Seroatlas · Human Serome Atlas

SVIL

Supervillin

Also known as: SVIL_HUMAN

Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
O95425
Gene
SVIL
Ensembl
ENSG00000197321
Chromosome
10
Canonical length
2214 aa
Protein class
Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
Subcellular location
Plasma membrane,Actin filaments,Cytosol

OverviewNCBI Gene

This gene encodes a bipartite protein with distinct amino- and carboxy-terminal domains. The amino-terminus contains nuclear localization signals and the carboxy-terminus contains numerous consecutive sequences with extensive similarity to proteins in the gelsolin family of actin-binding proteins, which cap, nucleate, and/or sever actin filaments. The gene product is tightly associated with both actin filaments and plasma membranes, suggesting a role as a high-affinity link between the actin cytoskeleton and the membrane. The encoded protein appears to aid in both myosin II assembly during cell spreading and disassembly of focal adhesions. Several transcript variants encoding different isoforms of supervillin have been described. [provided by RefSeq, Apr 2016]

Canonical amino-acid sequenceUniProt

2214 residues, UniProt reviewed canonical sequence.

>O95425|SVIL
     1  MKRKERIARR LEGIENDTQP ILLQSCTGLV THRLLEEDTP RYMRASDPAS PHIGRSNEEE
    61  ETSDSSLEKQ TRSKYCTETS GVHGDSPYGS GTMDTHSLES KAERIARYKA ERRRQLAEKY
   121  GLTLDPEADS EYLSRYTKSR KEPDAVEKRG GKSDKQEESS RDASSLYPGT ETMGLRTCAG
   181  ESKDYALHVG DGSSDPEVLL NIENQRRGQE LSATRQAHDL SPAAESSSTF SFSGRDSSFT
   241  EVPRSPKHAH SSSLQQAASR SPSFGDPQLS PEARPSTGKP KHEWFLQKDS EGDTPSLINW
   301  PSRVKVREKL VKEESARNSP ELASESVTQR RHQPAPVHYV SFQSEHSAFD RVPSKAAGST
   361  RQPIRGYVQP ADTGHTAKLV TPETPENASE CSWVASATQN VPKPPSLTVL EGDGRDSPVL
   421  HVCESKAEEE EGEGEGEEKE EDVCFTEALE QSKKTLLALE GDGLVRSPED PSRNEDFGKP
   481  AVSTVTLEHQ KELENVAQPP QAPHQPTERT GRSEMVLYIQ SEPVSQDAKP TGHNREASKK
   541  RKVRTRSLSD FTGPPQLQAL KYKDPASRRE LELPSSKTEG PYGEISMLDT KVSVAQLRSA
   601  FLASANACRR PELKSRVERS AEGPGLPTGV ERERGSRKPR RYFSPGESRK TSERFRTQPI
   661  TSAERKESDR CTSHSETPTV DDEEKVDERA KLSVAAKRLL FREMEKSFDE QNVPKRRSRN
   721  TAVEQRLRRL QDRSLTQPIT TEEVVIAATE PIPASCSGGT HPVMARLPSP TVARSAVQPA
   781  RLQASAHQKA LAKDQTNEGK ELAEQGEPDS STLSLAEKLA LFNKLSQPVS KAISTRNRID
   841  TRQRRMNARY QTQPVTLGEV EQVQSGKLIP FSPAVNTSVS TVASTVAPMY AGDLRTKPPL
   901  DHNASATDYK FSSSIENSDS PVRSILKSQA WQPLVEGSEN KGMLREYGET ESKRALTGRD
   961  SGMEKYGSFE EAEASYPILN RAREGDSHKE SKYAVPRRGS LERANPPITH LGDEPKEFSM
  1021  AKMNAQGNLD LRDRLPFEEK VEVENVMKRK FSLRAAEFGE PTSEQTGTAA GKTIAQTTAP
  1081  VSWKPQDSSE QPQEKLCKNP CAMFAAGEIK TPTGEGLLDS PSKTMSIKER LALLKKSGEE
  1141  DWRNRLSRRQ EGGKAPASSL HTQEAGRSLI KKRVTESRES QMTIEERKQL ITVREEAWKT
  1201  RGRGAANDST QFTVAGRMVK KGLASPTAIT PVASPICGKT RGTTPVSKPL EDIEARPDMQ
  1261  LESDLKLDRL ETFLRRLNNK VGGMHETVLT VTGKSVKEVM KPDDDETFAK FYRSVDYNMP
  1321  RSPVEMDEDF DVIFDPYAPK LTSSVAEHKR AVRPKRRVQA SKNPLKMLAA REDLLQEYTE
  1381  QRLNVAFMES KRMKVEKMSS NSNFSEVTLA GLASKENFSN VSLRSVNLTE QNSNNSAVPY
  1441  KRLMLLQIKG RRHVQTRLVE PRASALNSGD CFLLLSPHCC FLWVGEFANV IEKAKASELA
  1501  TLIQTKRELG CRATYIQTIE EGINTHTHAA KDFWKLLGGQ TSYQSAGDPK EDELYEAAII
  1561  ETNCIYRLMD DKLVPDDDYW GKIPKCSLLQ PKEVLVFDFG SEVYVWHGKE VTLAQRKIAF
  1621  QLAKHLWNGT FDYENCDINP LDPGECNPLI PRKGQGRPDW AIFGRLTEHN ETILFKEKFL
  1681  DWTELKRSNE KNPGELAQHK EDPRTDVKAY DVTRMVSMPQ TTAGTILDGV NVGRGYGLVE
  1741  GHDRRQFEIT SVSVDVWHIL EFDYSRLPKQ SIGQFHEGDA YVVKWKFMVS TAVGSRQKGE
  1801  HSVRAAGKEK CVYFFWQGRH STVSEKGTSA LMTVELDEER GAQVQVLQGK EPPCFLQCFQ
  1861  GGMVVHSGRR EEEEENVQSE WRLYCVRGEV PVEGNLLEVA CHCSSLRSRT SMVVLNVNKA
  1921  LIYLWHGCKA QAHTKEVGRT AANKIKEQCP LEAGLHSSSK VTIHECDEGS EPLGFWDALG
  1981  RRDRKAYDCM LQDPGSFNFA PRLFILSSSS GDFAATEFVY PARAPSVVSS MPFLQEDLYS
  2041  APQPALFLVD NHHEVYLWQG WWPIENKITG SARIRWASDR KSAMETVLQY CKGKNLKKPA
  2101  PKSYLIHAGL EPLTFTNMFP SWEHREDIAE ITEMDTEVSN QITLVEDVLA KLCKTIYPLA
  2161  DLLARPLPEG VDPLKLEIYL TDEDFEFALD MTRDEYNALP AWKQVNLKKA KGLF

