Pubmed abstracts for Protein-Protein Interaction search result :

Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.87462976
Activation of ERK was dependent on its protein protein assembly with FAK and c Src at focal adhesion complexes . 0.87462976^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Pretreatment of astrocytes with cytochalasin D or C 3 transferase , which inhibits actin polymerization or Rho activity , respectively , prevented the activation / phosphorylation of Src , FAK , and paxillin after ET 1 stimulation ; by contrast , the ERK pathway was not significantly affected . ^^^ This differential activation of FAK / Src and ERK pathways was also observed with astrocytes 10 and 60 min after replating on poly L ornithine precoated dishes . ^^^ Collectively , these findings indicate that activation of FAK and Src is dependent on actin cytoskeleton integrity , Rho activation , and adhesion to extracellular matrix , whereas ERK activation is independent of these intracellular events and seems to correlate with activation of the newly identified protein tyrosine kinase PYK 2 . ^^^ This study provides a demonstration of Rho and adhesion dependent activation of FAK / Src , which collaborates with adhesion independent activation of PYK2 / ERK for DNA synthesis in ET 1 stimulated astrocytes . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Attachment of cells to COL ( 1 ) stimulated tyrosine phosphorylation of focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) , a mitogen activated protein kinase ( MAPK ) , and enhanced MAPK activity . ^^^ Inhibition of tyrosine kinase by herbimycin A , destruction of focal adhesion by cytochalasin D , or overexpression of antisense FAK mRNA prevented the activation of ERK / MAPK and the increase in alkaline phosphatase ( ALP ) activity . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
FAK ( F397Y ) , which encodes a dominant negative mutant of FAK , attenuated the shear stress induced kinase activity of Myc epitope tagged ERK 2 and hemagglutinin epitope tagged JNK 1 . ^^^ These results demonstrate that FAK signaling is critical in the shear stress induced dual activation of ERK and JNK . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We have investigated the role of two GPCR regulated tyrosine phosphoproteins , p 125 ( FAK ) ( FAK ) and Shc , in the Ras dependent activation of Erk kinases by endogenously expressed GPCRs in Rat 1a fibroblasts . ^^^ In each case , the rapid stimulation of Erk 1 / 2 correlates with tyrosine phosphorylation of Shc but not of FAK . ^^^ The dissociation of FAK Grb 2 complex formation from receptor mediated activation of Erk 1 / 2 indicates that recruitment of Grb 2 mSos to the plasma membrane is not sufficient to mediate rapid Erk activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Pretreatment of MC3T3 E 1 cells with cytochalasin D completely prevented FAK and paxillin tyr phos without any alteration in the tyr phos of Shc proteins and activation of ERK 2 induced by AlFx . ^^^ This observation suggests that in confluent MC3T3 E 1 cells , there is no link between the activation of FAK induced by AlFx and the stimulation of ERK 2 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We have previously shown that IGF 1 activates the tyrosine phosphorylation of focal adhesion kinase ( FAK ) and extracellular signal regulated protein kinase ( ERK ) 2 . ^^^ Therefore , it is likely that FAK and ERK 2 tyrosine phosphorylations are regulated by separate pathways during IGF 1 signaling . ^^^ Our study suggests that integrity as well as dynamic motility of the actin cytoskeleton mediated by PI 3 K is required for IGF 1 induced FAK tyrosine phosphorylation , but not for ERK 2 activation . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Biochemical analyses indicated that FAK mutant DeltaC 14 was mislocalized and functioned as a dominant negative mutant by competing with endogenous FAK in focal contacts for binding signaling molecules such as Src and Fyn , resulting in a decreases of Erk activation in cell adhesion . ^^^ Consistent with this , we also observed inhibition of BrdU incorporation and Erk activation by FAK Y397F mutant and FRNK , but not FRNKDeltaC 14 , in transient transfection assays using primary human foreskin fibroblasts . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Endothelin 1 ( ET 1 ) mitogenic activity in astrocytes is mediated by the activation of the extracellular signal regulated kinase ( ERK ) pathway together with the Rho dependent activation of the focal adhesion kinase ( FAK ) pathway . ^^^ Selective disassembly of caveolae by filipin 3 impairs the ET 1 induced tyrosine phosphorylation of proteins including ERK and FAK . ^^^ This study reveals that structural integrity of caveolae is necessary for the adhesion dependent mitogenic signals induced by ET 1 in astrocytes , through compartmentation of ETB R with the upstream signaling molecules of the ERK and FAK pathways . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We found that pulsatile stretch rapidly phosphorylated p44 / p42 MAPKs ( extracellular signal regulated protein kinase [ ERK ] 1 / 2 ) , stress activated protein kinase ( SAPK ) , p38MAPK , and p 125 ( FAK ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
In response to adhesion on a fibronectin substrate , RPTPalpha / fibroblasts also exhibited characteristic deficiencies in integrin mediated signalling responses , such as decreased tyrosine phosphorylation of the c Src substrates Fak and p 130 ( cas ) , and reduced activation of extracellular signal regulated ( Erk ) MAP kinases . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
This enables FAK to function within a network of integrin stimulated signaling pathways leading to the activation of targets such as the ERK and JNK / mitogen activated protein kinase pathways . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We show here that the activation of FAK by anchoring to the cell membrane is itself sufficient to stimulate potently both ERK and JNK . ^^^ These effects were found to be phosphatidylinositol 3 kinase independent , as FAK effectively stimulated Akt , and wortmannin suppressed Akt but not ERK or JNK activation . ^^^ As previously reported by others , activation of ERK correlated with the ability of FAK to induce tyrosine phosphorylation of Shc . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
