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KIF26A

Chr 14q32.33

kinesin family member 26A

Aliases:
KIAA1236, DKFZP434N178
MANE:
ENST00000423312.7

Annotations refreshed 1 month ago.

Predicted protein structure

Clinical relevance (Genomics England PanelApp)

Diagnostic Grade (Green)

  • Fetal anomalies

    BIALLELIC, autosomal or pseudoautosomal
  • Hydrocephalus

    BIALLELIC, autosomal or pseudoautosomal
  • Intellectual disability

    BIALLELIC, autosomal or pseudoautosomal
  • Malformations of cortical development

    BIALLELIC, autosomal or pseudoautosomal
  • Paediatric pseudo-obstruction syndrome

    BIALLELIC, autosomal or pseudoautosomal

Disease associations (Open Targets)

  • cortical dysplasia, complex, with other brain malformations 11

    0.69
  • smoking initiation

    0.38
  • smoking cessation

    0.38
  • complex cortical dysplasia with other brain malformations

    0.37
  • diabetes mellitus

    0.36
  • stricture

    0.32
  • nicotine dependence

    0.31
  • mental disorder

    0.30
  • type 2 diabetes mellitus

    0.29
  • male reproductive organ cancer

    0.29

Score is the Open Targets composite evidence score (0-1). Higher = stronger gene-disease association.

Protein function (UniProt)

Kinesin-like protein KIF26A

Atypical kinesin that plays a key role in enteric neuron development. Acts by repressing a cell growth signaling pathway in the enteric nervous system development, possibly via its interaction with GRB2 that prevents GRB2-binding to SHC, thereby attenating the GDNF-Ret signaling (By similarity). Binds to microtubules but lacks microtubule-based motility due to the absence of ATPase activity (By similarity). Plays a critical role in cerebral cortical development. It probably acts as a microtubule stabilizer that regulates neurite growth and radial migration of cortical excitatory neurons (PubMed:36228617)

Data sources: HGNC (CC BY 4.0), AlphaFold (CC BY 4.0, Jumper et al. Nature 2021), Genomics England PanelApp (CC BY 4.0), ClinGen, Open Targets (CC0), UniProt.

Not for sole clinical decision-making. Always verify against primary sources.