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FLASH GENE
Symbol KIF3A contributors: shn/npt/pgu - updated : 07-09-2016
HGNC name kinesin family member 3A
HGNC id 6319
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • N terminal globular domain, motor domain with an ATP and the microtubule binding sites
  • a long alpha-helical coiled-coil region (stalk region), involved in dimerization
  • a small C terminal domain, potentially involved in interaction with other proteins, vesicles or organelles
  • mono polymer heteromer , dimer
    HOMOLOGY
    interspecies ortholog to KIF3A, Pan troglodytes
    ortholog to Kif3a, Mus musculus
    ortholog to kif3a, Danio rerio
    ortholog to Kif3a; Rattus norvegicus
    Homologene
    FAMILY
  • ATP dependent superfamily
  • kinesin-like protein family
  • Kinesin II subfamily
  • putative microtubule associated motor protein family
  • CATEGORY motor/contractile , transport
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,Golgi
    intracellular,cytoplasm,cytosolic
    intracellular,cytoplasm,cytoskeleton,microtubule,centrosome
    intracellular,cytoplasm,cytoskeleton,microfilament
    text
  • cilia
  • AXIN1, TNKS2 and KIF3A are co-localized with SLC2A4 on the trans-Golgi network
  • during spermatogenesis KIF3A and KBP localized in the cytoplasm of round spermatids and manchette of elongating spermatids
  • basic FUNCTION
  • involved in anterograde transport of membranous organelles in the axon, distinct from synaptic vesicles
  • required to transport opsin and arrestin from the inner to the outer segment of phosphoreceptor
  • ciliary activity in early embryo putatively involved in the nodal flow supposed to break symetry
  • required for the maintenance of primary cilia (playing a role in maintaining the differentiation of lumen-forming epithelia
  • required for HH response
  • kinesin-2 complex (KIF3A, KIF3B) plays an important role not only in interphase but also in mitosis
  • play a role in subcellular transport of several cancer-relatedproteins, including the b-catenin–cadherin(s) complex
  • required for normal craniofacial patterning
  • involved in truncation of primary cilia causing a gain of Hedgehog function, and aberrant neural crest cell proliferation in the facial midline
  • regulates hair cell polarization through both ciliary and non-ciliary mechanisms
  • key component of the hair cell-intrinsic polarity machinery, which acts in concert with the tissue polarity pathway
  • in addition to its ciliogenic roles, KIF3A recruits DCTN1 to the subdistal appendages of mother centrioles, critical for centrosomes to function as microtubule-organizing centres
  • is responsible for intraflagellar transport, which is required for protein delivery during axoneme formation in ciliated cells
  • essential role of KIF3A-mediated microtubular transport in the development of spermatozoa and male fertility
  • functions as an agonist of the Wnt signaling pathway in prostate cancer
  • midline cranial neural crest cells require KIF3A function in order to integrate and respond to Wnt signals from the surrounding epithelia
  • KIF3A, KIF3B (KIF3AB) is an N-terminal processive kinesin-2 family member best known for its role in intraflagellar transport
  • the kinesin-2 family motor KIF3A/KIF3B works together with dynein to bidirectionally transport intraflagellar particles, melanosomes, and neuronal vesicles
  • visual pigments transport to the retinal outer segment despite removal of KIF3A and IFT88, and KIF3A-mediated anterograde IFT88 is responsible for photoreceptor transition zone and axoneme formation
  • KIF17 and KIF3A do not act synergistically and did not prevent rhodopsin trafficking to rod outer segments
  • is required for the sperm tail formation and nuclear shaping during spermatogenesis
  • KIF3A, KIF3B, KIF3C is classified as a heterotrimeric kinesin-2 that is best known for organelle transport in neurons
  • is essential for glioblastoma multiforme (GBM) cell ciliogenesis, but its role in modulating GBM cell behavior is highly variable
  • anterograde intraflagellar transport motor protein, that regulates the integrity of primary cilia and various cellular functions
  • is important in the differentiation of dental follicle cells and human dental pulp cells through the Wnt pathway
  • plays a conserved role in photoreceptor outer segment formation and intracellular transport
  • CELLULAR PROCESS cell cycle, division, mitosis
    PHYSIOLOGICAL PROCESS development
    text determination of left-right asymetry
    PATHWAY
    metabolism
    signaling
    a component
  • KIF3A-PAK1 signaling coordinates planar polarization of the hair bundle and the basal body in hair cells
  • component of the kinesin-2 motor
  • intermolecular communication within the KIF3AC heterodimer modulates entry into the processive run regardless of whether the run is initiated by the KIF3A or KIF3C motor domain
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • CSPG6
  • VHL binding partner (mediates binding of VHL to microtubules)
  • KIF3B and KIF3C
  • Kinesin-Associated Protein 3 (KIFAP3)
  • Smoothened (SMO)
  • MAP kinase kinase kinase MLK2
  • Growth arrest and DNA-damage-indictible gene 34 (GADD34)
  • Never in mitosis gene A-related kinase 1 (NEK1)
  • TRIM60 most likely interacted with KIF3A-KIF3B independent of the adaptor kinesin-associated protein KIFAP3
  • AXIN1 interacts with TNKS2 and the kinesin motor protein KIF3A, forming a ternary complex crucial for SLC2A4 translocation in response to insulin
  • MAPK1 phosphorylates PARD3 and inhibits its binding with KIF3A, thereby controlling PARD3 transport and neuronal polarity
  • GLI1, GLI2, GLI3 interacts synergistically with KIFAP3 and KIF3A
  • GLI1 interactions with KIF3A-KIF3B-KIFAP3 complexes are essential for proper GLI1 transcriptional activity
  • cell & other
    REGULATION
    Other regulated by dual specificity phosphatase 26
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional       loss of function
    in polycystic kidney disease by inhibition of renal ciliogenesis
    constitutional   deletion    
    in ciliopathy with hydrocephalus, isolated craniosynostosis, hypertelorism, and clefting
    tumoral     --over  
    in the majority of human prostate cancer cell lines and primary tumor biopsies
    constitutional   deletion    
    selective deletion of KIF3A in osteoblasts disrupts primary cilia formation and/or function and impairs osteoblast-mediated bone formation through multiple pathways including intracellular calcium, hedgehog and Wnt signaling
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • mouse mutants lacking the KIF3A showed situs inversus and embryonic ciliary morphogenesis defects
  • mouse embryos lacking KIF3A die at 10 days postcoitum, exhibit randomized establishment of L-R asymmetry and display numerous structural abnormalities
  • complete loss of Kif3a led to large accumulations of opsin, arrestin and membranes within the photoreceptor inner segment and caused apoptotic photoreceptor cell death
  • Kif3a mutant zebrafish exhibited curved body axes and kidney cysts