Seroatlas · Human Serome Atlas

SWI5

DNA repair protein SWI5 homolog

Also known as: SWI5_HUMAN

Cross-references: UniProt · GeneCards · NCBI Gene

Protein identityUniProt · HPA

UniProt accession
Q1ZZU3
Gene
SWI5
Canonical length
235 aa
Protein class
Predicted intracellular proteins

OverviewNCBI Gene

No narrative summary is available for SWI5 in this catalog release; identity and structured annotations are shown without generated factual claims.

Canonical amino-acid sequenceUniProt

235 residues, UniProt reviewed canonical sequence.

>Q1ZZU3|SWI5
     1  MQRRGQRDLW RHNKSCARNR CPRPPRERGG AGFPWVRAQL SVRQFTLRVR VPGPVHLRGR
    61  SPTPALDPLA PLNPLIRGPR TPGLRRWIQS LALLLPNCSS SRIPTVPRPH SGLWVQSDFP
   121  LGFLSRTEPR LTRSCRGAFR SPRPLPKSGQ ADGTSEESLH LDIQKLKEKR DMLDKEISQF
   181  VSEGYSVDEL EDHITQLHEY NDIKDVGQML MGKLAVIRGV TTKELYPEFG LDMND

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against SWI5 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)
0.62
Highest tissue expression
149 nTPM

Expression across tissuesHPA

Tissue

  • testis: 149 nTPM
  • parathyroid gland: 71 nTPM
  • epididymis: 69 nTPM
  • choroid plexus: 67 nTPM
  • pituitary gland: 53 nTPM
  • thyroid gland: 43 nTPM

Single-cell type

  • late spermatids: 1,651 nCPM
  • early spermatids: 1,340 nCPM
  • late primary spermatocytes: 678 nCPM
  • platelets: 274 nCPM
  • epididymal principal cells: 223 nCPM
  • megakaryocytes: 198 nCPM

Immune cell

  • basophil: 56 nTPM
  • eosinophil: 26 nTPM
  • plasmacytoid DC: 22 nTPM
  • NK-cell: 22 nTPM
  • naive CD8 T-cell: 21 nTPM
  • naive B-cell: 21 nTPM

Brain region

  • choroid plexus: 24 nTPM
  • hypothalamus: 23 nTPM
  • cerebellum: 21 nTPM
  • basal ganglia: 21 nTPM
  • white matter: 21 nTPM
  • midbrain: 20 nTPM

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)
1.1
gnomAD pLI
0
gnomAD missense Z
-0.97
DepMap mean gene effect
-0.16
DepMap dependency class
selective

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

Cellular components

Protein domainsUniProt · Pfam · InterPro

  • DNA repair protein, Swi5
  • Swi5

KeywordsUniProt

InteractionsUniProt · HPA

Protein binding partners of SWI5 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 SWI5 as an antibody target. Whether an autoantibody or antibody against SWI5 could matter depends on whether native SWI5 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

SWI5 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 SWI5 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/SWI5. 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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