SCUBA

VIL1 — Villin 1

VIL1 belongs to a gene co-expression module in 2 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

VIL1's module in each cell type

Cell typeModuleShares the module with
EnterocytesMicrovillus actin cytoskeleton
Cytoskeletal
CYB5A, HSD17B11, PRXL2A, SCIN, SMPD3, TDP2View in SCUBA
Goblet cellsAdhesion & Transport
Cytoskeletal
AHCYL1, CHMP1B, DDX5, DYNC1H1, DYNC1LI2, EIF4G2, ITGB1, PTTG1IP +4 moreView in SCUBA

About the gene

SynonymsD2S1471, VIL
Chromosome2: 218419121-218453295
Predicted locationIntracellular
Essential geneNo
Protein classCancer-related genes, Disease related genes, Plasma proteins, Predicted intracellular proteins
Molecular functionActin capping, Actin-binding
Biological processApoptosis

Function

Epithelial cell-specific Ca(2+)-regulated actin-modifying protein that modulates the reorganization of microvillar actin filaments. Plays a role in the actin nucleation, actin filament bundle assembly, actin filament capping and severing. Binds phosphatidylinositol 4,5-bisphosphate (PIP2) and lysophosphatidic acid (LPA); binds LPA with higher affinity than PIP2. Binding to LPA increases its phosphorylation by SRC and inhibits all actin-modifying activities. Binding to PIP2 inhibits actin-capping and -severing activities but enhances actin-bundling activity. Regulates the intestinal epithelial cell morphology, cell invasion, cell migration and apoptosis. Protects against apoptosis induced by dextran sodium sulfate (DSS) in the gastrointestinal epithelium. Appears to regulate cell death by maintaining mitochondrial integrity. Enhances hepatocyte growth factor (HGF)-induced epithelial cell motility, chemotaxis and wound repair. Upon S.flexneri cell infection, its actin-severing activity enhances actin-based motility of the bacteria and plays a role during the dissemination.

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.