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the crystal structure of a catalytically active kinesin-13 monomer (Kif2A) in complex with two bent alphabeta-tubulin heterodimers in a head-to-tail array, providing a view of these interactions, is reported.
KIF2A expression was increased in human ovarian cancer patients and in tumor tissues and KIF2A mRNA contains two target sites for miR-206 binding and confirmed that miR-206 directly suppresses KIF2A; inhibits ovarian cancer cell proliferation, migration, and invasion; and induces apoptosis.
Furthermore, silencing KIF2A inhibited cell proliferation and induced apoptosis in lung adenocarcinoma(LUAD) cells. In conclusion, KIF2A may serve as a valuable prognostic indicator and promising therapeutic target of LUAD.
have identified a conserved WDR5 interaction (Win) motif, so far unique to the Mixed-lineage leukemia family
The effect of Kif2A Knockdown on spreading could be rescued by expression of Kif2A-GFP or FLAG-AGAP1, but not by Kif2C-GFP. The results support the hypothesis that the Kif2A.AGAP1 complex contributes to control of cytoskeleton remodeling involved in cell movement.
Study used high-resolution single-molecule microscopy to directly observe the stepping behavior of kinesin-1 and -2 family motors with different length neck-linker domains. Results provide a kinetic framework for explaining kinesin processivity and for mapping structural differences to functional differences in diverse kinesin isoforms.
these data provide the first evidence that increased KIF2A expression predicts poor prognosis in patients with diffuse large B cell lymphoma, and a rationale for treatment of DLBCL by targeting KIF2A.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (MMB-FOXM1) regulate the expression of mitotic kinesins in breast cancer cells.
Mdp3 (also known as MAP7D3) forms a complex with DDA3 (also known as PSRC1) and controls spindle dynamics at the minus end of Microtubuless by inhibiting DDA3-mediated Kif2a recruitment to the spindle.
High KIF2A expression is associated with Gastric Cancer.
KIF2A may be important in glioma progression.
This study demonstrated colorectal cancer (CRC) tissue-preferred expression pattern of the KIF2A and suggested that high KIF2A expression might serve as an independent maker for poor prognosis in CRC patients.
TTBK2 phosphorylates KIF2A and antagonizes KIF2A-induced depolymerization at microtubules plus ends for cell migration.
Ras regulates KIF2A to control cell migration pathways in transformed human bronchial epithelial cells.
KIF2A may play an important role in breast cancer progression and is potentially a novel predictive and prognostic marker for breast cancer.
up-regulation of KIF2C and KIF2A by ERK1/2 caused aberrant lysosomal positioning and mTORC1 activity in a mutant K-Ras-dependent cancer and cancer model.
Silencing Kif2a induces apoptosis and decreases the mRNA and protein level of PI3K, Akt and Bcell lymphoma 2 (Bcl2) in Tca8113 cells.
The distribution of Kif2A was limited to the distal ends of the central spindle through Aurora B-dependent phosphorylation and exclusion from the spindle midzone.
The kinesin-2 deficiency weakened intercellular adhesion, despite the maintenance of adherens junctions and other desmosome components at the plasma membrane.
Data show that 4-oxo-4-HPR inhibited tubulin polymerization and modulated gene expression of spindle aberration associated genes Kif 1C, Kif 2A, Eg5, Tara, tankyrase-1, centractin, and TOGp.
Heterodimeric KIF3AC and KIF3AB, two members of the mammalian kinesin-2 family, generate force for microtubule plus end-directed cargo transport. This study reveals the impact of heterodimerization of the motor polypeptides for microtubule association to start the processive run and the fundamental differences in the motile properties of KIF3C compared with KIF3A and KIF3B.
These data indicate that KIF2A regulates the spindle assembly, asymmetric cytokinesis and the metaphase I-anaphase I transition in mouse oocyte.
Kif2a may act as a microtubule depolymerase, regulating microtubule dynamics, spindle assembly and chromosome congression, and thus cell cycle progression during mouse oocyte meiotic maturation.
We further found that knockdown of Kif2a decreased the protein level of b-catenin, which is a critical molecule for neocortical neurogenesis. Together, these results reveal an important function of Kif2a in embryonic neocortical neurogenesis
Tubulin is transported in a non-particulate form requiring kinesin-2.
Authors identified two different sets of KIF2A phosphorylation profiles that accelerate (A-type) and brake (B-type) the MT depolymerization activity of KIF2A.
Kif2a is a pruning factor that regulates target innervation by sensory axons.
This study provided evidence from live-cell analysis that the conserved heterotrimeric kinesin-2 is required for the normal transport of opsin along the ciliary plasma membrane.
Kif2a functions in suppression of collateral extension.
Interaction between kif2a and importin-alpha could be the mechanism by which spindle and cell sizes are coordinated early in development.
Kif2a is required for the epiboly (spreading) of animal cap. In animal caps, Kif2a localizes to the spindle poles (centrosomes) and centromeres during mitosis and is required for spindle integrity and proper chromosome segregation.
The protein encoded by this gene is a plus end-directed motor required for normal mitotic progression. The encoded protein is required for normal spindle activity during mitosis and is necessary for normal brain development. Several transcript variants encoding different isoforms have been found for this gene.
Kinesin, heavy chain, 2
, kinesin-like protein KIF2A
, kinesin heavy chain member 2
, kinesin family member 2A
, kinesin heavy chain family, member 2
, kinesin-related protein XKIF2
, kinesin heavy chain member 2A