| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Furthermore , inhibition of PI3K , an upstream regulator in the JNK / SAPK pathway , decreased u PA promoter transcription . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| PI3K inhibitors dose dependently suppressed TGF beta 1 induced JNK , but not p 38 MAP kinase activation . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Furthermore , Nischarin does not affect Rac mediated JNK and PI3K activities . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| An upregulation of PI3K / AKT , Erk , and Jnk signaling pathways accompany these phenotypic changes . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| PI3K and JNK inhibitors had no effect . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Additionally , the beta 1 integrin downstream targets p130Cas and paxillin impaired survival regulating PI3K dependent JNK . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| JNK , p 38 ) able to overwhelm antiapoptotic signalling ( PI3K / Akt , Erk ) . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Only three phospho proteins ( JNK , p 38 , and PI3K ) have been previously shown to participate in stretch induced BSMC growth . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| However , this activation of NF kappaB requires the PI3K and PKC signaling pathways , but not ERK or JNK . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Treatment of BAEC with an inhibitor of PI3K , wortmannin , inhibited shear dependent activation of JNK but had no effect on that of ERK . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| In the MAPK family of kinases , ERK and JNK have been proposed to mediate apoptosis whereas the PI3K stimulated kinase , Akt / PKB , has been shown to inhibit apoptosis . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Analysis of three well defined signaling pathways , the mitogen activated protein kinase ( MAPK ) pathway , the Jun N terminal kinase ( JNK ) pathway , and the phosphoinositide 3 kinase ( PI3K ) / AKT pathway , demonstrated that only the PI3K / AKT pathway is constitutively activated in 5 Crk transformed CEF . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We have previously reported that NO triggers Ras activation and recruitment of an effector , phosphatidylinositol 3 ' kinase ( PI3K ) and Ras dependent activation of mitogen activated protein ( MAP ) kinases which include extracellular signal regulated kinases ( ERKs ) , c Jun NH ( 2 ) terminal kinase ( JNK ) , and p 38 MAP kinase . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Zn ( 2+ ) also induced stimulation of phosphoinositide 3 kinase ( PI3K ) The Zn ( 2+ ) induced JNK stimulation was blocked by LY 294002 , a PI3K inhibitor , or by a dominant negative mutant of PI3Kgamma . ^^^ The stimulatory effect of Zn ( 2+ ) on both PI3K and JNK was repressed by the free radical scavenging agent N acetylcysteine . ^^^ Taken together , our data suggest that Zn ( 2+ ) induces stimulation of the JNK signaling pathway through PI3K Rac 1 signals and that the free radical generation may be an important step in the Zn ( 2+ ) induction of the JNK stimulation . . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Tumor necrosis factor alpha ( TNFalpha ) activates various signal transduction pathways including those involving phosphatidylinositol 3 kinase ( PI3K ) , extracellular signal regulated kinases ( Erk ) , c Jun N terminal protein kinases ( JNK ) , and p 38 kinases . ^^^ The PI3K inhibitor LY 294002 significantly inhibited TNFalpha activation of Rac as well as Erk and abolished that of the PI3K target Akt , without showing any inhibitory effects on JNK and p 38 activation . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| In contrast , these studies demonstrated that the D816V c Kit mutant was constitutively associated with phosphorylated p85PI3K , and , downstream of PI3K , Jnk 1 and Jnk 2 were activated but Akt was not . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Finally , LY 294002 induced the blockade of phosphatidylinositol 3 kinase ( PI3K ) , one of the principal transducers of HGF / Met receptor signalling , prevented the enhancement of HIF 1 DNA binding and JNK activity , but the inhibition of p42 / 44 MAPK phosphorylation with PD 98059 was ineffective . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Altogether , our results show that S1P induces cardiomyocyte hypertrophy mainly via the EDG 1 receptor and subsequently via Gi through ERKs , p 38 MAPK , JNK , PI3K and via Rho pathway . . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Laminar shear stress activates c Jun NH ( 2 ) terminal kinase ( JNK ) by the mechanisms involving both nitric oxide ( NO ) and phosphatidylinositide 3 kinase ( PI3K ) . ^^^ Because protein kinase B ( Akt ) , a downstream effector of PI3K , has been shown to phosphorylate and activate endothelial NO synthase , we hypothesized that Akt regulates shear dependent activation of JNK by stimulating NO production . ^^^ These results and our previous findings strongly suggest that shear stress triggers activation of PI3K , Akt , and endothelial NO synthase , leading to production of NO , which ( along with O ( 2 ) , which is also produced by shear ) activates Ras JNK pathway . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Treatment of cells with the NO donors SNP , DETA NO , GEA 5024 , and SNAP resulted in phosphorylation of the antiapoptotic protein Bcl 2 , which was resistant to blockade of MEK , p 38 , and JNK pathways and sensitive to phosphoinositide 3 kinase ( PI3K ) inhibition . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Antimitogenic and proapoptotic activities of methylseleninic acid in vascular endothelial cells and associated effects on PI3K AKT , ERK , JNK and p 38 MAPK signaling . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The long form of c FLIP ( c FLIP ( L ) ) activates the Raf , which enhance the activity of Erk and PI3K , whereas short form ( c FLIPS ) are activated by c jun N terminal Kinase ( JNK ) through the TNF receptor associated factor ( TRAF ) 2 . ^^^ Since , however , recruitment of c FLIP ( L ) into FADD is later than that of c FLIP ( S ) , the activation of PI3K and Erk show the late response to activation of JNK . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Rac 1 and RhoG promote cell survival by the activation of PI3K and Akt , independently of their ability to stimulate JNK and NF kappaB . ^^^ Whereas the former is mediated through JNK , the latter is independent on the transcriptional activation of NF kappaB , a pro survival pathway , but results from the direct interaction of these GTPases with phosphatidylinositol 3 kinase ( PI3K ) and the stimulation of Akt . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We report that inhibition of the phosphatidylinositol 3 kinase ( PI3K ) Akt pathway enhances LPS induced activation of the mitogen activated protein kinase pathways ( ERK1 / 2 , p 38 , and JNK ) and the downstream targets AP 1 and Egr 1 . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Finally , the MKK 7 mutant , which activates JNK , reduced tyrosine phosphorylation of IRS 1 and IRS 2 and IRS associated PI3K activity without affecting expression of the IR , IRS 1 , or IRS 2 . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Paclitaxel induced p70S6K ( T421 / S424 ) phosphorylation requires both de novo RNA and protein synthesis via multiple signaling pathways including ERK1 / 2 MAP kinase , JNK , PKC , Ca ( ++ ) , PI3K , and mammalian target of rapamycin ( mTOR ) . ^^^ Inhibitors of mTOR , PI3K , and Ca ( ++ ) impair p70S6K activity , whereas inhibitors of JNK and PKC stimulate p70S6K activity . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| This includes radiation induced signaling via the EGFR and IGFI R to the PI3K , MAPK , JNK , and p 38 pathways as well as FAS R and TNF R signaling to pro caspases and NFKB . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Activation of ERK1 / 2 by deltaRaf 1 : ER * represses Bim expression independently of the JNK or PI3K pathways . ^^^ Thus , serum withdrawal induced expression of Bim ( EL ) occurs independently of the JNK > c Jun pathway and can be repressed by the ERK pathway independently of the PI3K pathway . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Both the JAK inhibitor AG 490 and the kinase deficient JAK 2 protein reduce the phosphorylation of JNK and phosphatidylinositol 3 kinase ( PI3K ) via LPS stimulation . ^^^ Pharmacological inhibition of the kinase activity of PI3K with LY 294002 decreases the phosphorylation of JNK . ^^^ PI3K and JNK are also important for the production of IL 1beta . ^^^ These results suggest that LPS induces tyrosine phosphorylation of JAK 2 via TLR 4 and that JAK 2 regulates phosphorylation of JNK mainly through activation of PI3K . ^^^ Phosphorylation of JAK 2 via LPS stimulation is important for the production of IL 1beta via the PI3K / JNK cascade . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Therefore , we propose that , in the setting of wild type PTEN , PI3K and MKK4 / JNK dependent pathways cooperate to maintain cell survival . . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Neuregulin is reported to stimulate synapse specific transcription of acetylcholine receptor ( AChR ) genes in the skeletal muscle fiber by multiple signaling pathways such as ERK , PI3K , and JNK . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The main pathway that leads to JNK activation downstream of the EGF receptor involves a sequential activation of c Src and phosphatidylinositol 3 kinase ( PI3K ) . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Selective activation of the c Jun N terminal kinase ( JNK ) pathway fails to elicit Bax activation or apoptosis unless the phosphoinositide 3 ' kinase ( PI3K ) pathway is inhibited . c Jun N terminal kinase ( JNK ) is activated when cells are exposed to noxious stimuli . ^^^ This PI3K inhibitable , JNK induced death response was not impeded , but actually accelerated , by cycloheximide . ^^^ However , if the PI3K cell survival pathway is not inhibited , even sustained activation of JNK exerts no overt proapoptotic effect in CC 139 cells . . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Addition of the MEK1 / 2 specific inhibitor U 0126 or the PI3K specific inhibitor LY 294002 ( but not p 38 kinase and JNK inhibitors ) completely nullified collagen 1 3 production and significantly decreased laminin beta 2 and fibronectin secretion . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| While investigating the signaling pathways responsible for HO 1 induction , we observed that carnosol activated the ERK , p 38 , and JNK pathways as well as the survival pathway driven by PI3K . ^^^ |
|
| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Inhibition of Syk with piceatannol or PI3K with wortmannin inhibited LPS induced JNK activation and decreased MCP 1 expression after exposure to LPS , suggesting that both Syk and PI3K reside in a signaling pathway leading to LPS induced JNK activation in neutrophils . ^^^ This Syk and PI3K dependent pathway leading to JNK activation after LPS exposure in non suspended neutrophils is specific for JNK , because inhibition of neither Syk nor PI3K decreased p 38 activation after LPS stimulation . ^^^ Overall our data suggests that LPS induces JNK activation only in non suspended neutrophils , which proceeds through Syk and PI3K dependent pathways , and that JNK activation is important for LPS induced MCP 1 expression but not for TNF alpha or IL 8 expression . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| A casein kinase 1 ( CKI ) inhibitor markedly suppressed the inhibitory effect of r 4 1BB on M CSF / RANKL induced osteoclast formation , suggesting that CKI might be involved in 4 1BB / 4 1BBL reverse signaling . r 4 1BB showed no effects on M CSF or RANKL induced phosphorylation of 1 kappaB , ERK1 / 2 , p 38 , or JNK , whereas RANKL induced phosphorylation of Akt , a downstream target of phosphatidylinositol 3 kinase ( PI3K ) , was completely abolished by r 4 1BB , suggesting that 4 1BB / 4 1BBL reverse signaling may interfere with PI3K / Akt pathway . r 4 1BB also abolished RANKL mediated induction of nuclear factor of activated T cells 2 . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| RET can activate various signaling pathways such as RAS / extracellular signal regulated kinase ( ERK ) , phosphatidylinositol 3 kinase ( PI3K ) / AKT , p 38 mitogen activated protein kinase ( MAPK ) and c Jun N terminal kinase ( JNK ) pathways . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Catalase induced COX 2 expression was abrogated by treatment of MG 132 ( a NF kappaB inhibitor ) or LY 294002 ( a PI3K inhibitor ) , but not by treatment of PD 98059 ( an ERK inhibitor ) , SB 203580 ( a p 38 inhibitor ) , or SP 600125 ( a JNK inhibitor ) . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| To study the role of MAPK ( ERK1 / 2 , JNK , p38MAPK ) and PI3K / Akt / GSK3beta signaling pathways in hypoxia induced ischemic tolerance , we examined the brains of newborn rats at different time points after exposure to sublethal hypoxia ( 8 % O ( 2 ) for 3 h ) . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Interestingly , unlike the delta opioid receptors , the mu opioid receptor required phosphatidylinositol 3 kinase ( PI3K ) to activate JNK . ^^^ The mu opioid receptor induced JNK activation was effectively inhibited by wortmannin or the coexpression of a dominant negative mutant of PI3K gamma . ^^^ Like the delta opioid receptor , activation of JNK by the kappa opioid receptor occurred in a PI3K independent manner . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| FGF 1 induced PN expression was blocked by the FGF 1 receptor antagonist PD 166866 and by inhibitors of phosphatidylinositol 3 kinase ( PI3K ) ( LY 294002 , wortmannin ) , p70S6K ( rapamycin ) , MEK1 / 2 ( U 0126 , PD 98059 ) , and p38MAPK ( SB 203580 ) but not of JNK ( SP 600125 ) . ^^^ In contrast , FGF 1 induced OPN expression was blocked by inhibitors of JNK or MEK1 / 2 but not of PI3K , p70S6K , or p38MAPK . ^^^ This study is the first to demonstrate that growth factor induced expression of PN in PASMCs is mediated through PI3K / p70S6K , Ras / MEK1 / 2 , and Ras / p38MAPK signaling pathways , whereas the expression of OPN is mediated through Ras / MEK1 / 2 and Ras / JNK signaling pathways . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The BTC dependent activation of JNK and PI3K / Akt pathways occurred predominantly via EGFR , whereas activation of the MEK 1 / ERK pathway occurred via all 4 c erbB receptors , although again predominantly via EGFR . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Up regulation of human beta defensin 2 by interleukin 1beta in A 549 cells : involvement of PI3K , PKC , p 38 MAPK , JNK , and NF kappaB . ^^^ HBD 2 mRNA expression in response to IL 1beta was attenuated by pretreatment of GF109203X , Go 6976 , and staurosporine [ inhibitors of protein kinase C ( PKC ) ] , SB 203580 [ an inhibitor of p 38 mitogen activated protein kinase ( MAPK ) ] , SP 600125 [ an inhibitor of c Jun N terminal kinase ( JNK ) ] , and LY 294002 [ an inhibitor of phosphatidylinositol 3 kinase ( PI3K ) ] , but not PD 98059 [ an inhibitor of extracellular signal regulated kinase ( ERK ) ] , suggesting involvement of PKC , p 38 MAPK , JNK , and PI3K in this response . ^^^ Together , these results suggest that IL 1beta induces HBD 2 mRNA expression in A 549 cells , and the induction seems to be at least in part mediated through activation of NF kappaB transcription factor as well as activation of signaling proteins of PKC , p 38 MAPK , JNK , and PI3K , but not ERK . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We therefore examined whether modulators of phosphatidylinositol 3 kinase ( PI3K ) / AKT signaling affected JNK activation . ^^^ PI3K inhibition led to increased JNK phosphorylation and islet cell death , which could be reversed by the specific JNK inhibitor SP 600125 . ^^^ In addition , IGF 1 suppressed cytokine mediated JNK activation in a PI3K dependent manner . ^^^ Taken together , these results demonstrate that PI3K / AKT suppresses the JNK pathway in islets , and this cross talk represents an important antiapoptotic consequence of PI3K / AKT activation . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Using specific inhibitors , we found that the apoptotic effect of GnRH a is mediated by c Jun NH 2 terminal kinase ( JNK ) and inhibited by the phosphatidylinositol 3 ' kinase ( PI3K ) protein kinase B ( PKB ) pathway . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| With relatively specific kinase inhibitors ( PD 98059 , SB 203580 , SP 600125 , wortmannin and LY 294002 , respectively ) the results showed that extracellular signal regulated kinase1 / 2 ( ERK1 / 2 ) , p 38 mitogen activated protein kinase ( p 38 MAPK ) and phosphatidylinositol 3 kinase ( PI3K ) were necessary for C5a induced migration , whereas c Jun N terminal kinase ( JNK ) was nonessential . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Inhibition of ERK and c jun NH ( 2 ) terminal kinase ( JNK ) , but not of p 38 MAPK and PI3K , blocked the effect of TGF beta 1 on CTGF mRNA and protein expression and on Smad2 / 3 phosphorylation . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| This review describes the possible mechanisms of induction of RANKL induced growth inhibition / apoptosis and discusses the role of various components in RANKL signaling in this phenomenon , including TNF receptor associated factor ( TRAF ) 6 , nuclear factor kappaB ( NF kappaB ) , c jun N terminal kinase JNK ) , phosphatidylinositol 3 kinase ( PI3K ) . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Finally , overexpression of a dominant negative form of Ets 2 blunted HO 1 promoter induction by LPS , and kinase inhibitors ( PI3K more than JNK ) that reduced Ets 2 expression markedly decreased endogenous HO 1 expression . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The effect of insulin on phosphorylation of both these sites required the activation of PI3K and the MAPKs ( mitogen activated protein kinases ) ERK1 / 2 ( extracellular signal regulated kinase 1 and 2 ) , but not the activation of mTOR ( mammalian target of rapamycin ) / p70S6 kinase , JNK ( c Jun N terminal kinase ) or p38MAPK . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| They are , respectively , the mitogen activated protein kinase ( MAPK ) , phosphatidylinositol 3 kinase ( PI3K ) , and Jun N terminal kinase ( JNK ) cascades . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We found that prior stimulation of primary murine B cells with CD40L markedly enhanced the level of ERK and JNK ( but not p 38 MAPK ) phosphorylation produced by subsequently added anti Ig Ab , and much , but not all , of this enhancement was independent of PI3K and phospholipase C . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We demonstrated that the participation of alpha isoform of PKC , phosphatidylinositol 3 kinase ( PI3K ) , extracellular signal regulated kinase ( ERK1 / 2 ) , and c Jun N terminal kinase ( JNK ) is crucial for the end point response . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Tumor cell killing correlates with regulation of proteins involved in the Wnt and PI3K pathways : beta catenin , APC , GSK 3 , JNK , and PTEN . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Src kinase inhibitors PP 1 and PP 2 , phosphatidylinositol 3 kinase ( PI3K ) inhibitors wortmannin and LY 294002 , Akt inhibitor , the c Jun N terminal kinase ( JNK ) inhibitor SP 600125 , antisense JNK and dominant negative MyD 88 , interleukin 1 receptor associated kinase ( IRAK ) 1 , IRAK 4 , and phosphatidylinositol 3 kinase expression all attenuated IL 18 mediated AP 1 binding and reporter activity , CXCL 16 promoter reporter activity , and CXCL 16 expression . ^^^ Thus IL 18 induced CXCL 16 expression via a MyD 88 > IRAK 1 IRAK4 TRAF 6 ( tumor necrosis factor receptor associated factor 6 ) > c Src > PI3K > Akt > JNK > AP 1 pathway . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Anti inflammatory effects of pharmacological agents targeted at tyrosine kinases , Syk , Itk , signal transducer and activator of transcription 1 , NF kappaB , GATA 3 , EGFR , PI3K , MEK1 / 2 , p 38 MAPK and JNK have been reported in animal models of allergic airway inflammation . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We further show that OX40L induces activation of p 38 mitogen activated protein kinase ( MAPK ) and phosphotidyl inositol 3 kinase ( PI3K ) in T cells , and using specific inhibitors , we find that increased mRNA half life is dependent upon both these pathways but is independent of c jun N terminal kinase ( JNK ) . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| CONCLUSIONS : These findings show the role of PI3K in KIT ( Asn822Lys ) mediated constitutive activation through the Akt independent downstream signaling pathway of JNK , and also demonstrate the mutant ' s susceptibility to STI 571 , which may therefore have therapeutic potential in CBFL patients with susceptible KIT mutations . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| JNK and PI3k / Akt signaling pathways are required for establishing persistent SARS CoV infection in Vero E 6 cells . ^^^ Our previous studies demonstrated that signaling pathways of extracellular signal related kinase ( ERK1 / 2 ) , c Jun N terminal protein kinase ( JNK ) , p 38 mitogen activated protein kinase ( MAPK ) , and phosphatidylinositol 3 ' kinase ( PI3K ) / Akt were activated in SARS CoV infected Vero E 6 cells . ^^^ In the present study , we showed that the inhibitors of JNK and PI3K / Akt inhibited the establishment of persistence , but those of MAPK / ERK kinase ( MEK ; as an inhibitor for ERK1 / 2 ) and p 38 MAPK did not . ^^^ These results indicated that two signaling pathways of JNK and PI3K / Akt were important for the establishment of persistence in Vero E 6 cells . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The gamma subunit demonstrates remarkable regulatory complexity including induction by chloride ions rather than sodium , the differential expression of at least 2 isoforms , involvement of separate MAP kinase signaling pathways for transcription ( JNK ) and translation ( PI3K ) as well as cell type regulation of expression . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| These findings suggest that , in glioma cells , the PI3K / Cdc42 / p38MAPK and PI3K / Rac1 / JNK pathways are equally important for LPA ( 1 ) receptor mediated migration . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The neuroprotection of insulin on ischemic brain injury in rat hippocampus through negative regulation of JNK signaling pathway by PI3K / Akt activation . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Further characterisation of signalling intermediates downstream of the BCR revealed a perturbation of MAPK signalling pathways in p85alpha null and p110delta null B cells , and our data suggests that cross talk exists between the PI3K and JNK pathways . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Concurrent inhibition of the PI3K / Akt and MKK4 / JNK pathways showed enhanced antiproliferative effects on H 1299 cells in vitro and in vivo by increasing apoptosis . ^^^ CONCLUSIONS : PI3K / Akt and MKK4 / JNK pathways cooperate to stimulate NSCLC cell proliferation by maintaining cell survival , suggesting that simultaneously targeting these two pathways might be an effective therapeutic strategy against NSCLC . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| KGF induces lipogenic genes through a PI3K and JNK / SREBP 1 pathway in H 292 cells . ^^^ Induction of SREBP 1 , SCD 1 , and FAS by KGF was inhibited by the JNK inhibitor SP 600125 and the phosphatidylinositol 3 kinase ( PI3K ) inhibitor LY 294002 but not by the ERK inhibitor PD 98059 . ^^^ In summary , we conclude that KGF requires both PI3K and JNK signaling pathways to induce SREBP 1 , which in turn induces SCD 1 and FAS expression in H 292 cells . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
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 . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The activity of GCH was increased up to 5 fold after the NGF treatment , and the increase was repressed by pretreatment with U 0126 , an MEK1 / 2 inhibitor , but not with protein kinase A ( PKA ) , phosphoinositide 3 kinase ( PI3K ) , p 38 mitogen activated protein kinase ( MAPK ) , and c Jun NH 2 terminal kinase ( JNK ) inhibitors . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| In vitro , LMP 1 activates numerous signaling pathways including p 38 , c Jun N terminal kinase ( JNK ) , phosphatidylinositol 3 kinase ( PI3K ) / Akt , and NF kappaB through interactions with tumor necrosis receptor associated factors ( TRAFs ) . ^^^ In this study , interactions between LMP 1 and TRAFs and the activation of PI3K / Akt , JNK , p 38 , and NF kappaB were examined in LMP 1 transgenic mice . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| This implies that DORs activate JNK through a novel pathway dependent on PI3K and Akt , thereby regulating the function of activator protein 1 transcription complexes containing c jun and other transcription partners . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| PI3K , ERK , JNK , and p 38 kinases , known to mediate PDGF BB signaling in the canonic dedifferentiative and proliferative response of smooth muscle cells ( SMC ) were rapidly activated by PDGF BB but only p 38 remained activated after 2 day stimulation . ^^^ Immunofluorescence and immunoblotting experiments showed that in 4 day treatment : ( 1 ) continuous inhibition of PI3K , of ERK , of JNK , failed to inhibit either cell enlargement and formation of prominent alpha SM actin containing stress fibers or the typical increase in alpha SM actin ; ( 2 ) when stimulated in the presence of the p 38 inhibitor SB 203580 both responses were significantly inhibited and cytofluorimetric analysis of cell size showed a remarkable reduction of the hypertrophic response . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Inhibitor studies showed that enhanced expression was insensitive to inhibitors of JAK / STAT , p 38 , JNK , and PI3K signaling pathways , but sensitive to inhibitors of MEK1 / 2 and NF kappaB activation , suggesting a MEK / NF kappaB based mechanism . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| The effect of EPA on ERK1 / 2 , c jun NH 2 terminal kinase ( JNK ) , p 38 or phosphoinositide 3 kinase ( PI3K ) activity in MMCs was examined using Western blot . ^^^ EPA and specific inhibitors of ERK1 / 2 , JNK and PI3K decreased levels of MCP 1 in MMCs . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We found that acidosis triggers the phosphorylation of Akt ( the main downstream target of PI3K ) and ERK MAPK , but not that of p 38 and JNK MAPK . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| METHODS : DNA fragmentation , nuclear condensation and activated apoptotic caspases were measured by agarose gel electrophoresis , nuclear DAPI ( 4 ' , 6 diamidine 2 phenylindole dihydrochloride ) stain and western blotting analysis following the surrounding medium of P . gingivalis and / or pre administration of SB 203580 ( p 38 inhibitor ) , U 0126 [ mitogen activated protein kinase ( MAPK ) extracellular signal regulated kinase 1 / 2 ( ERK1 / 2 ) inhibitor ] , LY 294002 [ phosphoinositide 3 kinase ( PI3K ) inhibitor ] , cyclosporine A ( CsA : calcineurin inhibitor ) , and Sp 600125 [ c Jun N terminal kinase ( JNK ) inhibitor ] in cultured cardiac H9c2 cells . ^^^ Porphyromonas gingivalis related cardiac cell apoptosis was also partially mediated by PI3K or calcineurin signaling pathways , whereas the JNK pathway might play a protective role in P . gingivalis related cardiac cell apoptosis . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Our data showed that extracellular signal regulated kinase ( ERK ) pathway inhibitor PD 98059 , but not the c Jun N terminal kinase ( JNK ) inhibitor SP 600125 , p 38 kinase inhibitor SB 203580 , and PI3K inhibitor wortmannin , attenuated Src induced MMP 2 promoter activity . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Glc HSA induced E selectin expression was suppressed by the phosphatidylinositol 3 kinase ( PI3K ) inhibitors wortmannin and LY 294002 , the protein kinase B ( PKB ) inhibitor ML 9 , the IkappaB kinase ( IKK ) inhibitor BAY 117082 , and the Jun N terminal kinase ( JNK ) inhibitor SP 600125 , On the other hand , the protein kinase C inhibitors calphostin C and H 7 did not suppress Glc HSA induced E selectin expression . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We demonstrate that heparin , like epidermal growth factor ( EGF ) and heparin binding EGF ( HB EGF ) , elicits phosphorylation of the EGF receptor and activation of the phosphatidyl inositol 3 kinase ( PI3K ) , the extracellular signal related kinase 1 / 2 ( ERK1 / 2 ) and the c Jun NH 2 terminal kinase ( JNK ) signal transduction pathways in primary villous trophoblast . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| METHODS : Matrix metalloproteinase ( MMP ) 2 and MMP 9 activities and cellular morphology were measured by gelatin zymography and immunofluorescence after P . gingivalis medium treatment with or without SB 203580 ( p 38 mitogen activated protein kinase cascade [ p 38 ] inhibitor ) , U 0126 ( mitogen activated protein kinase kinase [ MAPKK ] inhibitor ) , LY 294002 ( phosphoinositide 3 kinase [ PI3K ] inhibitor ) , cyclosporin A ( CsA ; calcineurin inhibitor ) , SP 600125 ( c Jun N terminal kinase [ JNK ] inhibitor ) , proinflammatory interleukin ( IL ) 1 , or anti inflammatory IL 10 in cultured cardiomyoblast H9c2 cells . ^^^ The increased activity of MMP 9 treated with P . gingivalis medium was not mediated through p 38 , extracellular regulated kinase ( ERK ) , PI3K , calcineurin , and JNK signaling pathways and was not inhibited by IL 10 . ^^^ However , P . gingivalis induced H9c2 cell hypertrophy was mediated through p 38 , ERK , PI3K , calcineurin , and JNK signaling pathways , which are in a totally different regulatory pathway from P . gingivalis elevated MMP 9 activity . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Furthermore , inhibiting phosphoinositide 3 kinase ( PI3K ) activity prevented Rac 1 and JNK activation as well as collagen 1 induced N cadherin up regulation . ^^^ These data implicate PI3K Rac 1 JNK signaling in collagen 1 induced changes in NMuMG cells . ^^^ In addition , we showed that cord formation and branching in three dimensional culture ( EMT dependent events ) required N cadherin expression and PI3K Rac 1 JNK signaling . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| We found that sustained Lnk mediated activation of PI3K in TNFalpha activated ECs correlated with the inhibition of ERK1 / 2 phosphorylation , whereas phosphorylation of p 38 and c Jun NH ( 2 ) terminal kinase ( JNK ) mitogen activated protein kinases ( MAPKs ) was unchanged . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| JNK and PI3K differentially regulate MMP 2 and MT 1 MMP mRNA and protein in response to actin cytoskeleton reorganization in endothelial cells . ^^^ Inhibition of phosphoinositide 3 kinase ( PI3K ) , but not JNK , significantly decreased the amount of active MMP 2 following cytochalasin D stimulation with a concurrent decrease in MT 1 MMP protein . ^^^ In summary , our results provide novel insight into the signaling cascades initiated in the early stages of angiogenesis through the reorganization of the actin cytoskeleton and demonstrate a critical role for JNK in regulating MMP 2 and MT 1 MMP mRNA expression , whereas PI3K regulates protein levels of both MMP 2 and MT 1 MMP . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| EGF induced cell migration in a dose dependent manner ; EGF induced EGFR phosphorylation and downstream activation of c Jun N terminal protein kinase ( JNK ) , p 38 MAP kinase ( p 38 ) , extracellular signal regulated kinase ( ERK1 / 2 ) and AKT , were inhibited by PD 153035 ( EGFR inhibitor ) , JNKi ( JNK inhibitor ) , SB 203580 ( p 38 inhibitor ) , U 0126 ( MEK / ERK inhibitor ) , and LY 294002 ( PI3K / AKT inhibitor ) , respectively . ^^^ EGF induced MMP 2 activity was significantly inhibited by treatment of PD 153035 , U 0126 , and LY 294002 , but not SB 203580 and JNK inhibitor , suggesting that ERK and the phosphatidylinositol 3 kinase ( PI3K ) / AKT pathways selectively mediate EGF stimulated MMP 2 activity and cell migration in cultured HLECs in vitro . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Multiple MAP kinases ( MAPK ) , including MEK / ERK , p 38 kinase , PI 3 kinase ( PI3K ) but not JNK were involved in the regulation of IL 1alpha stimulated alpha secretase activity and sAPPalpha release . p 38 MAPK seems to be the most proximal of these MAPKs , as it was the earliest to be activated by IL 1alpha and blocking this pathway attenuated activation of IL 1alpha induced MEK and PI3K pathways . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Some cultures were pretreated with the phosphatidylinositol 3 kinase ( PI3K ) inhibitor Ly 294002 or specific inhibitors of the mitogen activated protein kinase ( MAPK ) family members such as the mitogen activated protein kinase kinase ( MEK 1 ) inhibitor PD 098059 , Jun N terminal kinase ( JNK ) inhibitor SP 600125 , p 38 MAPK inhibitor SB 203580 . ^^^ Inhibition of PI3K and MEK 1 but not JNK or p 38 MAPK increased the apoptotic rate of cardiomyocytes treated with cruzipain . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| Primary human ASM cells pretreated with inhibitors of MAPK p 38 , p42 / p44 ERK , JNK , or JAK but not PI3K , showed a significant decrease in eotaxin 1 / CCL11 release upon IL 17A treatment . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| A receptor mutant lacking all the binding sites for SHP 2 , GAP , PI3K , and PLC gamma fails to activate JNK 1 . ^^^ Receptor mutants with no binding site for either SHP 2 or GAP can fully activate JNK 1 but those which do not bind either PI3K or PLC gamma are unable to induce JNK 1 activation . ^^^ Altogether , these results indicate that PDGF activates JNK 1 through a pathway that involves both PI3K and PLC gamma and subsequent activation of protein kinase C . . ^^^ |
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| Interacting proteins: P45983 and P27986 |
Pubmed |
SVM Score :0.0 |
| They further suggest a possible triptolide induced inhibitory signal for tumor cell proliferation that is initiated by the decrease in PI3K activity , which in turn leads to the augmentation of JNK 1 phosphorylation via the Akt and / or PKC independent pathway ( s ) . ^^^ |
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