This resulted in a marked inhibition of PDGF induced FAK tyrosine phosphorylation together with the expected reduction of PDGF induced extracellular signal regulated kinase activity ( ERK ) . ^^^ PDGF induced FAK tyrosine phosphorylation , ERK activity and intracellular calcium increase , as well as the biological effects of this growth factor , ( i . e . , mitogenesis and cell migration ) were effectively blocked by GGTI 298 , an inhibitor of geranylgeranyltransferase 1 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Exposure of the cells to two structurally unrelated mitogen activated protein kinase or ERK kinase ( MEK ) inhibitors , PD 98059 and U 0126 , completely abrogated ERK activation but did not prevent tyrosine phosphorylation of p 125 ( Fak ) , p 130 ( Cas ) , and paxillin . ^^^ Thus , our results demonstrate that the activation of the ERK pathway is not necessary for the increase of the tyrosine phosphorylation of p 125 ( Fak ) , p 130 ( Cas ) , and paxillin induced by either GPCRs or tyrosine kinase receptors in Swiss 3T3 cells . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We compared focal adhesion kinase ( FAK ) and paxillin protein and phosphorylation , extracellular signal regulated kinase ( ERK ) 1 , ERK 2 , and p 38 activation , as well as FAK and paxillin organization in static and migrating human intestinal Caco 2 cells on matrix proteins and anionically derivatized polystyrene dishes ( tissue culture plastic ) . ^^^ We also studied effects of FAK , ERK , and p 38 blockade in a monolayer wounding model . ^^^ Caco 2 motility was inhibited by transfection of FRNK ( the COOH terminal region of FAK ) and PD 98059 , a mitogen activated protein kinase ERK kinase inhibitor , but not by SB 203580 , a p 38 inhibitor , suggesting that FAK and ERK modulate Caco 2 migration . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Both HA and F 1 induced tyrosine phosphorylation of p 125 ( FAK ) , paxillin , and p42 / 44 ERK in HMVEC L and HPAEC , which was blocked by an anti RHAMM antibody . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
In addition , Pyk 2 and FPhy 2 to a greater extent also inhibited Erk activation in cell adhesion whereas FAK and PFhy 1 stimulated it , suggesting a role for Erk activation in mediating differential regulation of cell cycle by Pyk 2 and FAK . ^^^ A role for Erk and JNK pathways in mediating the cell cycle regulation by FAK and Pyk 2 was also confirmed by using chemical inhibitors for these pathways . ^^^ This suggested that they may inhibit Erk activation in an analogous manner as the mislocalized FAK mutant ( & Dgr ; ) C 14 described previously by competing with endogenous FAK for binding signaling molecules such as Src and Fyn . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
It has been proposed that integrins activate ERK through the adaptor protein Shc independently of focal adhesion kinase ( FAK ) or through FAK acting on multiple target effectors , including Shc . ^^^ We show that disruption of the actin cytoskeleton by cytochalasin D causes a complete inhibition of FAK but does not inhibit Shc signaling and activation of ERK . ^^^ Analysis of these cells indicates that FAK is not necessary for efficient tyrosine phosphorylation of Shc , association of Shc with Grb 2 , and activation of ERK in response to matrix adhesion . ^^^ In addition , integrin mediated activation of FAK does not appear to be required for signaling to ERK following growth factor stimulation . ^^^ To examine if FAK could contribute to the activation of ERK in a cell type specific manner through the Rap1 / B Raf pathway , we have used Swiss 3T3 cells , which in contrast to primary fibroblasts express B Raf . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Expression of the C terminal domain of Pyk 2 or of FAK is sufficient to block neurite outgrowth , but not activation of extracellular signal regulated kinase ( ERK ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Integrin initiated extracellular signal regulated kinase ( ERK ) activation by matrix adhesion may require focal adhesion kinase ( FAK ) or be FAK independent via caveolin and Shc . ^^^ FAK , ERK , and p 130 ( cas ) tyrosine phosphorylation were activated after 10 min adhesion to collagen 4 . ^^^ Transfection with FAK related nonkinase , but not substrate domain deleted p 130 ( cas ) , strongly inhibited ERK 2 activation in response to collagen 4 , indicating Caco 2 ERK activation is at least partly regulated by FAK . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We , therefore , investigated the organization of actin , FAK , paxillin , and activated ERK and activated p 38 during Caco 2 motility across collagen 1 , fibronectin , laminin , and tissue culture treated glass . ^^^ Expression of actin , FAK , paxillin , phospho ERK , and phospho p 38 were examined by immunofluorescent staining in static and motile cells . ^^^ Like FAK , phosphorylated ERK was expressed in the central region of migrating cells but was dramatically decreased at areas of cell cell contact and free lamellipodia . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Abbreviations : CAS , CRK associated substrate ; CH , calponin homology domain ; CSK , C terminal SRC kinase ; E 6 , Papillomavirus E 6 protein ; FAK , focal adhesion kinase ; GIT , GRK interacter ; GPCR , heterotrimeric G protein coupled receptor ; GRK , G protein coupled receptor kinase ; MAPK , mitogen activated protein kinase ( ERK , p 38 , JNK ) ; PAK , p 21 activated kinase ; PBS , paxillin binding subdomain ; PIX , PAK interacting exchange factor ; PKL , paxillin kinase linker ; POR 1 , partner of Rac ; PS , phosphoserine ; PT , phosphothreonine ; PY , phosphotyrosine ; RTK , growth factor receptor tyrosine kinase ; SH , SRC homology domain . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Receptor tyrosine kinases , FAK , Gbetagamma , and beta arrestin , which were implicated in some G protein coupled receptor signaling to MAPK cascades , do not play a role in the GnRH to ERK pathway . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Strain rapidly and time dependently activated focal adhesion kinase ( FAK ) , paxillin , ERK 1 and 2 , and p 38 on collagen . c Jun NH ( 2 ) terminal kinase ( JNK ) 1 and 2 exhibited delayed activation . ^^^ FAK inhibition by FAK 397 transfection blocked ERK 2 and JNK 1 activation by in vitro kinase assays , but pharmacological protein kinase C inhibition did not block ERK 1 or 2 activation by strain . ^^^ Strain induced ERK signals mediate strain ' s mitogenic effects and may require integrins and FAK activation . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The reduced survival of G1E ER 2 cells on FN H 296 correlated with reduced activation of Akt and expression of Bcl 2 and Bcl 10 ( L ) , whereas increase in proliferation on FN CH 271 correlated with significantly enhanced and sustained activation of focal adhesion kinase ( FAK ) and extracellular regulated kinase ( ERK ) pathways . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The protrusive phase and full development of integrin dependent adhesions in colon epithelial cells require FAK and ERK mediated actin spike formation : deregulation in cancer cells . ^^^ Furthermore , phosphorylated ERK was targeted to newly forming cell matrix adhesions in the carcinoma cells but not the adenoma cells , and inhibition of FAK tyrosine 397 phosphorylation or MEK suppressed the appearance of phosphorylated ERK at peripheral sites . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
