Seroatlas · Human Serome Atlas

DEFB123

Beta-defensin 123

Also known as: DB123_HUMAN, DEFB-23

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

Protein identityUniProt · HPA

UniProt accession
Q8N688
Gene
DEFB123
Ensembl
ENSG00000180424
Chromosome
20
Canonical length
67 aa
Protein class
Predicted secreted proteins
Secretome location
Secreted in other tissues

OverviewNCBI Gene

Defensins are cysteine-rich cationic polypeptides that are important in the host immunologic response to invading microorganisms. This antimicrobial protein is secreted and is a member of the beta defensin protein family. Beta defensin genes are found in several clusters throughout the genome, with this gene mapping to a cluster at 20q11.1. Two transcript variants, one protein-coding and the other not, have been found for this gene. [provided by RefSeq, Nov 2014]

Canonical amino-acid sequenceUniProt

67 residues, UniProt reviewed canonical sequence.

>Q8N688|DEFB123
     1  MKLLLLTLTV LLLLSQLTPG GTQRCWNLYG KCRYRCSKKE RVYVYCINNK MCCVKPKYQP
    61  KERWWPF

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against DEFB123 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
Secreted
Secreted
Yes
Transmembrane segments
0
Mean surface accessibility (rSASA)
0.49
Highest tissue expression
207 nTPM

Expression across tissuesHPA

Tissue

  • testis: 207 nTPM
  • epididymis: 150 nTPM
  • small intestine: 0.3 nTPM
  • spleen: 0.3 nTPM
  • prostate: 0.2 nTPM
  • vagina: 0.2 nTPM

Single-cell type

  • sertoli cells: 230 nCPM
  • epididymal principal cells: 119 nCPM
  • late spermatids: 60 nCPM
  • late primary spermatocytes: 21 nCPM
  • early spermatids: 16 nCPM
  • leydig cells: 5.2 nCPM

Immune cell

  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • gdT-cell: 0 nTPM
  • intermediate monocyte: 0 nTPM
  • MAIT T-cell: 0 nTPM

Brain region

  • amygdala: 0 nTPM
  • basal ganglia: 0 nTPM
  • cerebellum: 0 nTPM
  • cerebral cortex: 0 nTPM
  • choroid plexus: 0 nTPM
  • hippocampal formation: 0 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)
1.68
gnomAD pLI
0.41
gnomAD missense Z
0.32
DepMap mean gene effect
0.08
DepMap dependency class
selective

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 2% 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

KeywordsUniProt

Antibody and autoantibody relevanceSeroatlas analysis

Seroatlas reads DEFB123 as an antibody target. Whether an autoantibody or antibody against DEFB123 could matter depends on whether native DEFB123 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

DEFB123 is annotated as secreted, so native DEFB123 circulates and is directly accessible to antibodies. Secreted and cell-surface proteins are the autoantibody targets most likely to act like drugs, blocking or depleting the native protein.

Annotation status

The present source text does not explicitly label DEFB123 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/DEFB123. 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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