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against SVIL 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
Cell surface
Secreted
No
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.51
Highest tissue expression
751 nTPM

Expression across tissuesHPA

Tissue

  • skeletal muscle: 751 nTPM
  • tongue: 519 nTPM
  • colon: 300 nTPM
  • urinary bladder: 194 nTPM
  • heart muscle: 151 nTPM
  • blood vessel: 128 nTPM

Single-cell type

  • myonuclei: 4,265 nCPM
  • neutrophils: 2,216 nCPM
  • smooth muscle cells: 2,169 nCPM
  • thymic myoid cells: 1,390 nCPM
  • salivary myoepithelial cells: 1,299 nCPM
  • neutrophil progenitors: 1,240 nCPM

Immune cell

  • neutrophil: 261 nTPM
  • eosinophil: 59 nTPM
  • basophil: 44 nTPM
  • non-classical monocyte: 30 nTPM
  • naive CD4 T-cell: 17 nTPM
  • NK-cell: 15 nTPM

Brain region

  • cerebral cortex: 28 nTPM
  • medulla oblongata: 23 nTPM
  • thalamus: 19 nTPM
  • white matter: 19 nTPM
  • spinal cord: 18 nTPM
  • midbrain: 18 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about SVIL.

Disease | AllUniProt

Conditions SVIL is implicated in, by any mechanism.

Disease | GeneticClinVar

8 pathogenic / likely-pathogenic of 579 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

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)
0.36
gnomAD pLI
0
gnomAD missense Z
0.89
DepMap mean gene effect
-0.01
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).

OntologyGO

Biological processes

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of SVIL in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads SVIL as an antibody target. Whether an autoantibody or antibody against SVIL could matter depends on whether native SVIL is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

SVIL is annotated at the cell surface, where native SVIL is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.

Annotation status

The present source text does not explicitly label SVIL as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/SVIL. Study-independent annotations aggregated from UniProt, Human Protein Atlas, PubMed, IEDB, Pfam, InterPro, Gene Ontology, AlphaFold, gnomAD, DepMap, ClinVar, TCGA. Catalog release seroatlas-reviewed-human-uniprot-20260313.

Seroatlas is the reference for exploring autoantibody and antibody serology at the human-protein level: the autoreactome and human serome, multiplex serology (HuProt, HuScan, VirScan, PhIP-Seq).

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