However , beta 1 and beta 4 integrin mediated differentiation of PaTu 2 cells was independent from FAK , ERK , and JNK activation levels . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We investigated the role of tyrosine phosphorylation of FAK in the stretch induced MAPKs ( extracellular signal regulated kinase ( ERK ) , p38MAPK ) activation in mutant FAK transfected fibroblasts . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Finally , we showed that FAK regulation of cyclin D 1 depends on integrin mediated cell adhesion and is likely through its activation of the Erk signaling pathway . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Several potential ERK phosphorylation sites in paxillin flank the paxillin FAK association domains , so the ability of HGF to regulate paxillin FAK association was examined . ^^^ HGF induced an increase in paxillin FAK association that was inhibited by pretreatment with U 0126 and reproduced by in vitro phosphorylation of paxillin with ERK . ^^^ Thus , these data suggest that HGF can induce serine / threonine phosphorylation of paxillin most probably mediated directly by ERK , resulting in the recruitment and activation of FAK and subsequent enhancement of cell spreading and adhesion . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We investigated the influence of stretch and contractile activity on load induced activation of focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) 1 / 2 in isolated rat hearts . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Integrin activation by cell adhesion to fibronectin increased the phosphorylation level of focal adhesion kinase ( FAK ) upstream of the ERK pathway . angiotensin 2 induced a high increase in the phosphorylation level of FAK with integrin activation , but not in suspended cells . ^^^ These results suggest that simultaneous stimulation of integrin and angiotensin 2 receptors cause synergistic interaction in the activation of ERK pathway , possibly via phosphorylation of FAK , which may play a critical role in angiotensin 2 mediated mitogenic response in VSMCs . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Downstream signals of collagen integrin might be FAK Ras extracellular signal regulated kinase ( ERK ) in osteoblastic cells . ^^^ These observations suggest that the Ras ERK pathway downstream of integrin FAK is involved in Smad 1 signals activated by BMP and provide a possible mechanism for cooperation between intracellular signals activated by integrin and BMPRs in osteoblastic cells . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
OPN and PDGF synergistically activated focal adhesion kinase ( FAK ) , as well as extracellular signal regulated kinase ( ERK ) , which seems to be a reason for OPN induced enhancement of PDGF mediated DNA synthesis . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
ETs stimulated astroglial proliferation by both adhesion dependent and independent mechanisms , where FAK and ERK plays key roles , respectively . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
These cells overexpress urokinase receptor ( uPAR ) which , by activating alpha5beta1 integrin , initiates an intracellular signal through FAK and Src leading to ERK activation and tumorigenicity in vivo . ^^^ The FAK signaling pathway in T HEp 3 cells , measured by FAK phosphorylation , GTP loaded Ras and ERK activation , was inhibited by transient or stable transfection of FAK related non kinase ( FRNK ) , known to have a dominant negative function , but not by a FRNK mutant version ( S 1034 FRNK ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
PDGF BB also induced activation of p 38 MAP kinase , its downstream effector , heat shock protein ( HSP ) 27 , ERK 1 and ERK 2 , and p 125 focal adhesion kinase ( FAK ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Endostatin blocked VEGF induced tyrosine phosphorylation of KDR / Flk 1 and activation of ERK , p 38 MAPK , and p 125 ( FAK ) in human umbilical vein endothelial cells . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
In a manner independent of Met , beta ( 4 ) integrin mCLCA 1 ligation leads to complexing with and activation of focal adhesion kinase ( FAK ) and downstream signaling to extracellular signal regulated kinase ( ERK ) . ^^^ FAK / ERK signaling is Src dependent and is interrupted by adhesion blocking antibodies and by dominant negative ( dn ) FAK mutants . ^^^ Levels of ERK activation in B 16 F10 cells transfected with wild type or mutant FAK are closely associated with rates of proliferation and bromodeoxyuridine ( BrdUrd ) incorporation of tumor cells grown in mCLCA 1 coated dishes , the ability to form tumor cell colonies on CLCA expressing endothelial cell monolayers , and the extent of pulmonary metastatic growth . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Therefore , expression and phosphorylation of these kinases was determined 48 h after AII treatment , revealing a significant increase in Pyk 2 and FAK protein levels ( up to 2 fold , both p < 0 . 05 ) and increased phosphorylation of Pyk 2 ( 2 fold , p < 0 . 05 ) and ERK 1 / 2 ( 4 fold , p < 0 . 05 ) as compared to controls . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Inhibition of ERK activation during reoxygenation with U 0126 , an inhibitor of the ERK activator , MAPK / ERK kinase 1 / 2 , prevented both barrier restoration and stress fibre formation , but did not prevent recruitment of FAK to focal contacts . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Sachs et al . illustrate the application of Bayesian networks to an example cellular pathway involving the activation of focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) in response to fibronectin binding to an integrin . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Experimental clustering of chimeras containing integrin beta cytoplasmic domains or FAK induced FAK tyrosine phosphorylation and trans phosphorylation of endogenous FAK , as well as strong ERK activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Moreover , FAK overexpression was able to enhance HGF elicited signals , leading to sustained activation of ERK , JNK , and AKT , which could be prevented by the expression of the Src homology 3 domain of p 130 ( cas ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The effect of HFG / SF on cell growth , motility , and phosphorylation of the signaling proteins FAK and Erk was determined . ^^^ Incubation of FaDu cells in the presence of HGF / SF led to a rapid increase in phosphorylation of both FAK and the growth promoting kinase Erk . ^^^ HGF / SF induced phosphorylation of FAK and Erk was observed in both detached and attached SCCHN cells . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Furthermore , cell adhesion was abolished when we used a recombinant LAP TGFbeta 1 protein in which the RGD site was mutated to RGE . alpha8beta1 binding to LAP TGFbeta 1 increased cell proliferation and phosphorylation of FAK and ERK , but did not activate of TGFbeta 1 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
