Inverted Formin 2 Regulates Actin Dynamics by Antagonizing Rho/Diaphanous-related Formin Signaling

• Published in: Journal of the American Society of Nephrology Vol. 24; no. 6; pp. 917 - 929
• Main Authors: HUA SUN, SCHLONDORFF, Johannes, HIGGS, Henry N, POLLAK, Martin R
• Format: Journal Article
• Language: English
• Published: Washington, DC American Society of Nephrology 01.06.2013
• Subjects: Actins - metabolism; Basic Research; Biological and medical sciences; Carrier Proteins - metabolism; Cell Line, Transformed; Cytosol - metabolism; Dimerization; Glomerulosclerosis, Focal Segmental - genetics; Glomerulosclerosis, Focal Segmental - metabolism; Humans; Medical sciences; Membrane Microdomains - metabolism; Membrane Proteins - metabolism; Microfilament Proteins - chemistry; Microfilament Proteins - genetics; Microfilament Proteins - metabolism; Nephrology. Urinary tract diseases; Podocytes - cytology; Podocytes - metabolism; Point Mutation; Protein Structure, Quaternary; Protein Transport - physiology; Pseudopodia - metabolism; rhoA GTP-Binding Protein - metabolism; RNA, Small Interfering - metabolism; Signal Transduction - physiology; Signal transduction; Nephrology; Regulation(control); Actin; Dynamics; Contractile protein; Urology

Mutations in inverted formin 2 INF2 are a common cause of familial FSGS. INF2 interacts with diaphanous-related formins (mDia) and antagonizes mDia-mediated actin polymerization in response to active Rho signaling, suggesting that dysregulation of these pathways may mediate the development of INF2-r...