SHP-2 regulates myogenesis by coupling to FAK signaling pathway

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]}

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

• 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