FRNK expression disrupted the formation of a 5 Src FAK signaling complex , inhibited p130Cas tyrosine phosphorylation , and attenuated 5 Src stimulated ERK and JNK kinase activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Although integrin reportedly regulates the transcription of the IRS 1 gene via FAK mediated JNK activation , no impairment of fibronectin stimulated activation of FAK , ERK , or JNK was observed in MEKK 1 deficient cells . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
To investigate the intracellular signaling pathways involved in this process , we examined the effects of UII on activation of extracellular signal regulated kinase ( ERK ) and focal adhesion kinase ( FAK ) in VSMCs . ^^^ On the other hand , UII induced an increase in the phosphorylation level of ERK , but not FAK , in cells adherent to fibronectin . ^^^ Our results suggested that activation of integrin mediated signaling pathways play a critical role in UII induced phosphorylation of ERK , leading to proliferation of VSMCs , which does not involved increased phosphorylation of FAK . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Because gonadotropin releasing hormone analogue ( GnRHa ) therapy often causes leiomyoma regression , in part through alteration of growth factor and receptor expression , we determined whether GnRHa therapy alters the expression of extracellular signal regulated kinase ( ERK ) and focal adhesion kinase ( FAK ) , which are linked to intracellular signaling pathways activated by ovarian steroids , growth factors , and adhesion molecules . ^^^ We determined the expression of ERK 1 , ERK 2 , FAK , phosphorylated ERK ( pERK1 / 2 ) , and pFAK using Western blotting and immunohistochemical analysis . ^^^ Leiomyoma and myometrium expressed ERK 1 ( 44 kD ) , ERK 2 ( 42 kD ) , and FAK ( 125 kD ) at variable levels with increased ERK 2 , pERK , and FAK expression in leiomyoma . ^^^ We found that GnRHa therapy resulted in a noticeable decrease in ERK 2 and FAK , with significant reduction in pERK1 / 2 and low or undetectable levels of pFAK in both leiomyoma and myometrium compared with the untreated group ( P < . 05 ) . ^^^ Immunohistochemically ERK 1 , ERK 2 , FAK , pERK1 / 2 , and pFAK were localized in smooth muscle cells and connective tissue fibroblasts in GnRHa treated and untreated leiomyoma and myometrium , with considerable reduction in their intensity as indicated by HScore in GnRHa treated tissues . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Phosphorylation of extracellular signal regulated kinase ( ERK ) and focal adhesion kinase ( FAK ) was increased by BMP 4 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Cells that overexpress FRNK have reduced adhesion mediated tyrosine phosphorylation of FAK with a coincident decrease in ERK phosphorylation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Treatment with the ERK inhibitors U 0126 and PD 98059 prevented FAK phosphorylation at Ser 910 in response to all of the stimuli tested . ^^^ Furthermore , incubation of activated ERK 2 with FAK immunocomplexes leads to FAK phosphorylation at Ser 910 in vitro . ^^^ Our results demonstrate , for the first time , that stimulation with bombesin , lysophosphatidic acid , PDB , or EGF induces phosphorylation of endogenous FAK at Ser 910 via an ERK dependent pathway in Swiss 3T3 cells . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The phosphorylation statuses of focal adhesion kinase ( FAK ) , extracellular signal regulated kinase ( ERK ) , p 38 , and c Jun amino terminal kinase ( JNK ) were also determined in NHOK cells cultured on ECM proteins , to evaluate the functions of integrins with respect to cellular responses to ECM proteins . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
An integrin inhibitory peptide with an RGD motif blocked TUDC induced FAK , Src , ERK , and p 38 ( MAPK ) activation , suggesting that integrin signaling toward FAK / Src is required for TUDC induced MAPK activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
FAK deficiency did not affect the three types of mitogen activated protein kinases , ERK , JNK , and p 38 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Cytochalasin D , which inhibits protein I / II induced phosphorylation of FAK ( Tyr 397 ) , had no effect either on activation of ERK 1 / 2 and JNKs or on IL 6 and IL 8 release . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
By examining the role of FAK involved in LTP induction in dentate gyrus in vivo with medial perforant path stimulation , we found that both FAK and mitogen activated protein kinase ( MAPK ) / extracellular signal regulated kinase ( ERK ) phosphorylation were increased significantly 5 and 10 min after LTP induction , whereas cAMP responsive element binding protein ( CREB ) phosphorylation was increased 40 min later . ^^^ Further , transfection of the HA FAK ( Y397F ) construct decreased FAK , MAPK / ERK , and CREB phosphorylation , and the inhibition of MAPK / ERK decreased CREB phosphorylation . ^^^ Moreover , blockade of NMDA receptor ( NMDAR ) did not decrease FAK , MAPK / ERK , and CREB phosphorylation although LTP induction was blunted by NMDAR antagonist . ^^^ These results together suggest that FAK is required , but not sufficient , for the induction of LTP in a NMDAR independent manner and that MAPK / ERK and CREB are the downstream events of FAK activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The available data suggests that increased levels of FAK protein and activity may contribute to an increased ERK activity and cell proliferation in vivo in these tumors . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Tyr / Phe deprivation inhibits expression and phosphorylation of focal adhesion kinase ( FAK ) and extracellular regulated kinase ( ERK ) in DU 145 but not PC 3 or normal cells . ^^^ Met deprivation inhibits phosphorylation but not protein expression of FAK and ERK in PC 3 . ^^^ Therefore , apoptosis of DU 145 and PC 3 cells by amino acid restriction is FAK and ERK dependent . ^^^ The inhibition of invasion by Tyr / Phe restriction in DU 145 and Met restriction in PC 3 is consistent with the inhibition on FAK / ERK signaling . ^^^ The inhibition of Tyr / Phe restriction in PC 3 and Gln restriction in DU 145 is not associated with inhibition of FAK / ERK . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
