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FLASH GENE
Symbol KIF1C contributors: mct/npt/shn - updated : 28-12-2018
HGNC name kinesin family member 1C
HGNC id 6317
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a FHA domain
  • N terminal motor domain
  • PTPD-binding domain
    • mono polymer monomer
    HOMOLOGY
    interspecies ortholog to murine Kif1c
    homolog to C.elegans M116.5
    intraspecies homolog to kinesin-like motor protein KIF1 c
    Homologene
    FAMILY
  • Kinesin-3 family
    • CATEGORY motor/contractile , transport
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    intracellular,cytoplasm,organelle,Golgi
    intracellular,cytoplasm,cytoskeleton,microtubule
    text Golgi apparatus and endoplasmic reticulum
    basic FUNCTION
  • act as microtubule-based molecular motors involved in intracellular transport
  • podosome regulation
  • microtubule motor KIF1C contributes to persistent cell migration primarily through stabilization of an extended cell rear
  • may likely be involved in transport around the Golgi apparatus rather than only Golgi-to-ER transport
  • the kinesin KIF1C is known to regulate podosomes, actin-rich adhesion structures that remodel the extracellular matrix during physiological processes
  • KIF1C is a player in the podosome-inducing signaling cascade
  • KIF1C can protect Golgi membranes from fragmentation in cells lacking an intact microtubule network
  • KIF1A or KIF1C must have an effect on the cycle of division before differentiation
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS cellular trafficking transport
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • PTPD1
  • transports RAB6A-vesicles and can influence Golgi complex organization
  • RAB6A binding to the motor domain inhibits microtubule interaction and in cells, decreasing the amount of motile KIF1C
    • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) SPAX2
    Susceptibility to autoimmune orchitis
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • kif1C(-/-) mice are viable and showed no obvious abnormalities
  • no significant difference in the distribution of the Golgi apparatus or in the transport from the Golgi apparatus to the endoplasmic reticulum in fibroblasts from kif1C(-/-) mice
  • Expression of mutation constructs or small interfering RNA-/short hairpin RNA-based depletion of KIF1C resulted in decreased podosome dynamics and ultimately in podosome deficiency