| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| HGF stimulated Gab 1 association with c Met , Grb 2 , SHP 2 , PI3K , Shc , Crk isoforms and CrkL , but not with PLCgamma 1 . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Tyrosine phosphorylation stimulates PI3K and PLCgamma 1 enzymatic activity , and on ShcA creates binding sites for Grb 2 with its associated Sos 1 and Gab 1 . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Here , we show that Abi 1 ( also known as E3b1 ) recruits PI3K , via p 85 , into a multimolecular signaling complex that includes Eps 8 and Sos 1 . ^^^ The recruitment of p 85 to the Eps 8 Abi1 Sos 1 complex and phosphatidylinositol 3 , 4 , 5 phosphate ( PIP 3 ) , the catalytic product of PI3K , concur to unmask its Rac GEF activity in vitro . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| In both M 23 and MM 55 cells , HGF induces association with MET / HGFR and increased tyrosine phosphorylation of the SH 2 domain containing proteins PI3K , GAP and NCK . ^^^ We therefore suggest that the second messenger proteins PI3K , GAP and NCK , and possibly the protein products of the c fos , c jun , junB , junD and c myc genes , are important elements in the HGF induced mitogenic pathway in the normal mouse epithelial cell lines M 23 and MM55 . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The transducers involved in HGF triggered gene inductions were investigated using different protein kinase inhibitors : genistein for the receptor tyrosine kinase , herbimycin A for the nonreceptor tyrosine kinase ( pp 60 ( c src ) ) , wortmannin for phosphatidylinositol 3 kinase ( PI3K ) and H 7 for protein kinase C ( PKC ) . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| HGF stimulated DNA synthesis in 184B5 and 32D / c Met cells , while HGF / NK2 was mitogenically inactive , despite the ability of HGF / NK2 to stimulate c Met autophosphorylation , mitogen activated protein kinase ( MAPK ) , and phosphatidylinositol 3 kinase ( PI3K ) in both cell systems . ^^^ These data suggest that ( 1 ) alternative HGF isoforms signaling through c Met generate both common and distinct biological responses , ( 2 ) the extent and duration of ligand stimulated c Met and MAPK activities are dependent on the cellular context and are not predictive of mitogenic signaling , and ( 3 ) in at least some HGF target cells , the activation of both MAPK and PI3K signaling pathways is insufficient for mitogenesis elicited through c Met . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The ability of HGF / SF to induce both chemoresistance and DNA repair was inhibited by wortmannin , suggesting that these activities of HGF / SF are due , in part , to a phosphatidylinositol 3 ' kinase ( PI3K ) dependent signaling pathway . ^^^ Consistent with this finding , HGF / SF induced the phosphorylation of c Akt ( protein kinase B ) , a PI3K substrate implicated in apoptosis inhibition ; and an expression vector encoding a dominant negative kinase inactive Akt partially but significantly inhibited HGF / SF mediated cell protection and DNA repair . ^^^ These findings suggest that HGF / SF activates a cell survival and DNA repair pathway that involves signaling through PI3K and c Akt and stabilization of the expression of Bcl XL ; and they implicate Bcl XL in the DNA repair process . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Based on our previous observations that active ERK associates with and phosphorylates Gab 1 in response to HGF , and the prediction that the ERK phosphorylation site is adjacent to one of the phosphatidylinositol 3 kinase ( PI3K ) SH 2 binding motifs , we examined the possibility that ERK phosphorylation can regulate the Gab1 / PI3K association . ^^^ These results suggest that activated ERK can phosphorylate Gab 1 in response to HGF stimulation and thereby potentiate the Gab1 / PI3K association and subsequent PI3K activation . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| HGF induced phosphorylation of mitogen activated protein / extracellular signal regulated kinase kinase ( MEK ) pathway substrate p42 / p44 ( erk ) and phosphatidylinositol 3 ' kinase ( PI3K ) pathway substrate Akt provided evidence for downstream activation of MEK and PI3K pathways in HNSCC . ^^^ Inhibitors of MEK ( U 0126 ) and PI3K ( LY 294002 ) blocked p42 / p44 ( erk ) and Akt , respectively , and partially blocked HGF induced production of IL 8 and VEGF , whereas the combination of U 0126 and LY 294002 completely inhibited expression of IL 8 and VEGF by UMSCC 11A . ^^^ Our results demonstrate that HGF can promote expression of angiogenesis factors in tumor cells through both MEK and PI3K dependent pathways . ^^^ |