A novel role for FAK as a protease targeting adaptor protein : regulation by p 42 ERK and Src . ^^^ ERK / MAP kinase mediated activation of the protease Calpain 2 also promotes focal adhesion turnover ; however , it is not known if this is linked to the activities of Src and FAK . ^^^ We show that both complex formation and MEK / ERK activity are associated with Calpain mediated proteolysis of FAK and focal adhesion turnover during transformation and migration . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Multiple kinases , such as focal adhesion kinase ( FAK ) , Ras extracellular signal regulated kinase ( ERK ) , phosphatidylinositol 3 kinase ( PI3K ) , and Akt serine / threonine kinase were related to Smads signal transduction . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Compared with GEC on plastic substratum , adhesion to collagen increased activation of focal adhesion kinase ( FAK ) , c Src , and ERK and facilitated survival ( prevented apoptosis ) . ^^^ Stable expression of constitutively active mutants of FAK ( CD 2 FAK ) or MEK ( R4F MEK ) activated the ERK pathway and supplanted the requirement of collagen for survival . ^^^ Glomeruli isolated from rats with PAN revealed increased beta 1 integrin expression , along with increased activation of FAK , c Src , and ERK , compared with controls . ^^^ Therefore , adhesion to collagen , resulting in activation of FAK and the Ras ERK pathway , supports GEC survival . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Human intestinal epithelial crypt cell survival and death : Complex modulations of Bcl 2 homologs by Fak , PI 3 K / Akt 1 , MEK / Erk , and p 38 signaling pathways . ^^^ Pharmacological inhibitors and / or dominant negative constructs were used to inhibit focal adhesion kinase ( Fak ) and p 38 isoforms , as well as the phosphatidylinositol 3 ' kinase ( PI 3 K ) / Akt 1 and mitogen activated protein kinase [ MAPK ] kinase ( MEK ) / extracellular regulated kinases ( Erk ) pathways . ^^^ Herein , we report that beta 1 integrins , Fak , and the PI 3 K / Akt 1 pathway , but not beta 4 integrins or the MEK / Erk pathway , are crucial for the survival of HIEC 6 cells . ^^^ These results indicate that integrins , Fak , PI 3 K / Akt 1 , MEK / Erk , and p 38 isoforms perform distinct roles in the regulation of HIEC 6 cell survival and / or death . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Our previous work indicates intestinal epithelial cell ERK activation by collagen 4 , a major component of the intestinal epithelial basement membrane , requires focal adhesion kinase ( FAK ) and suggests FAK and ERK may have important roles in regulating intestinal epithelial cell migration . ^^^ We therefore sought to identify FAK downstream targets regulating intestinal epithelial cell spreading , migration , and ERK activation on collagen 4 and the integrins involved . ^^^ Additionally , FAK Y925F expression blocked collagen 4 ERK activation . alpha ( 1 ) beta ( 1 ) Or alpha ( 2 ) beta ( 1 ) integrin blockade with alpha ( 1 ) or alpha ( 2 ) integrin subunit antibodies indicated that either integrin can mediate adhesion , cell spreading , and FAK , Src , and ERK activation on collagen 4 . ^^^ These results suggest a pathway for collagen 4 ERK activation requiring Src phosphorylation of FAK Y 925 not previously described for this matrix protein and suggest either alpha ( 1 ) beta ( 1 ) or alpha ( 2 ) beta ( 1 ) integrins can regulate Caco 2 spreading and ERK activation on collagen 4 via Src . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The expression of a C terminal splice variant of FAK , FRNK , had no affect on VEGF induced activation of p 38 ; however , expression of a dominant negative RAFTK / Pyk2 mutant led to a decrease in the activation of p 38 , but had no affect on extracellular signal regulated kinase ( ERK ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We assessed binding affinity by detachment assay ; integrin surface expression by flow cytometry ; and focal adhesion kinase ( FAK ) , Src , and extracellular signal regulated kinase ( ERK ) activation by Western analysis and Src in vitro kinase assay . ^^^ Pressure activated SW 620 FAK and Src , but not ERK . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
FAK Src signalling through paxillin , ERK and MLCK regulates adhesion disassembly . ^^^ Using these assays , we show that kinases and adaptor molecules , including focal adhesion kinase ( FAK ) , Src , p130CAS , paxillin , extracellular signal regulated kinase ( ERK ) and myosin light chain kinase ( MLCK ) are critical for adhesion turnover at the cell front , a process central to migration . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Extracellular pressure stimulates macrophage phagocytosis by inhibiting a pathway involving FAK and ERK . ^^^ We hypothesized that changes in extracellular pressure during inflammation or infection regulate macrophage phagocytosis through modulating the focal adhesion kinase ( FAK ) ERK pathway . ^^^ THP 1 macrophages constitutively expressed activated FAK , ERK , and Src . ^^^ Exposure of macrophages to pressure decreased ERK and FAK Y 397 phosphorylation ( 77 . 6 + / 7 . 9 % , n = 7 , P < 0 . 05 ) but did not alter FAK Y 576 or Src phosphorylation . ^^^ Pressure also inhibited ERK activation after mock transfection or transfection with scrambled SiRNA , but transfection of FAK SiRNA abolished ERK inhibition by pressure . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
AC 100 increased cell proliferation and alkaline phosphatase activity and activated focal adhesion kinase ( FAK ) and extracellular signal regulated protein kinase ( ERK ) in human primary osteoblasts . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Vinculin modulation of paxillin FAK interactions regulates ERK to control survival and motility . ^^^ Thus , vinculin regulates survival and motility via ERK by controlling the accessibility of paxillin for FAK interaction . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
