| Full text | |
| Author(s): |
de Oliveira, Michel V.
[1]
;
Marin, Talita M.
[1]
;
Clemente, Carolina F.
[1]
;
Dalla Costa, Ana Paula
[1]
;
Judice, Carla C.
[1]
;
Franchini, Kleber G.
[1, 2]
Total Authors: 6
|
| Affiliation: | [1] Univ Estadual Campinas, Dept Internal Med, Sch Med, Campinas, SP - Brazil
[2] Brazilian Assoc Synchrotron Light Technol, Ctr Struct Mol Biol, Campinas, SP - Brazil
Total Affiliations: 2
|
| Document type: | Journal article |
| Source: | FEBS Letters; v. 583, n. 18, p. 2975-2981, 2009. |
| Web of Science Citations: | 11 |
| Abstract | |
Transient dephosphorylation of FAK at Tyr-397 is required for cell cycle withdrawal early on during myogenesis. Here, we show that upon serum starvation of C2C12 myoblasts, FAK is transiently dephosphorylated in parallel with SHP-2 activation and association with FAK. SHP-2 knockdown by RNA interference suppressed the transient upregulation of SHP-2 and dephosphorylation of FAK during myogenesis. Furthermore, depletion of SHP-2 retarded the cell cycle withdrawal and the differentiation of serum-starved myoblasts into myotubes. These data provide a mechanistic basis for the reduction in FAK activity in differentiating myoblasts, indicating that myogenesis is critically triggered by FAK/SHP-2 complex. (AU) | |
| FAPESP's process: | 06/54878-3 - Pathogenesis of cardiac hypertrophy and failure: mechanisms activated by mechanical stress |
| Grantee: | Kleber Gomes Franchini |
| Support Opportunities: | Research Projects - Thematic Grants |