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these findings demonstrate that p53 (show TP53 Proteins) can repress MCAK promoter activity indirectly via down-regulation of Sp1 (show PSG1 Proteins) expression level, and suggest that MCAK elevation in human tumor cells might be due to p53 (show TP53 Proteins) mutation
Results show that three residues (K524, E525 and R528), which are located in the C-terminal half of the a4-helix, play a crucial role in the ability of MCAK to distinguish between the microtubule lattice and the microtubule end.
Authors find that 3D ECM engagement uncouples MCAK-mediated regulation of MT growth persistence from myosin-II-mediated regulation of growth persistence specifically within EC branched protrusions.
REVIEW: Conformation changes in MCAK related to its depolymerization activity and function are described. A model of its regulation by multiple mitotic kinases is proposed and its potential involvement in oncogenesis and drug resistance its highlighted.
GTSE1 (show GTSE1 Proteins) inhibition of MCAK activity regulates the balance of MT stability that determines the fidelity of chromosome alignment, segregation, and chromosomal stability.
MCAC (show SLC25A20 Proteins) role in microtubule assembly
Our results reveal an underlying mechanism by which NuSAP (show NUSAP1 Proteins) controls kinetochore microtubule dynamics spatially and temporally by modulating the depolymerisation function of MCAK in an Aurora B kinase (show AURKB Proteins)-dependent manner.
MCAK is involved in directional migration and invasion of tumor cells.
the Aurora B (show AURKB Proteins)-PLK1 signaling at the kinetochore orchestrates MCAK activity, which is essential for timely correction of aberrant kinetochore attachment to ensure accurate chromosome segregation during mitosis.
MCAK activity is modulated by Plk1 phosphorylation on S632/S633 in mitosis.
PAK1 (show PAK1 Proteins) phosphorylates MCAK and regulates both its localization and function.
MCAK appears to possess a unique distribution and function in oocyte maturation.
MCAK contributes to chromosome alignment in meiosis I, but is not necessary for preventing chromosome segregation errors.
Possible functions of MCAK at the inner centromere domain and at the perikinetochoric ring during both meiotic divisions.
Shugoshin 2 is necessary for the loading of MCAK at the inner centromere, but is dispensable for the loading of the outer kinetochore proteins BubR1 (show BUB1B Proteins) and CENP-E (show CENPE Proteins).
MCAK colocalized with NuMA and XMAP215 at the center of Ran asters where its activity is regulated by Aurora A (show AURKA Proteins)-dependent phosphorylation of S196, which contributes to proper pole focusing
This study reveals a new role for Aurora B (show AURKB Proteins), which is to prevent excess MCAK binding to chromatin to facilitate chromatin-nucleated spindle assembly.
MCAK regulation of cytoplasmic and spindle-associated (show HAUS1 Proteins) microtubules can be differentiated by Aurora B (show AURKB Proteins)-dependent phosphorylation
These data support a model in which Nup98 (show NUP98 Proteins) interacts with microtubules and antagonizes MCAK activity, thus promoting bipolar spindle assembly.
The protein encoded by this gene is a member of kinesin-like protein family. Proteins of this family are microtubule-dependent molecular motors that transport organelles within cells and move chromosomes during cell division. This protein is important for anaphase chromosome segregation and may be required to coordinate the onset of sister centromere separation.
kinesin family member 2C
, kinesin-like protein KIF2C
, kinesin-like protein KIF2C-like
, kinesin-like 6
, kinesin-like protein 6
, mitotic centromere-associated kinesin
, kinesin-related protein 2
, Kinesin-like protein 6
, kinesin central motor 1