PDGF and FGF induce focal adhesion kinase ( FAK ) phosphorylation at Ser 910 : dissociation from Tyr 397 phosphorylation and requirement for ERK activation . ^^^ Conversely , treatment with U 0126 , a potent inhibitor of MEK mediated ERK activation , prevented FAK phosphorylation at Ser 910 induced by PDGF but did not interfere with PDGF induced FAK phosphorylation at Tyr 397 . ^^^ FGF but not insulin promoted a striking ERK dependent phosphorylation of FAK at Ser 910 . ^^^ Our results indicate that FAK phosphorylation at Tyr 397 and FAK phosphorylation at Ser 910 are induced in response to PDGF stimulation through different signaling pathways , namely PI 3 kinase and ERK , respectively . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The expression of beta ( 1 ) integrin receptor , as well as Src , son of sevenless protein ( SOS ) and phosphorylated mitogen activated protein ( MAP ) kinases ( MAPK ) , extracellular signal regulated kinase 1 ( ERK ( 1 ) ) and kinase 2 ( ERK ( 2 ) ) but not focal adhesion kinase pp 125 ( FAK ) ( FAK ) , Shc , and Grb 2 was significantly decreased in cells incubated for 24 h with 10 microM AB ( 1 ) compared to the control , whereas in the same conditions chlorambucil did not evoke any changes in expression of all these signaling proteins , as shown by Western immunoblot analysis . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Melanoma chondroitin sulfate proteoglycan enhances FAK and ERK activation by distinct mechanisms . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Caspase 8 activity was reduced in cells cultured on matrix , whereas focal adhesion kinase ( FAK ) , protein kinase B ( PKB , or Akt ) , and extracellular signal regulated kinase ( ERK ) phosphorylation was augmented . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We also show that alpha 3 beta 1 mediated adhesion activates focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) , and that inhibition of either FAK or ERK signaling leads to apoptosis of keratinocytes attached to laminin 5 . alpha 6 beta 4 mediated adhesion to laminin 5 only partially protects cells from apoptosis in the absence of alpha 3 beta 1 , and alpha 6 beta 4 is not necessary for cell survival in the presence of alpha 3 beta 1 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
RhoE expressing cells failed to accumulate cyclin D 1 or p 21 ( cip 1 ) protein or to activate E2F regulated genes in response to serum , although ERK , PI 3 K / Akt , FAK , Rac , and cyclin D 1 transcription was activated normally . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Focal adhesion kinase ( FAK ) regulates adhesion dynamics , acting in part by modulating RhoA activity , and FAK is implicated in ERK and PI 3 kinase activation . ^^^ TSP1 / hep 1 stimulates a transient increase in FAK phosphorylation that requires calreticulin and Galphai , but not ERK or PI 3 kinase . ^^^ Hep 1 does not activate ERK or PI 3 kinase in FAK knockout fibroblasts , suggesting activation occurs downstream of FAK . ^^^ TSP1 / hep 1 stimulates RhoA inactivation with kinetics corresponding to focal adhesion disassembly in a FAK , ERK , and PI 3 kinase dependent manner . ^^^ This is the first work to illustrate a connection between FAK phosphorylation in response to a soluble factor and RhoA inactivation , as well as the first report of PI 3 kinase and ERK in FAK regulation of RhoA activity . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Erk governs cell movement by phosphorylating myosin light chain kinase ( MLCK ) , calpain or FAK . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The actin cytoskeleton disruptor , cytochalasin D ( 20 microM ) , abolished FAK phosphorylation in response to CCh but did not alter CCh induced EGFr or ERK MAPK activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Paxillin serves as an ERK regulated scaffold for coordinating FAK and Rac activation in epithelial morphogenesis . ^^^ In the present study we demonstrate that activated ERK phosphorylates paxillin on serine 83 and that mutation of this site eliminates HGF stimulated increased association of paxillin and FAK in subconfluent cells . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
However , integrin beta 1 is not required for cell growth or activation of FAK and ERK signalling in vitro or in vivo . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We have previously demonstrated that constant 20 mmHg extracellular pressure increases serum opsonized latex bead phagocytosis by phorbol 12 myristate 13 acetate ( PMA ) differentiated THP 1 macrophages in part by inhibiting focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) . ^^^ SB 203580 did not affect basal or pressure reduced FAK activation in THP 1 macrophages , but significantly attenuated the reduction in ERK phosphorylation associated with pressure . p 38 MAPKalpha siRNA reduced total FAK protein by 40 50 % , and total ERK by 10 15 % , but increased phosphorylated ERK 1 . 4 + / 0 . 1 fold . p 38 MAPKalpha siRNA transfection did not affect the inhibition of FAK Y 397 phosphorylation by pressure but prevented inhibition of ERK phosphorylation . ^^^ Changes in extracellular pressure during infection or inflammation regulate macrophage phagocytosis by a FAK dependent inverse effect on p 38 MAPKalpha that might subsequently downregulate ERK . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
In order to determine the mechanism of increased FAK production , we investigated the relationship of FAK production and ERK activation . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The oligomerization promotes integrin clustering , thereby increasing cell adhesion , spreading , formation of prominent peripheral focal contacts , and integrin mediated activation of focal adhesion kinase ( FAK ) and extracellular signal regulated kinase ( ERK ) signaling pathways . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Prolidase activity and collagen biosynthesis are supposed to be regulated by beta ( 1 ) integrins , which initiate a signaling pathway in which several kinases and intracellular proteins are involved , including focal adhesion kinase pp 125 ( FAK ) ( FAK ) , Src , Shc , growth factor receptor bound protein 2 ( Grb 2 ) , son of sevenless protein ( SOS ) , Ras , Raf and mitogen activated protein kinases ( MAPK ) , extracellular signal regulated kinase 1 ( ERK ( 1 ) ) and kinase 2 ( ERK ( 2 ) ) . ^^^ We studied the effects of echistatin , a well known disintegrin and thrombin , a serine protease capable of activation of platelet integrin alpha ( 2 ) beta ( 1 ) receptor on collagen production , prolidase activity , expression of prolidase , beta ( 1 ) integrin receptor , FAK , SOS protein and phosphorylated MAP kinases ( ERK ( 1 ) and ERK ( 2 ) ) in confluent human dermal fibroblasts . ^^^ These phenomena were accompanied by a decrease in the expression of FAK , SOS protein and phosphorylated MAP kinases , ERK ( 1 ) and ERK ( 2 ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Signal transduction molecules activated by these neuropeptides include Src , focal adhesion kinase ( FAK ) , ERK , and PI3K / Akt , with subsequent activation of Elk 1 , NF kappaB , and c myc transcription factors . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
