| UniProt functional annotation for L0N7N1 | |||
| UniProt code: L0N7N1. |
| Organism: | Mus musculus (Mouse). | |
| Taxonomy: | Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus. | |
| Function: | Microtubule motor protein that binds to microtubules with high affinity through each tubulin heterodimer and has an ATPase activity (PubMed:24949858). Plays a role in many processes like cell division, cytokinesis and also in cell proliferation and apoptosis (By similarity). During cytokinesis, targets to central spindle and midbody through its interaction with PRC1 and CIT respectively (By similarity). Regulates cell growth through regulation of cell cycle progression and cytokinesis. During cell cycle progression acts through SCF-dependent proteasomal ubiquitin-dependent protein catabolic process which controls CDKN1B degradation, resulting in positive regulation of cyclins, including CCNE1, CCND1 and CCNB1 (By similarity). During late neurogenesis, regulates the cerebellar and cerebral cortex development and olfactory bulb development through regulation of apoptosis, cell proliferation and cell division (PubMed:23308235, PubMed:24931760). Also is required for chromosome congression and alignment during mitotic cell cycle process (By similarity). Regulates cell spreading, focal adhesion dynamics, and cell migration through its interaction with RADIL resulting in regulation of RAP1A-mediated inside-out integrin activation by tethering RADIL on microtubules (By similarity). {ECO:0000250|UniProtKB:Q15058, ECO:0000269|PubMed:23308235, ECO:0000269|PubMed:24931760, ECO:0000269|PubMed:24949858}. | |
| Biophysicochemical properties: | Kinetic parameters: KM=62 uM for ATP {ECO:0000269|PubMed:24949858}; KM=33 uM for ATP (in the presence of microtubule) {ECO:0000269|PubMed:24949858}; | |
| Subunit: | Directly interacts with PRC1 within a complex also containing KIF4A, KIF20A and KIF23; targets to the central spindle. Directly interacts with CIT depending on the activation state of the kinase (stronger interaction with the kinase-dead form); targets to the midbody. Interacts with ARRB2; the interaction is detected in the nucleus upon OR1D2 stimulation (By similarity). Interacts with AKT1; the interaction is detected in the plasma membrane upon INS stimulation and promotes AKT1 phosphorylation. Interacts with SVIL; at midbody during cytokinesis. Interacts with RADIL (via PDZ domain); recruits RADIL to the microtubule network restricting RADIL from interaction with activated RAP1A. {ECO:0000250|UniProtKB:Q15058}. | |
| Subcellular location: | Nucleus {ECO:0000250|UniProtKB:Q15058}. Cytoplasm {ECO:0000250|UniProtKB:Q15058}. Cytoplasm, cytoskeleton, spindle {ECO:0000250|UniProtKB:Q15058}. Midbody {ECO:0000250|UniProtKB:Q15058}. Note=Nuclear localization observed during interphase. Nuclear localization triggered by entry into mitosis. Cytoplasmic in interphase. Cytoplasmic in metaphase cells. From prophase to metaphase, accumulates at the developing spindle poles and their associated microtubules. During anaphase, accumulates at the spindle midzone. Localization to the central spindle and midbody during anaphase is dependent upon PRC1 and CIT presence. In cells ready to undergo abscission, concentrates at the contractile ring. {ECO:0000250|UniProtKB:Q15058}. | |
| Domain: | The kinesin motor domain binds to microtubules with high affinity and has a robust ATPase activity but a very slow motility. The kinesin motor domain protects microtubules from cold depolymerization. Binds to each tubulin heterodimer resulting in a microtubule complexes. Binds at the tubulin intradimer interface, at the crest of the protofilament, and orients slightly toward the next protofilament. {ECO:0000269|PubMed:24949858}. | |
| Disruption phenotype: | The lag homozygous mutant mice that lack detectable Kif14 expression are indistinguishable from normal littermates at birth. At P10, mutants exhibit an overt ataxic phenotype that increased in severity over time. At P12, lag homozygous mutant mice are unable to stand for 10 s on a narrow platform. Their gait is wide and uncoordinated, and they frequently fell on their backs while walking. These defects in voluntary movement control, posture and balance are accompanied by progressive weakness and failure to gain body weight. By P14, the homozygous mutants in a litter could be identified by their small size and uncontrolled movements. The homozygous mutants all died by P21. The lag homozygous mutant mice also display a flathead, a reduction in brain size, slender optic nerves, and a translucent spinal cord. {ECO:0000269|PubMed:23308235}. | |
| Similarity: | Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Kinesin family. {ECO:0000255|PROSITE-ProRule:PRU00283}. | |
Annotations taken from UniProtKB at the EBI.