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anti-Human KIF2C Anticorps:
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Human Monoclonal KIF2C Primary Antibody pour IF, IHC (p) - ABIN564770
Sanhaji, Friel, Kreis, Krämer, Martin, Howard, Strebhardt, Yuan: Functional and spatial regulation of mitotic centromere-associated kinesin by cyclin-dependent kinase 1. dans Molecular and cellular biology 2010
Show all 2 Pubmed References
Human Polyclonal KIF2C Primary Antibody pour IP, WB - ABIN251028
Pakala, Nair, Reddy, Kumar: Signaling-dependent phosphorylation of mitotic centromere-associated kinesin regulates microtubule depolymerization and its centrosomal localization. dans The Journal of biological chemistry 2012
Show all 2 Pubmed References
Human Monoclonal KIF2C Primary Antibody pour FACS, ICC - ABIN4328842
Xie, Zhang, Zhao, Bai, Fan, Zhu, Yu, Li, Liang, Sun, Li, Qiao: Poly(ADP-ribose) mediates asymmetric division of mouse oocyte. dans Cell research 2018
KIF-2C expression in tumor tissues may serve as an independent prognostic marker for male, but not female, patients with operable esophageal squamous cell carcinomas.
these findings demonstrate that p53 can repress MCAK promoter activity indirectly via down-regulation of Sp1 expression level, and suggest that MCAK elevation in human tumor cells might be due to p53 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 inhibition of MCAK activity regulates the balance of MT stability that determines the fidelity of chromosome alignment, segregation, and chromosomal stability.
MCAC role in microtubule assembly
Our results reveal an underlying mechanism by which NuSAP controls kinetochore microtubule dynamics spatially and temporally by modulating the depolymerisation function of MCAK in an Aurora B kinase-dependent manner.
MCAK is involved in directional migration and invasion of tumor cells.
the Aurora B-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.
These results demonstrate that the structural change of Kif2C-ATP upon binding to microtubule ends is sufficient for tubulin release, whereas ATP hydrolysis is not required
Ras regulates KIF2C to control cell migration pathways in transformed human bronchial epithelial cells.
A dynamic interaction of MCAK-TIP150 orchestrated by Aurora A-mediated phosphorylation governs entosis via regulating microtubule plus-end dynamics and cell rigidity.
this study suggests a new mechanism by which Plk1 regulates MCAK: by regulating its degradation and hence controlling its turnover in mitosis.
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.
A Rac1-Aurora A-MCAK signaling pathway mediates endothelial cell polarization and directional migration by promoting regional differences in microtubule dynamics.
result suggested E403K mutation in mitotic centromere-associated kinesin protein as highly damaging and showed strong concordance to the previously observed colorectal cancer mutations aggregation tendency and energy value changes
A CENP-E mediated wall-tethering event and a MCAK-mediated wall-removing event show that human chromosome-microtubule attachment is achieved through a set of deterministic sequential events rather than stochastic direct capture of microtubule ends.
expression has no effect on the level of the TRAIL receptors DR4 and DR5. These findings might have clinical implications since the combination of TRAIL therapy with administration of Pgp modulators might sensitize TRAIL resistant tumors.
PAK1 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 and CENP-E.
MCAK colocalized with NuMA and XMAP215 at the center of Ran asters where its activity is regulated by Aurora A-dependent phosphorylation of S196, which contributes to proper pole focusing
This study reveals a new role for Aurora B, which is to prevent excess MCAK binding to chromatin to facilitate chromatin-nucleated spindle assembly.
MCAK regulation of cytoplasmic and spindle-associated microtubules can be differentiated by Aurora B-dependent phosphorylation
These data support a model in which Nup98 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