Seroatlas · Human Serome Atlas

KCNA5

Potassium voltage-gated channel subfamily A member 5

Also known as: HK2, HPCN1, KCNA5_HUMAN, Kv1.5

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

Protein identityUniProt · HPA

UniProt accession
P22460
Gene
KCNA5
Ensembl
ENSG00000130037
Chromosome
12
Canonical length
613 aa
Protein class
Disease related genes, FDA approved drug targets, Human disease related genes, Predicted membrane proteins, Transporters, Voltage-gated ion channels
Quaternary structure
Homotetramer

OverviewNCBI Gene

Potassium channels represent the most complex class of voltage-gated ino 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. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shaker-related subfamily. This member contains six membrane-spanning domains with a shaker-type repeat in the fourth segment. It belongs to the delayed rectifier class, the function of which could restore the resting membrane potential of beta cells after depolarization and thereby contribute to the regulation of insulin secretion. This gene is intronless, and the gene is clustered with genes KCNA1 and KCNA6 on chromosome 12. Defects in this gene are a cause of familial atrial fibrillation type 7 (ATFB7). [provided by RefSeq, May 2012]

Canonical amino-acid sequenceUniProt

613 residues, UniProt reviewed canonical sequence.

>P22460|KCNA5
     1  MEIALVPLEN GGAMTVRGGD EARAGCGQAT GGELQCPPTA GLSDGPKEPA PKGRGAQRDA
    61  DSGVRPLPPL PDPGVRPLPP LPEELPRPRR PPPEDEEEEG DPGLGTVEDQ ALGTASLHHQ
   121  RVHINISGLR FETQLGTLAQ FPNTLLGDPA KRLRYFDPLR NEYFFDRNRP SFDGILYYYQ
   181  SGGRLRRPVN VSLDVFADEI RFYQLGDEAM ERFREDEGFI KEEEKPLPRN EFQRQVWLIF
   241  EYPESSGSAR AIAIVSVLVI LISIITFCLE TLPEFRDERE LLRHPPAPHQ PPAPAPGANG
   301  SGVMAPPSGP TVAPLLPRTL ADPFFIVETT CVIWFTFELL VRFFACPSKA GFSRNIMNII
   361  DVVAIFPYFI TLGTELAEQQ PGGGGGGQNG QQAMSLAILR VIRLVRVFRI FKLSRHSKGL
   421  QILGKTLQAS MRELGLLIFF LFIGVILFSS AVYFAEADNQ GTHFSSIPDA FWWAVVTMTT
   481  VGYGDMRPIT VGGKIVGSLC AIAGVLTIAL PVPVIVSNFN YFYHRETDHE EPAVLKEEQG
   541  TQSQGPGLDR GVQRKVSGSR GSFCKAGGTL ENADSARRGS CPLEKCNVKA KSNVDLRRSL
   601  YALCLDTSRE TDL

LocalizationUniProt · AlphaFold · HPA

Whether an antibody against KCNA5 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)
0.47
Highest tissue expression
57 nTPM

Expression across tissuesHPA

Tissue

  • choroid plexus: 57 nTPM
  • blood vessel: 42 nTPM
  • heart muscle: 37 nTPM
  • retina: 7 nTPM
  • basal ganglia: 6.7 nTPM
  • pituitary gland: 6.5 nTPM

Single-cell type

  • retinal bipolar cells: 102 nCPM
  • vascular smooth muscle cells: 61 nCPM
  • retinal amacrine cells: 31 nCPM
  • pancreatic islet cells: 23 nCPM
  • pdcs: 20 nCPM
  • choroid plexus epithelial cells: 12 nCPM

Immune cell

  • plasmacytoid DC: 12 nTPM
  • basophil: 0 nTPM
  • classical monocyte: 0 nTPM
  • eosinophil: 0 nTPM
  • gdT-cell: 0 nTPM
  • intermediate monocyte: 0 nTPM

Brain region

  • choroid plexus: 114 nTPM
  • hypothalamus: 16 nTPM
  • midbrain: 14 nTPM
  • hippocampal formation: 13 nTPM
  • thalamus: 12 nTPM
  • white matter: 10 nTPM

DiseaseUniProt · ClinVar · IEDB · PubMed

Four sources answering four different questions about KCNA5.

Disease | AllUniProt

Conditions KCNA5 is implicated in, by any mechanism.

Disease | GeneticClinVar

3 pathogenic / likely-pathogenic of 594 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)
0.92
gnomAD pLI
0
gnomAD missense Z
-0.05
DepMap mean gene effect
0.02
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 KCNA5 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 KCNA5 as an antibody target. Whether an autoantibody or antibody against KCNA5 could matter depends on whether native KCNA5 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.

KCNA5 is annotated at the cell surface, where native KCNA5 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 KCNA5 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.

Canonical record: https://seroatlas.com/gene/KCNA5. 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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