Seroatlas · Human Serome Atlas

VIM

Vimentin

Also known as: VIME_HUMAN

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

Protein identityUniProt · HPA

UniProt accession
P08670
Gene
VIM
Ensembl
ENSG00000026025
Chromosome
10
Canonical length
466 aa
Protein class
Disease related genes, Human disease related genes, Plasma proteins, Predicted intracellular proteins
Subcellular location
Intermediate filaments

OverviewNCBI Gene

This gene encodes a type III intermediate filament protein. Intermediate filaments, along with microtubules and actin microfilaments, make up the cytoskeleton. The encoded protein is responsible for maintaining cell shape and integrity of the cytoplasm, and stabilizing cytoskeletal interactions. This protein is involved in neuritogenesis and cholesterol transport and functions as an organizer of a number of other critical proteins involved in cell attachment, migration, and signaling. Bacterial and viral pathogens have been shown to attach to this protein on the host cell surface. Mutations in this gene are associated with congenital cataracts in human patients. [provided by RefSeq, Aug 2017]

Canonical amino-acid sequenceUniProt

466 residues, UniProt reviewed canonical sequence.

>P08670|VIM
     1  MSTRSVSSSS YRRMFGGPGT ASRPSSSRSY VTTSTRTYSL GSALRPSTSR SLYASSPGGV
    61  YATRSSAVRL RSSVPGVRLL QDSVDFSLAD AINTEFKNTR TNEKVELQEL NDRFANYIDK
   121  VRFLEQQNKI LLAELEQLKG QGKSRLGDLY EEEMRELRRQ VDQLTNDKAR VEVERDNLAE
   181  DIMRLREKLQ EEMLQREEAE NTLQSFRQDV DNASLARLDL ERKVESLQEE IAFLKKLHEE
   241  EIQELQAQIQ EQHVQIDVDV SKPDLTAALR DVRQQYESVA AKNLQEAEEW YKSKFADLSE
   301  AANRNNDALR QAKQESTEYR RQVQSLTCEV DALKGTNESL ERQMREMEEN FAVEAANYQD
   361  TIGRLQDEIQ NMKEEMARHL REYQDLLNVK MALDIEIATY RKLLEGEESR ISLPLPNFSS
   421  LNLRETNLDS LPLVDTHSKR TLLIKTVETR DGQVINETSQ HHDDLE

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against VIM 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)
0.54
Highest tissue expression
5,524 nTPM

Expression across tissuesHPA

Tissue

  • blood vessel: 5,524 nTPM
  • ovary: 3,586 nTPM
  • adipose tissue: 3,318 nTPM
  • breast: 2,291 nTPM
  • cervix: 1,648 nTPM
  • fallopian tube: 1,375 nTPM

Single-cell type

  • müller glia: 6,804 nCPM
  • decidual stromal cells: 5,626 nCPM
  • schwann cells: 5,554 nCPM
  • mast cells: 5,505 nCPM
  • ovarian stromal cells: 4,974 nCPM
  • lymphatic endothelial cells: 4,530 nCPM

Immune cell

  • myeloid DC: 867 nTPM
  • classical monocyte: 752 nTPM
  • basophil: 670 nTPM
  • total PBMC: 615 nTPM
  • T-reg: 483 nTPM
  • non-classical monocyte: 474 nTPM

Brain region

  • medulla oblongata: 927 nTPM
  • choroid plexus: 706 nTPM
  • thalamus: 538 nTPM
  • white matter: 407 nTPM
  • spinal cord: 388 nTPM
  • hypothalamus: 368 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about VIM.

Disease | AllUniProt

Conditions VIM is implicated in, by any mechanism.

Disease | GeneticClinVar

3 pathogenic / likely-pathogenic of 149 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

Disease | ImmuneIEDB

Conditions an epitope on VIM was assayed in.

Disease | AutoantibodyPubMed

Conditions in which antibodies against VIM are reported. Each links to that disease's full target list.

Showing 6 of 7 — disease pages carrying at least 10 antigens.

ReferencesPubMed · IEDB

Publications for VIM from three distinct lines of evidence, kept separate because they answer different questions: whether antibodies are directed at the protein, whether a B-cell epitope has been mapped on it, and whether a T-cell epitope has. Each is labelled with its source.

Reference: AutoantibodyPubMed

71 publications

Show 20 more of 71 total

Reference: B cellIEDB

29 publications

Show 20 more of 29 total

Reference: T cellIEDB

20 publications

Show 15 more

Sources: PubMed — antigen-level antibody evidence from a custom retrieval. Records matching a controlled set of autoantibody terms (the MeSH descriptors Autoantibodies and Autoantigens, with title and abstract term variants) were obtained through NCBI E-utilities, and their titles and abstracts parsed for constructions that direct an antibody at a named protein rather than for co-occurrence. Captured names were resolved against UniProt nomenclature and each antigen adjudicated individually against the source text. IEDB — curated epitope assays from the Immune Epitope Database (Vita et al., Nucleic Acids Research 2019). Bibliographic records from PubMed and MeSH, U.S. National Library of Medicine; citation metrics from NIH iCite (Hutchins et al., PLoS Biology 2016). Titles link to PubMed; abstracts are not reproduced here. The NLM does not endorse this analysis.

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)
0.42
gnomAD pLI
0.71
gnomAD missense Z
1.21
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 VIM 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 VIM as an antibody target. Whether an autoantibody or antibody against VIM could matter depends on whether native VIM is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

VIM is annotated at the cell surface, where native VIM 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 VIM as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/VIM. 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).

© 2026 · Seroatlas, Discover Oregon LLC · Terms of use

Loading the interactive Seroatlas protein explorer...