Seroatlas · Human Serome Atlas

KCNV2

Potassium voltage-gated channel subfamily V member 2

Also known as: KCNV2_HUMAN, Kv8.2

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

Protein identityUniProt · HPA

UniProt accession
Q8TDN2
Gene
KCNV2
Ensembl
ENSG00000168263
Chromosome
9
Canonical length
545 aa
Protein class
Disease related genes, Human disease related genes, Potential drug targets, Predicted membrane proteins, Transporters, Voltage-gated ion channels
Quaternary structure
Homomultimer

OverviewNCBI Gene

Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. This gene encodes a member of the potassium voltage-gated channel subfamily V. This member is identified as a 'silent subunit', and it does not form homomultimers, but forms heteromultimers with several other subfamily members. Through obligatory heteromerization, it exerts a function-altering effect on other potassium channel subunits. This protein is strongly expressed in pancreas and has a weaker expression in several other tissues. [provided by RefSeq, Jul 2008]

Canonical amino-acid sequenceUniProt

545 residues, UniProt reviewed canonical sequence.

>Q8TDN2|KCNV2
     1  MLKQSERRRS WSYRPWNTTE NEGSQHRRSI CSLGARSGSQ ASIHGWTEGN YNYYIEEDED
    61  GEEEDQWKDD LAEEDQQAGE VTTAKPEGPS DPPALLSTLN VNVGGHSYQL DYCELAGFPK
   121  TRLGRLATST SRSRQLSLCD DYEEQTDEYF FDRDPAVFQL VYNFYLSGVL LVLDGLCPRR
   181  FLEELGYWGV RLKYTPRCCR ICFEERRDEL SERLKIQHEL RAQAQVEEAE ELFRDMRFYG
   241  PQRRRLWNLM EKPFSSVAAK AIGVASSTFV LVSVVALALN TVEEMQQHSG QGEGGPDLRP
   301  ILEHVEMLCM GFFTLEYLLR LASTPDLRRF ARSALNLVDL VAILPLYLQL LLECFTGEGH
   361  QRGQTVGSVG KVGQVLRVMR LMRIFRILKL ARHSTGLRAF GFTLRQCYQQ VGCLLLFIAM
   421  GIFTFSAAVY SVEHDVPSTN FTTIPHSWWW AAVSISTVGY GDMYPETHLG RFFAFLCIAF
   481  GIILNGMPIS ILYNKFSDYY SKLKAYEYTT IRRERGEVNF MQRARKKIAE CLLGSNPQLT
   541  PRQEN

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against KCNV2 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
6
Mean surface accessibility (rSASA)
0.41
Highest tissue expression
268 nTPM

Expression across tissuesHPA

Tissue

  • retina: 268 nTPM
  • testis: 4.5 nTPM
  • cerebellum: 0.4 nTPM
  • basal ganglia: 0.2 nTPM
  • ovary: 0.2 nTPM
  • blood vessel: 0.1 nTPM

Single-cell type

  • cone photoreceptor cells: 733 nCPM
  • rod photoreceptor cells: 532 nCPM
  • early spermatids: 121 nCPM
  • epicardial cells: 82 nCPM
  • late spermatids: 41 nCPM
  • oocytes: 37 nCPM

Immune cell

  • naive B-cell: 0.1 nTPM
  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • gdT-cell: 0 nTPM
  • intermediate monocyte: 0 nTPM

Brain region

  • cerebral cortex: 5.8 nTPM
  • amygdala: 5.4 nTPM
  • basal ganglia: 5.2 nTPM
  • hippocampal formation: 4.3 nTPM
  • hypothalamus: 3.9 nTPM
  • white matter: 3.3 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about KCNV2.

Disease | AllUniProt

Conditions KCNV2 is implicated in, by any mechanism.

  • Cone dystrophy with supernormal rod responses (CDSRR) MIM:610356

Disease | GeneticClinVar

84 pathogenic / likely-pathogenic of 820 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)
1.97
gnomAD pLI
0
gnomAD missense Z
-4.48
DepMap mean gene effect
0.08
DepMap dependency class
none

Cancer expressionTCGA

Across TCGA tumor cohorts, this protein is over-expressed in roughly 5% 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 KCNV2 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 KCNV2 as an antibody target. Whether an autoantibody or antibody against KCNV2 could matter depends on whether native KCNV2 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

KCNV2 is annotated at the cell surface, where native KCNV2 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 KCNV2 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/KCNV2. 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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