Seroatlas · Human Serome Atlas

WAS

Actin nucleation-promoting factor WAS

Also known as: IMD2, THC, WASP, WASP_HUMAN, WASPA

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

Protein identityUniProt · HPA

UniProt accession
P42768
Gene
WAS
Ensembl
ENSG00000015285
Chromosome
X
Canonical length
502 aa
Protein class
Cancer-related genes, Disease related genes, Human disease related genes, Predicted intracellular proteins
Subcellular location
Plasma membrane,Cytosol

OverviewNCBI Gene

The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

502 residues, UniProt reviewed canonical sequence.

>P42768|WAS
     1  MSGGPMGGRP GGRGAPAVQQ NIPSTLLQDH ENQRLFEMLG RKCLTLATAV VQLYLALPPG
    61  AEHWTKEHCG AVCFVKDNPQ KSYFIRLYGL QAGRLLWEQE LYSQLVYSTP TPFFHTFAGD
   121  DCQAGLNFAD EDEAQAFRAL VQEKIQKRNQ RQSGDRRQLP PPPTPANEER RGGLPPLPLH
   181  PGGDQGGPPV GPLSLGLATV DIQNPDITSS RYRGLPAPGP SPADKKRSGK KKISKADIGA
   241  PSGFKHVSHV GWDPQNGFDV NNLDPDLRSL FSRAGISEAQ LTDAETSKLI YDFIEDQGGL
   301  EAVRQEMRRQ EPLPPPPPPS RGGNQLPRPP IVGGNKGRSG PLPPVPLGIA PPPPTPRGPP
   361  PPGRGGPPPP PPPATGRSGP LPPPPPGAGG PPMPPPPPPP PPPPSSGNGP APPPLPPALV
   421  PAGGLAPGGG RGALLDQIRQ GIQLNKTPGA PESSALQPPP QSSEGLVGAL MHVMQKRSRA
   481  IHSSDEGEDQ AGDEDEDDEW DD

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against WAS 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)
0.55
Highest tissue expression
80 nTPM

Expression across tissuesHPA

Tissue

  • spleen: 80 nTPM
  • bone marrow: 62 nTPM
  • lymph node: 56 nTPM
  • appendix: 56 nTPM
  • thymus: 43 nTPM
  • tonsil: 37 nTPM

Single-cell type

  • neutrophils: 458 nCPM
  • hofbauer cells: 174 nCPM
  • monocytes: 172 nCPM
  • neutrophil progenitors: 144 nCPM
  • monocyte progenitors: 131 nCPM
  • cdc: 104 nCPM

Immune cell

  • eosinophil: 46 nTPM
  • neutrophil: 38 nTPM
  • non-classical monocyte: 11 nTPM
  • intermediate monocyte: 10 nTPM
  • classical monocyte: 9.5 nTPM
  • myeloid DC: 6.6 nTPM

Brain region

  • white matter: 26 nTPM
  • medulla oblongata: 23 nTPM
  • thalamus: 20 nTPM
  • pons: 19 nTPM
  • hypothalamus: 18 nTPM
  • cerebral cortex: 17 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about WAS.

Disease | AllUniProt

Conditions WAS is implicated in, by any mechanism.

Disease | GeneticClinVar

209 pathogenic / likely-pathogenic of 774 ClinVar records.

Conditions with pathogenic or likely-pathogenic variants.

  • Wiskott-Aldrich syndrome
  • Thrombocytopenia 1
  • X-linked severe congenital neutropenia
  • WAS-related disorder
  • Thrombocytopenia

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)
0.15
gnomAD pLI
1
gnomAD missense Z
1.98
DepMap mean gene effect
0
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

Molecular functions

Cellular components

Protein domainsUniProt · Pfam · InterPro

KeywordsUniProt

InteractionsUniProt · HPA

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

WAS 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 WAS as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/WAS. 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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