VIL1
Villin-1
Also known as: D2S1471, VIL, VILI_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P09327
- Gene
- VIL1
- Ensembl
- ENSG00000127831
- Chromosome
- 2
- Canonical length
- 827 aa
- Protein class
- Cancer-related genes, Disease related genes, Plasma proteins, Predicted intracellular proteins
- Subcellular location
- Plasma membrane
- Quaternary structure
- Homodimer
OverviewNCBI Gene
This gene encodes a member of a family of calcium-regulated actin-binding proteins. This protein represents a dominant part of the brush border cytoskeleton which functions in the capping, severing, and bundling of actin filaments. Two mRNAs of 2.7 kb and 3.5 kb have been observed; they result from utilization of alternate poly-adenylation signals present in the terminal exon. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
827 residues, UniProt reviewed canonical sequence.
>P09327|VIL1
1 MTKLSAQVKG SLNITTPGLQ IWRIEAMQMV PVPSSTFGSF FDGDCYIILA IHKTASSLSY
61 DIHYWIGQDS SLDEQGAAAI YTTQMDDFLK GRAVQHREVQ GNESEAFRGY FKQGLVIRKG
121 GVASGMKHVE TNSYDVQRLL HVKGKRNVVA GEVEMSWKSF NRGDVFLLDL GKLIIQWNGP
181 ESTRMERLRG MTLAKEIRDQ ERGGRTYVGV VDGENELASP KLMEVMNHVL GKRRELKAAV
241 PDTVVEPALK AALKLYHVSD SEGNLVVREV ATRPLTQDLL SHEDCYILDQ GGLKIYVWKG
301 KKANEQEKKG AMSHALNFIK AKQYPPSTQV EVQNDGAESA VFQQLFQKWT ASNRTSGLGK
361 THTVGSVAKV EQVKFDATSM HVKPQVAAQQ KMVDDGSGEV QVWRIENLEL VPVDSKWLGH
421 FYGGDCYLLL YTYLIGEKQH YLLYVWQGSQ ASQDEITASA YQAVILDQKY NGEPVQIRVP
481 MGKEPPHLMS IFKGRMVVYQ GGTSRTNNLE TGPSTRLFQV QGTGANNTKA FEVPARANFL
541 NSNDVFVLKT QSCCYLWCGK GCSGDEREMA KMVADTISRT EKQVVVEGQE PANFWMALGG
601 KAPYANTKRL QEENLVITPR LFECSNKTGR FLATEIPDFN QDDLEEDDVF LLDVWDQVFF
661 WIGKHANEEE KKAAATTAQE YLKTHPSGRD PETPIIVVKQ GHEPPTFTGW FLAWDPFKWS
721 NTKSYEDLKA ELGNSRDWSQ ITAEVTSPKV DVFNANSNLS SGPLPIFPLE QLVNKPVEEL
781 PEGVDPSRKE EHLSIEDFTQ AFGMTPAAFS ALPRWKQQNL KKEKGLFLocalizationUniProt · AlphaFold · HPA
Whether an antibody against VIL1 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.28
- Highest tissue expression
- 411 nTPM
Expression across tissuesHPA
Tissue
- small intestine: 411 nTPM
- duodenum: 371 nTPM
- rectum: 172 nTPM
- colon: 165 nTPM
- liver: 29 nTPM
- pancreas: 28 nTPM
Single-cell type
- enterocytes: 559 nCPM
- colonocytes: 252 nCPM
- enteric transient amplifying cells: 180 nCPM
- enteric stem cells: 167 nCPM
- goblet cells: 160 nCPM
- tuft cells: 150 nCPM
Immune cell
- total PBMC: 4 nTPM
- neutrophil: 1.3 nTPM
- basophil: 0.3 nTPM
- plasmacytoid DC: 0.2 nTPM
- myeloid DC: 0.1 nTPM
- classical monocyte: 0 nTPM
Brain region
- cerebellum: 1.3 nTPM
- cerebral cortex: 1.1 nTPM
- basal ganglia: 0.8 nTPM
- hippocampal formation: 0.8 nTPM
- white matter: 0.8 nTPM
- amygdala: 0.7 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about VIL1.
Disease | ImmuneIEDB
Conditions an epitope on VIL1 was assayed in.
- narcolepsy B cell
- multiple sclerosis B cell
- peripheral nervous system disease B cell
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.86
- gnomAD pLI
- 0
- gnomAD missense Z
- 0.9
- DepMap mean gene effect
- -0.04
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 3% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- actin filament capping
- actin filament depolymerization
- actin filament polymerization
- actin filament severing
- actin polymerization or depolymerization
- apoptotic process
- barbed-end actin filament capping
- cellular response to epidermal growth factor stimulus
- cellular response to hepatocyte growth factor stimulus
- cytoplasmic actin-based contraction involved in cell motility
- epidermal growth factor receptor signaling pathway
- epithelial cell differentiation
- intestinal D-glucose absorption
- positive regulation of actin filament bundle assembly
- positive regulation of actin filament depolymerization
- positive regulation of cell migration
- positive regulation of epithelial cell migration
- positive regulation of lamellipodium morphogenesis
- positive regulation of multicellular organism growth
- positive regulation of protein localization to plasma membrane
- protein-containing complex assembly
- regulation of actin nucleation
- regulation of cell shape
- regulation of lamellipodium morphogenesis
- regulation of microvillus length
- regulation of wound healing
- response to bacterium
- terminal web assembly
Molecular functions
- actin filament binding
- calcium ion binding
- cysteine-type endopeptidase inhibitor activity involved in apoptotic process
- identical protein binding
- lysophosphatidic acid binding
- phosphatidylinositol-4,5-bisphosphate binding
- protein homodimerization activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
KeywordsUniProt
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads VIL1 as an antibody target. Whether an autoantibody or antibody against VIL1 could matter depends on whether native VIL1 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
VIL1 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label VIL1 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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