INF2mediated

INF2-mediated refers to cellular processes governed by inverted formin-2 (INF2), a member of the formin family of actin-nucleating proteins. INF2 participates in remodeling the actin cytoskeleton by promoting the assembly and turnover of actin filaments in response to cellular signals.

INF2 contains characteristic formin domains, including an actin-nucleating FH2 domain and a profilin-binding FH1 domain, arranged within an autoinhibitory DID–DAD module. In resting cells INF2 is held in an inactive conformation, and signaling relieves autoinhibition to promote localized actin polymerization. INF2 activity is regulated by calcium signals and by interactions at endoplasmic reticulum membranes.

INF2 localizes to the endoplasmic reticulum and concentrates at mitochondria-associated membranes, where calcium flux triggers transient actin polymerization. This INF2-mediated actin remodeling supports mitochondrial fission, ER morphology, and organelle contact site dynamics, and it contributes to processes such as vesicle trafficking and cell movement in some contexts.

Mutations in INF2 are associated with kidney disease, most notably focal segmental glomerulosclerosis (FSGS) and nephrotic syndrome, highlighting its importance in podocyte and renal cell function. The precise mechanisms by which INF2 dysfunction leads to disease remain under investigation.

INF2-mediated processes are studied with genetic knockdown or knockout models, overexpression of wild-type or mutant INF2, and imaging of actin dynamics and organelle morphology. Understanding INF2-mediated actin remodeling contributes to insights into cell biology and disease.