Focal adhesion kinase - The basis of local hypertrophic signaling domains

Autor(es)

Franchini, K. G.

• Tipo de documento: Artigo Científico
• Fonte: JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY; v. 52, n. 2, p. 8-pg., 2012-02-01.

Resumo

Focal adhesion kinase (FAK), a broadly expressed non-receptor tyrosine kinase which transduces signals from integrins, growth and hormonal factors, is a key player in many fundamental biological processes and functions, including cell adhesion, migration, proliferation and survival. The involvement of FAK in this range of functions supports its role in important aspects of organismal development and disease, such as central nervous system and cardiovascular development, cancer, cardiac hypertrophy and tissue fibrosis. Many functions of FAK are correlated with its tyrosine kinase activity, which is temporally and spatially controlled by complex intra-molecular autoinhibitory conformation and inter-molecular interactions with protein and lipid partners. The inactivation of FAK in mice results in embryonic lethality attributed to the lack of proper development and function of the heart. Accordingly, embryonic FAK myocyte-specific knockout mice display lethal cardiac defects such as thin ventricle wall and ventricular septum defects. Emerging data also support a role for FAK in the reactive hypertrophy and failure of adult hearts. Moreover, the mechanisms that regulate FAK in differentiated cardiac myocytes to biomechanical stress and soluble factors are beginning to be revealed and are discussed here together with data that connect FAK to its downstream effectors. This article is part of a Special Issue entitled "Local Signaling in Myocytes". (C) 2011 Elsevier Ltd. All rights reserved. (AU)

• Processo FAPESP: 06/54878-3 - Patogênese da hipertrofia e insuficiência cardíacas: mecanismos ativados por estimulo mecânico
• Beneficiário: Kleber Gomes Franchini
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 07/59442-1 - interacao com aB-cristalina protege a FAK da degradacao e promove a sobrevivencia de miocitos cardiacos durante o estresse mecanico
• Beneficiário: Michelle Bueno de Moura Pereira
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 08/53457-0 - Efeitos da hiperexpressao transgenica de fak no coracao de camundongos.
• Beneficiário: carolina fernanda manfredi zambon clemente
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 08/57629-0 - Novas quinazolinas 2,8-dissubstituídas com potencial atividade de inibição da quinase de adesão focal (FAK)
• Beneficiário: João Eustáquio Antunes
• Modalidade de apoio: Bolsas no Brasil - Doutorado