Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Mitotic , tyrosine phosphorylated Sam 68 bound selectively to recombinant SH 2 domains with significantly different affinities ( c Src approximately Ras GTPase activating protein > p 85 alpha ( amino terminal ) > Grb 2 > > p 85 alpha ( COOH terminal ) ) . ^^^ In vitro translated Sam 68 also bound selectively to recombinant SH 3 domains , with the highest affinity for the Src and p 85 alpha SH 3 domains . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Only one peptide inhibited binding of Sam 68 to the p85alpha SH 3 domain , whereas several peptides inhibited binding of Sam 68 to c src SH 3 domain , suggesting that Sam 68 uses different proline rich motifs to bind to different SH 3 domains . ^^^ A peptide derived from residues 32 44 of Sam 68 which fits the class 2 SH 3 domain binding consensus sequence inhibited binding of Sam 68 to both p85alpha SH 3 domain and c src SH 3 domain , but with differential potency , suggesting a differential affinity of these SH 3 domains for this proline rich motif . . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Employing antibodies specific to two p 85 isoforms , p85alpha and p85beta , we demonstrate that HTC IR cells express both p 85 isoforms , and these isoforms induce the formation of similar signaling complexes in response to insulin . p 60 70 , present in both alpha p85alpha and alpha p85beta immunoprecipitates , is a GAP associated protein , but is distinct from the p 68 src associated protein in mitosis ( Sam 68 ) by several criteria . ^^^ These data suggest that 1 ) GAP associated protein , but not Sam 68 , is a part of insulin signaling complexes ; and 2 ) p85alpha and p85beta form similar , but distinct , insulin receptor signaling complexes . . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Indeed , three amino acids important for ligand binding in Src SH 3 were replaced in the Slap SH 3 sequence ; Slap SH 3 did not bind to the Src SH 3 partners p85alpha , Shc , and Sam 68 in vitro , and the chimeric tyrosine kinase Slap / SrcK , composed of SlapDeltaC fused to the SH 2 linker kinase sequence of Src , was not regulated in vivo . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Sam 68 is a docking protein linking GAP and PI3K in insulin receptor signaling . ^^^ We have recently found that Sam 68 is a substrate of the insulin receptor ( IR ) and that Tyr phosphorylated Sam 68 associates with the SH 2 domains of p 85 PI3K . ^^^ Thus , Sam 68 is co precipitated with p 85 PI3K , IRS 1 and IR . ^^^ The association of Sam 68 with these complexes is mediated by the SH 2 domains of PI3K . ^^^ Thus , Sam 68 is linking p120GAP to PI3K signaling pathway . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
Human leptin activates PI3K and MAPK pathways in human peripheral blood mononuclear cells : possible role of Sam 68 . ^^^ Moreover , tyrosine phosphorylation of IRS 1 and Sam 68 promotes their association with p 85 , the regulatory subunit of PI3K , and this association leads to the stimulation of PI3K activity . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
We have recently found that Sam 68 is a substrate of the insulin receptor ( IR ) that translocates from the nucleus to the cytoplasm and that Tyr phosphorylated Sam 68 associates with the SH 2 domains of p 85 PI3K and GAP , in vivo and in vitro . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
In the present work , we have found that Sam 68 is tyrosine phosphorylated in peripheral blood mononuclear cells ( PBMC ) from HIV infected subjects , leading to the formation of signalling complexes with p 85 the regulatory subunit of PI3K , GAP and STAT 3 , and decreasing its RNA binding capacity . ^^^ |
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Interacting proteins: Q07666 and P27986 |
Pubmed |
SVM Score :0.0 |
We investigated whether phosphatidylinositol 3 kinase ( PI3K ) and 68 kDa Src associated during mitosis ( SAM 68 ) are involved in angiotensin 2 ( ANG 2 ) growth signaling in vascular smooth muscle cells ( VSMCs ) from spontaneously hypertensive rats ( SHR ) . ^^^ The PI3K SAM 68 interaction was assessed by coimmunoprecipitation , and SAM 68 activity was evaluated by poly ( U ) binding . ^^^ ANG 2 increased the phosphorylation of p85alpha and kinase activity of the 110 kDa PI3K subunit in VSMCs from SHR and transiently increased p85alpha SAM 68 association . ^^^ ANG 2 stimulated phosphoinositol phosphate synthesis by PI3K in SAM 68 immunoprecipitates in both groups , with significantly enhanced effects in SHR . ^^^ Inhibition of PI3K , using the selective inhibitor LY 294002 , and downregulation of SAM 68 , by antisense oligonucleotides , significantly decreased ANG 2 stimulated incorporation of [ 3H ] leucine and [ 3H ] thymidine in VSMCs , showing the functional significance of PI3K and SAM 68 . ^^^ |
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