PP 2 and RGD peptide also inhibited high pressure induced binding of FAK with the effector Grb 2 and blocked activation of extracellular regulated kinase ( ERK ) 1 / 2 in vessels at 150 mm Hg . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
DFMO did not affect phosphorylation of FAK or Akt , but increased ERK phosphorylation by approximately threefold . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Here , cannabinergic activation of extracellular signal regulated kinase ( ERK ) and focal adhesion kinase ( FAK ) occurred correspondingly in long term hippocampal slice cultures . ^^^ Both events of ERK and FAK activation were selectively blocked by N ( morpholin 4 yl ) 1 ( 2 , 4 dichlorophenyl ) 5 ( 4 iodophenyl ) 4 methyl 1H pyrazole 3 carboxamide ( AM 281 ) , a cannabinoid CB 1 receptor antagonist , and the blockage was associated with a gradual decline in synaptic markers . ^^^ Interestingly , the integrin antagonist Gly Arg Gly Asp Ser Pro also caused the disruption of R methanandamide mediated ERK and FAK responses and upset the integrity of excitatory synapses . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Both the focal adhesion kinase ( FAK ) and the extracellular signal regulated kinase / activated mitogen activated protein kinase ( ERK / MAPK ) signaling pathways are required for efficient cell migration . ^^^ Cells adherent to FBG were lysed and analyzed for FAK and ERK / MAPK activation by immunoblotting followed by image analysis densitometry . ^^^ Inhibition of alphavbeta 3 mediated migration by the integrin alpha5beta1 correlates with altered intensity and duration of ERK / MAPK activation , but not FAK activation , in response to adhesion . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
These effects were explained in part by our observation in endothelial cells that Sema ECD inhibited VEGF mediated Src , FAK and ERK phosphorylation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The phosphorylation of focal adhesion kinase ( FAK ) was decreased by treatment with PPARgamma antagonists , and resulted in decreases in phosphorylation of Erk and mitogen activated protein kinase . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Hyposmolarity also activated the non receptor tyrosine kinases , Src , focal adhesion kinase ( FAK ) , extracellular signal regulated protein kinase ( ERK ) 1 / 2 , and the tyrosine kinase target phosphatidyl inositol 3 kinase ( PI3K ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Pkhd 1 silenced cells developed abnormalities in cell cell contact , actin cytoskeleton organization , cell ECM interactions , cell proliferation , and apoptosis , which may be mediated by dysregulation of extracellular regulated kinase ( ERK ) and focal adhesion kinase ( FAK ) signaling . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Adhesion of rat glomerular epithelial cells ( GEC ) to collagen activates focal adhesion kinase ( FAK ) and the Ras extracellular signal regulated kinase ( ERK ) pathway and supports survival ( prevents apoptosis ) . ^^^ Parental GEC ( adherent to collagen ) and GEC stably transfected with constitutively active mutants of mitogen activated protein kinase kinase ( R4F MEK ) or FAK ( CD 2 FAK ) ( on plastic ) showed ERK activation , low levels of apoptosis , and a cortical distribution of F actin . ^^^ However , disruption of the actin cytoskeleton with cytochalasin D or latrunculin B in parental GEC ( on collagen ) and in GEC that express R4F MEK or CD 2 FAK ( on plastic ) decreased ERK activation and increased apoptosis . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We investigated the mechanism of collaboration between integrins and platelet derived growth factor ( PDGF ) in focal adhesion kinase ( FAK ) and extracellular signal related kinase ( ERK ) 1 / 2 mediated signal pathways that lead to monocyte chemoattractant protein ( MCP ) 1 expression in cultured rat mesangial cells ( MCs ) . ^^^ METHODS : Serum starved MCs were plated on fibronectin or polylysine coated plates with or without PDGF , and examined for phosphorylation of ERK1 / 2 , mitogen activated protein or ERK kinase ( MEK ) 1 / 2 and FAK by western blotting , and for expression of MCP 1 mRNA and protein by reverse transcription polymerase chain reaction ( RT PCR ) and enzyme linked immunosorbent assay ( ELISA ) , respectively . ^^^ CONCLUSIONS : Our results suggest the cooperative role of integrin and PDGF receptor in activation of the ERK pathway possibly via FAK in MCs . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
To investigate the possible mechanisms involved in these events , we performed Western blot analysis using phospho specific antibodies , and found that emodin inhibited phosphorylation of focal adhesion kinase ( FAK ) , extracellular regulated protein kinase ( ERK ) 1 / 2 and Akt / PKB ; emodin also suppressed the transcriptional activity of two transcription factors , activator protein 1 ( AP 1 ) and nuclear factor kappaB ( NF kappaB ) , in glioma cells . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Finally , PE treatment suppressed the active ( phosphorylated ) forms of VEGFR 2 , Akt , ERK , FAK and paxillin , which are involved in endothelial cell survival , proliferation , adhesion and migration . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
However , the expression of the Y397F mutant rendered 5 Src transformed FAK ( / ) cells susceptible to anoikis , correlated with suppression on 5 Src stimulated activation of ERK and AKT . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We have previously shown that RET signals through focal adhesion kinase ( FAK ) in medullary thyroid cancer cells and that extracellular signal regulated kinase ( ERK ) activity can be blocked by pp 2 , an inhibitor of both Src and RET . ^^^ We hypothesized that RET could directly phosphorylate FAK and ERK . ^^^ CONCLUSIONS : RET directly phosphorylates tyrosine residues on FAK , ERK 1 / 2 , DOK 1 , the p 85 subunit of of phosphatidylinositol 3 ' kinase , JNK 1 and 2 , P 38 , and phospholipase gamma . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Extracellularly regulated kinase ( ERK ) , Jun N terminal kinase ( JNK ) and phosphatidylinositol 3 kinase ( PI3K ) were found to be negatively involved in M CSF induced FAK phosphorylation , as their inhibition resulted in FAK hyper phosphorylation . ^^^ Following M CSF treatment , FAK and the active forms of M CSFR and Src were redistributed to the cytoskeleton , where active ERK , JNK and PI3K were detectable . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
