Entity Details

Primary name KIF2A_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionO00139
EntryNameKIF2A_HUMAN
FullNameKinesin-like protein KIF2A
TaxID9606
Evidenceevidence at protein level
Length706
SequenceStatuscomplete
DateCreated1998-07-15
DateModified2021-06-02

Ontological Relatives

GenesKIF2A

GO terms

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GOName
GO:0000226 microtubule cytoskeleton organization
GO:0000922 spindle pole
GO:0003774 cytoskeletal motor activity
GO:0003777 microtubule motor activity
GO:0005524 ATP binding
GO:0005654 nucleoplasm
GO:0005730 nucleolus
GO:0005737 cytoplasm
GO:0005813 centrosome
GO:0005814 centriole
GO:0005819 spindle
GO:0005829 cytosol
GO:0005871 kinesin complex
GO:0005874 microtubule
GO:0006890 retrograde vesicle-mediated transport, Golgi to endoplasmic reticulum
GO:0007018 microtubule-based movement
GO:0007019 microtubule depolymerization
GO:0007052 mitotic spindle organization
GO:0007399 nervous system development
GO:0008017 microtubule binding
GO:0016020 membrane
GO:0016604 nuclear body
GO:0016887 ATP hydrolysis activity
GO:0019886 antigen processing and presentation of exogenous peptide antigen via MHC class II
GO:0030154 cell differentiation
GO:0030334 regulation of cell migration
GO:0051301 cell division
GO:0090307 mitotic spindle assembly
GO:0120103 centriolar subdistal appendage

Subcellular Location

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Subcellular Location
Cytoplasm

Domains

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DomainNameCategoryType
IPR001752 Kinesin motor domainDomainDomain
IPR019821 Kinesin motor domain, conserved siteSiteConserved site
IPR027417 P-loop containing nucleoside triphosphate hydrolaseFamilyHomologous superfamily
IPR027640 Kinesin-like proteinFamilyFamily
IPR036961 Kinesin motor domain superfamilyFamilyHomologous superfamily

Diseases

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Disease IDSourceNameDescription
615411 OMIMCortical dysplasia, complex, with other brain malformations 3 (CDCBM3)A disorder of aberrant neuronal migration and disturbed axonal guidance. Clinical features include early-onset epilepsy, and various malformations of cortical development such as agyria, posterior or frontal pachygyria, subcortical band heterotopia, and thin corpus callosum. The disease is caused by variants affecting the gene represented in this entry.