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| Interacting proteins: Q07889 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 . ^^^ In conclusion , we suggest that HGF triggers a signal transduction cascade involving PI3K and ultimately activates HIF 1 . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Following Met activation , alpha6beta4 is tyrosine phosphorylated and combines with Shc and PI3K , generating an additional signaling platform that potentiates HGF triggered activation of Ras and PI3K dependent pathways . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| All melanocytic cells expressed the HGF receptor c Met , and autocrine HGF caused constitutive activation of c Met , MAPK and PI3K . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| In support of this divergent effect of ERK on Gab1 / PI3K association following HGF and EGF stimulation , U 0126 decreased the HGF stimulated association of p 85 and the Gab 1 c Met binding domain but did not alter the EGF stimulated association of p 85 and the c Met binding domain . ^^^ These experiments demonstrate that EGF and HGF mediated ERK activation result in divergent effects on Gab1 / PI3K signaling . ^^^ HGF stimulated ERK activation increases the Gab1 / PI3K association , whereas EGF stimulated ERK activation results in a decrease in the tyrosine phosphorylation of Gab 1 and a decreased association with the PI3K . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| In this study , we define the role of these effectors in response to HGF by utilizing Met mutants , designed to obtain preferential coupling of Met to either Grb 2 or PI3K or both . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Whereas in BLM rapid increases in 1 , 2 diacylglycerol , PtdIns ( 3 , 4 , 5 ) P ( 3 ) and PtdIns ( 3 , 4 ) P ( 2 ) were observed , suggesting that in BLM HGF activates both phospholipase C ( PLC ) and phosphoinositide 3 kinase ( PI3K ) , in BBM only HGF induced transient accumulation of PtdIns3P was seen , which was temporarily delayed from signalling events in BLM and could be blocked by the PtdIns specific PLC inhibitor ET 18 OCH ( 3 ) and the calpain inhibitor calpeptin , suggesting that 3 kinase activation in BBM lies downstream of PLC activation in BLM and is a calpain mediated event . ^^^ Moreover , the increase in immunoprecipitable PI3K C 2 beta activity , which is sensitive to wortmannin ( 10 nM ) and shows strong preference for PtdIns over PtdIns4P as a substrate , was observed only in BBM upon stimulation of renal cortical slices with HGF and could be mimicked by the Ca ( 2+ ) ionophore A 23187 and blocked by the cell penetrant Ca ( 2+ ) chelator BAPTA AM [ 1 , 2 bis ( 2 aminophenoxy ) ethane N , N , N ' , N ' tetra acetic acid tetrakis ( acetoxymethyl ester ) ] . ^^^ On Western blots PI3K C 2 beta revealed a single immunoreactive band of 180 kDa in BLM and BBM , while after stimulation with HGF a gel shift of 18 kDa was noticed only in BBM , suggesting that the observed enzyme activation is achieved by proteolysis . ^^^ When BBM were subjected to short term ( 15 min ) exposure to mu calpain , a similar gel shift together with an increase in PI3K C 2 beta activity was observed , when compared with the BBM harvested after HGF stimulation . ^^^ The data presented in this report show that in renal cells there is a spatial separation of the inositol lipid signalling system between BLM and BBM , and that HGF causes activation of PLC and PI3K primarily in BLM , which leads to calpain mediated activation of PI3K C 2 beta in BBM with a concomitant increase in PtdIns3P . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Although phosphatidylinositol 3 kinase ( PI3K ) inhibitors diminished HGF induced mitogenesis , anti apoptosis , and MAP kinase activation , IL 4 enhanced HGF signaling persisted even in the presence of these inhibitors . ^^^ Our results suggest that the IL 4 and HGF pathways converge at multiple levels , and that IL 4 dependent Jak 3 and STAT 6 activities modulate signaling events independent of PI3K to enhance HGF dependent mitogenesis in myeloid cells , and possibly other common cellular targets . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| PAK 4 is activated via PI3K in HGF stimulated epithelial cells . ^^^ LY 294002 , a phosphoinositide 3 kinase ( PI3K ) inhibitor , inhibits HGF induced PAK 4 kinase activation , relocalisation , and cell rounding . ^^^ These results indicate that HGF stimulates PAK 4 through PI3K , and that PAK 4 could contribute to HGF induced changes in actin organisation and cell substratum adhesion . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Utilizing unique phospho specific antibodies generated against various tyrosines of c Met , we show that Y 1003 ( binding site for c Cbl and a negative regulatory site ) , Y 1313 ( binding site for PI3K ) , Y1230 / Y1234 / Y1235 ( autophosphorylation site ) , Y 1349 ( binding site for Grb 2 ) , Y 1365 ( important in cell morphogenesis ) are phosphorylated in response to HGF ( 40 ng / ml , 7 . 