| Interacting proteins: P16473 and P27986 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P16473 and P27986 |
Pubmed |
SVM Score :0.0 |
| Our results show that ( 1 ) the TSHR ( M 623 ) or ( M 632 ) cDNAs give rise to 3T3 clones presenting a fully neoplastic phenotype ( growth in agar and nude mouse tumorigenesis ) ; this phenotype was weaker in the cells transformed by the 632 cDNA ; ( 2 ) suggest that the fully transformed phenotype of our 3T3 cells , may be the consequence of the additive effect of the activation of at least two different pathways : the cAMP pathway through G ( alpha ) s and the Ras dependent MAPK pathway through G ( beta ) gamma and PI3K and ( 3 ) show that the PI3K isoform playing a key role as an effector in the MAPK pathway activation in our 3T3 transformed cells is PI3Kgamma . ^^^ |
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| Interacting proteins: P16473 and P27986 |
Pubmed |
SVM Score :0.0 |
| This study investigated the roles of the phosphatidylinositol 3 kinase ( PI3K ) , PDK 1 , FRAP / mammalian target of rapamycin , and ribosomal S 6 kinase 1 ( S6K1 ) signaling mechanism by which TSH and the stimulating type TSHR antibodies regulate thyrocyte proliferation and the follicle activities in vitro and in vivo . ^^^ The TSHR immunoprecipitates exhibited PI3K activity , which was higher in the cells treated with either TSH or 8 bromo cAMP . ^^^ TSH and cAMP increased the tyrosine phosphorylation of TSHR and the association between TSHR and the p85alpha regulatory subunit of PI3K . ^^^ These findings suggest an interaction between TSHR and PI3K , which is stimulated by TSH and cAMP and might involve the downstream S6K1 but not Akt / protein kinase B . ^^^ |
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