When triggered by laminins , NEU 3 clearly stimulated phosphorylation of FAK ( focal adhesion kinase ) and ERK ( extracellular signal regulated kinase ) , whereas there was no activation on fibronectin . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
L 59 activated Src ( a known substrate of LAR ) , FAK and TrkB and also activated downstream signalling intermediates including PKC , ERK , AKT and CREB . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Acquisition of chemoresistance following discontinuous exposures to cisplatin is associated in ovarian carcinoma cells with progressive alteration of FAK , ERK and p 38 activation in response to treatment . ^^^ The simultaneous study of activation pattern of key proteins of different signaling pathways revealed that cisplatin induced both activation of ERK and p 38 and inhibition of P FAK in the sensitive cells , whereas it progressively failed to elicit such a response in the resistant variants . ^^^ CONCLUSIONS : Our results suggested that emergence of chemoresistance was accompanied with the progressive loss of ERK and p 38 activation and with the maintenance of FAK activation in response to cisplatin , and they demonstrated that these alterations were early events in the course of treatments . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
We show that Ang 2 interacts with alpha ( 5 ) beta ( 1 ) integrin in Tie 2 deficient human glioma cells , activating focal adhesion kinase ( FAK ) , p 130 ( Cas ) , extracellular signal regulated protein kinase ( ERK ) 1 / 2 , and c jun NH ( 2 ) terminal kinase ( JNK ) and substantially enhancing MMP 2 expression and secretion . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The alphav and beta 1 integrin , actin , FAK , and ERK gene expression were found to be different with adhesion time and with materials . ^^^ Indeed , the signal transduction pathways involved in adhesion of Saos 2 cells on HA and titanium were confirmed by the sequential expression of alphav and beta 1 integrins , FAK , and ERK genes followed by the expression of c jun and c fos genes for proliferation and alkaline phosphatase gene for differentiation . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Examination of focal adhesion kinase ( FAK ) , and extracellular signal regulated kinase ( ERK 1 / 2 ) , important mediators of adhesion and growth factor related signalling events , revealed a comparative reduction in phosphorylation of these signalling proteins in cells grown on co polymers in comparison to those cultured on tissue culture polystyrene ( TCP ; used as a control surface ) . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Ectopic expression of the FAK C terminal domain FRNK attenuated FAK and ERK phosphorylation and micromotion . ^^^ Further , cytochalasin D inhibited FAK phosphorylation and cleavage , cell adhesion , locomotion , and ERK phosphorylation , thus showing FAK activation downstream of actin assembly . ^^^ We also found a pivotal role for FAK Tyr ( 861 ) phosphorylation in cell motility and ERK activation . ^^^ Our results reveal a novel functional connection between integrin alpha 2 engagement , FAK , ERK , and mu calpain activation in cell motility and a direct link between FAK cleavage and enhanced cell motility . ^^^ The data suggest that blocking the integrin alpha2 / FAK / ERK / mu calpain pathway may be an important strategy to reduce cancer progression . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
BB 94 treatment promoted stable focal adhesion formation concomitant with enhanced phosphorylation of tyrosine 397 of focal adhesion kinase ( FAK ) and reduced ERK activation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
US stimulation increased the phosphorylation of focal adhesion kinase ( FAK ) , extracellular signal regulated kinases ( ERK ) , p 85 subunit of PI3K , and serine 473 of Akt . ^^^ Cotransfection with dominant negative mutant of FAK ( Y397F ) , p 85 ( Deltap 85 ) , Akt ( K179A ) , or ERK 2 ( K52R ) inhibited the potentiating action of US on COX 2 promoter activity . ^^^ Taken together , our results provide evidence that US stimulation increases COX 2 expression and promotes bone formation in osteoblasts via the integrin / FAK / PI3K / Akt and ERK signaling pathway . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
CCK stimulated an association of Lyn with PKC delta , Shc , p 125 ( FAK ) and PYK 2 as well as with their autophosphorylated forms , but not with Cbl , p 85 , p 130 ( CAS ) or ERK 1 / 2 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
The expression of beta ( 1 ) integrin receptor , as well as Sos 1 and phosphorylated MAPK , ERK ( 1 ) and ERK ( 2 ) but not FAK , Shc , and Grb 2 was significantly decreased in cells incubated for 24h with 20 microM AB 4 compared to the control , not treated cells , whereas in the same conditions melphalan did not evoke any changes in expression of all these signaling proteins , as shown by Western immunoblot analysis . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Specifically , osteogenesis on vitronectin correlated with enhanced focal adhesion formation , the activation of focal adhesion kinase ( FAK ) and paxillin , and the diminished activation of extracellular signal regulated kinase ( ERK ) and phosphatidylinositol 3 kinase ( PI3K ) pathways . ^^^ By contrast , MSCs on type 1 collagen exhibited reduced focal adhesion formation , reduced activation of FAK and paxillin , and increased activation of ERK and PI3K . ^^^ Inhibition of ERK and FAK blocked mineral deposition on both substrates , suggesting that the observed differences in signaling pathways ultimately converge to the same cell fate . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
FAK regulation of cell cycle progression in tumor cells requires Erk activity , cyclin D 1 transcription , and the cyclin dependent kinase ( cdk ) inhibitor p27Kip1 . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
In addition , HPSE unexposed cells did not phosphorylate extracellular signal related kinase ( ERK ) or focal adhesion kinase ( FAK ) in response to FGF 2 . ^^^ Conversely , in cells treated with HPSE , FGF 2 stimulated ERK and FAK phosphorylation . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
Immunoblotting analysis revealed that l CaD overexpression reduced PDGF induced phosphorylation of both FAK and extracellular signal regulated kinase ( ERK ) . ^^^ CONCLUSIONS : Overexpression of l CaD suppressed cell growth and survival in VSMCs and inhibited neointimal formation after experimental angioplasty , partly by regulating the cytoskeletal tension FAK ERK axis . . ^^^
Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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Interacting proteins: P29323 and Q05397	Pubmed	SVM Score :0.0
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