5 min ) in H 69 cells . ^^^ Since multiple biological and biochemical effects are transduced through the PI3K pathway , we determine the role of PI3K in the c Met / HGF stimulation pathway . ^^^ Finally , we determined the downstream signal transduction of HGF stimulation of c Met with and without inhibition of c Met ( with geldanamycin , an anisamycin antibiotic that inhibits c Met in SCLC ) or PI3K ( with LY 294002 ) . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Bcl xL deficient keratinocytes cultured in vitro readily underwent apoptosis in the absence of growth factors , but the addition of HGF or EGF resulted in restoration of cell survival , which was reversed by treatment with wortmannin , an inhibitor of phosphoinositide 3 kinase ( PI3K ) . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Stimulation of MM cells with HGF led to the activation of the RAS / mitogen activated protein kinase and phosphatidylinositol 3 kinase / protein kinase B ( PI3K / PKB ) pathways , signaling routes that have been implicated in the regulation of cell proliferation and survival . ^^^ Furthermore , by applying specific signal transduction inhibitors , we demonstrated that MEK is required for HGF induced proliferation , whereas activation of PI3K is required for both HGF induced proliferation and for rescue of MM cells from apoptosis . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| These results suggest that HGF stimulates eNOS activity by a PI3K / Akt dependent phosphorylation in a Ca ( 2+ ) sensitive manner in vascular endothelial cells . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The activation of AKT , p 70 ( s6k ) , and ERK1 / 2 induced by HGF was abolished by pre treatment with LY 294002 , a phosphoinositide 3 OH kinase ( PI3K ) inhibitor , and U 0126 , a mitogen activated protein kinase / ERK kinase ( MEK ) inhibitor , respectively . ^^^ When the cells were pre treated with LY 294002 prior to the HGF stimulation , the proliferative action of HGF was completely abrogated , implying that the PI3K / AKT signaling pathway is responsible for the biological effect of HGF . ^^^ These in vitro data indicate that HGF exerts a proliferative action on hepatic oval cells via activation of the PI3K / AKT signaling pathway . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The transforming growth factors beta 1 and beta 2 also evoked cell proliferation which was independent of activation of the MAPKs investigated . bFGF evoked a release of VEGF and of HGF by the cells ; these effects were independent of MAPK activation and were possibly mediated by activation of the PI3K signaling pathway . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| HGF activated survival pathways such as the phosphatidylinositol 3 kinase ( PI3K ) / Akt pathway , the mitogen activated protein kinase / extracellular signal regulated kinase ( ERK ) kinase / ERK and the signal transducer and activator of transcription 3 ( STAT 3 ) pathway . ^^^ Pretreatment of PHH with the PI3K inhibitor LY 294002 as well as adenoviral transduction of dominant negative Akt 1 prevented HGF mediated Mcl 1 induction and reversed the antiapoptotic effects of HGF . ^^^ In conclusion , HGF confers survival of PHH by activation of the PI3K / Akt pathway . ^^^ PI3K / Akt activation by HGF results in the induction of antiapoptotic proteins such as Mcl 1 . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Cytokines , such as HGF , IGF 1 , and IL 6 also protects cells against apoptosis induced by radiation through PI3K / AKT pathway . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| In this study , we have compared the ability of HGF and IGF 1 to activate PI3K and MAPK / ERK in i 28 myogenic cells . ^^^ In agreement with this observation , IGF 1 is much more potent than HGF in stimulating phosphorylation of Akt / PKB , a protein kinase downstream of PI3K . ^^^ Moreover , the specific PI3K inhibitor , Wortmannin , abolished MAPK / ERK and Elk 1 phosphorylation in HGF treated cells , suggesting the requirement of PI3K in mediating the HGF induced MAPK pathway . ^^^ UO 126 , a specific MAPK pathway inhibitor , had no effect on PI3K activity or Akt phosphorylation , implying that at least in muscle cells , the MAPK / ERK pathway is not required for HGF induced PI3K activation . ^^^ These results provide a biochemical rationale for the previous observations that HGF and IGF 1 have opposite effects on myogenic cells , consistent with studies linking PI3K activation to differentiation and MAPK / ERK activation to proliferation in these cells . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Like VEGF , hepatocyte growth factor ( HGF ) activated the PI3K Akt forkhead pathway . ^^^ However , HGF PI3K Akt forkhead signaling was insensitive to diphenyleneiodonium and AS p47phox . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Production of MUC 20 reduced HGF induced matrix metalloproteinase expression and proliferation , which require the Grb 2 Ras pathway , whereas cell scattering , branching morphogenesis , and survival via the Gab1 / phosphatidylinositol 3 kinase ( PI3K ) pathways was not affected . ^^^ Thus , MUC 20 reduces HGF induced activation of the Grb 2 Ras pathway but not the Gab1 / PI3K pathways . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The results showed that HGF , but not FGF 2 , stimulated MMP 9 expression , and that the stimulation was mediated through the activation of phosphoinositide 3 kinase ( PI3K ) which was not associated with FGF 2 signal transduction . ^^^ Moreover , the specific role of HGF through the PI3K signal pathway is the induction of MMP 9 expression in , and the migration of , myoblasts . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Our findings suggest that HGF promotes myeloma cells to adhere via activation of the phosphatidylinositol 3 kinase ( PI3K ) pathway independently of AKT , but possibly through the involvement of nuclear factor kappa B ( NF kappaB ) . ^^^ INA 6 cells adhered to fibronectin after stimulation by insulin like growth factor or stromal cell derived factor 1alpha , but this adhesion was less dependent on PI3K than HGF mediated adhesion . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Taken together , these results indicate that HGF not only phosphorylates eNOS through the PI3K / Akt pathway , but also partially through the MAPK pathway , and that these two pathways may interact . ^^^ Our study thus demonstrates a novel activity of HGF the stimulation of NO production which occurs via eNOS phosphorylation that may in turn be mediated by cross talk between the PI3K / Akt and MAPK pathways . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| In this context , we show that short term exposure of mesenchymal stem cells ( MSCs ) to HGF can induce the activation of its cognate Met receptor and the downstream effectors ERK1 / 2 , p38MAPK , and PI3K / Akt , while long term exposure to HGF resulted in cytoskeletal rearrangement , cell migration , and marked inhibition of proliferation through the arrest in the G 1 S checkpoint . ^^^ HGF ' s effect on MSC proliferation was reversed by p 38 inhibitor SB 203580 , while the effects on cell migration were abrogated by PI3K inhibitor Wortmannin , suggesting that HGF acts through different pathways to determine its complex effects on MSCs . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| This study demonstrates that concomitant activation of the Ras / ERK , PI3K / Akt , and Rac1 / p38 pathways is required to achieve full capacity of cortical neurons to migrate upon HGF stimulation . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The blebbing response was dependent on autocrine HGF ( hepatocyte growth factor ) activation of c Met and prevented by inhibition of RhoA , ROCK and p 38 MAPK ( p 38 mitogen activated protein kinase ) , but not ERK ( extracellular signal regulated kinase ) or PI3K ( phosphoinositide 3 kinase ) . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Our investigation demonstrated that luteolin similar to PD 98059 , which acts as a specific inhibitor of MEK , an up stream kinase regulating ERK1 / 2 , and wortmannin , a PI3K inhibitor , inhibited the invasiveness induced by HGF . ^^^ In conclusion , the luteolin inhibited HGF induced HepG 2 cell invasion involving both MAPK / ERKs and PI3K Akt pathways . . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| The invasive / migratory phenotype activated by HGF can be blocked by specific inhibitors of the phosphatidylinositol 3 kinase ( PI3K ) cascade , inhibitor of p 70 ( S6K ) , and also the expression of a dominant negative Akt , demonstrating that HGF transmits the motogenic signal through PI3K and Akt to p 70 ( S6K ) . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| HGF activated phosphatidylinositol 3 kinase ( PI3K ) Akt that in turn inhibited its downstream transducer glycogen synthase kinase ( GSK ) 3 . ^^^ Blockade of the PI3K Akt pathway with specific inhibitors abrogated HGF induced inhibitory phosphorylation of GSK 3 and suppression of E selectin . ^^^ |
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| Interacting proteins: Q07889 and P27986 |
Pubmed |
SVM Score :0.0 |
| Since phosphatidylinositol 3 kinase ( PI3K ) / Akt pathway is essential for cell survival , the present study has examined whether the preventive effect of hepatocyte growth factor ( HGF ) on ActD induced apoptotic cell death in a human hepatocyte derived cell line ( HL 7702 ) is associated with PI3K / Akt activation . ^^^ HGF was found to significantly activate Akt phosphorylation while pre treatment with PI3K specific inhibitor wortmannin further enhanced ActD induced apoptotic effect , and also significantly prevented HGF ' s protection against ActD induced apoptosis . ^^^ These results suggest that HGF ' s prevention of ActD induced apoptotic cell death in HL 7702 cells is associated with the activation of PI3K / Akt signaling . . ^^^ |
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