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KIF18A is a member of the kinesin superfamily of microtubule-associated molecular motors (see MIM 148760) that use hydrolysis of ATP to produce force and movement along microtubules (Luboshits and Benayahu, 2005 [PubMed 15878648]).[supplied by OMIM, Aug 2008].. Additionally we are shipping KIF18A Kits (3) and and many more products for this protein.
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Human Polyclonal KIF18A Primary Antibody for EIA, WB - ABIN953072
Zhang, Zhu, Chen, Li, Guo, Jiang, Lu: Kif18A is involved in human breast carcinogenesis. in Carcinogenesis 2010
Show all 5 references for ABIN953072
Human Polyclonal KIF18A Primary Antibody for ICC, IF - ABIN4328804
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
Cdk1 (show CDK1 Antibodies)-mediated inhibitory phosphorylation of Kif18A promotes chromosome oscillations in early metaphase. PP1 (show PPA1 Antibodies) induces metaphase plate thinning by directly dephosphorylating Kif18A.
Confocal microscopy shows that cells expressing SUMO-resistant Kif18A display a compromised dissociation of BubR1 (show BUB1B Antibodies) from kinetochores after anaphase onset.
that the human mitotic kinesin-8, KIF18A, directly interacts with PP1gamma through a conserved RVxF motif
the motion of yeast (Kip3) and human (Kif18A) kinesin-8s
Mechanisms controlling the temporal degradation of Nek2A (show NEK2 Antibodies) and Kif18A by the APC (show APC Antibodies)/C-Cdc20 (show CDC20 Antibodies) complex.
Kif18A (kinesin-8) attenuates centromere movement by directly promoting microtubule pausing in a concentration- dependent manner.
there is a mutual regulation of kinetochore MT plus-end dynamics and Kif18A accumulation, which may contribute to the highly regulated and ordered changes in kinetochore spindle microtubule dynamics during chromosome congression and oscillation
Kif18A controls spindle length independently of its role in chromosome positioning. This is mediated by an ATP-independent spindle microtubule (MT) binding site at C-terminal end of the Kif18A tail that has a strong affinity for MTs (show TIMM8A Antibodies) in vitro and in cells.
The heightened processivity of Kif18A, conferred by its tail domain, thus promotes concentration of Kif18A at K-MT plus ends, where it suppresses their dynamics to control chromosome movements.
Kif18A overexpression is associated with colorectal cancer progression.
Kif18a is specifically required for mitotic progression during germ line development.
In conclusion, Kif18a is critical for colorectal carcinogenesis in the setting of inflammation by mechanisms of increased PI3K-AKT (show AKT1 Antibodies) signaling.
KIF18A is a member of the kinesin superfamily of microtubule-associated molecular motors (see MIM 148760) that use hydrolysis of ATP to produce force and movement along microtubules (Luboshits and Benayahu, 2005
kinesin family member 18A
, kinesin-like protein KIF18A
, kinesin-like protein KIF18A-like
, N-8 kinesin
, kinesin superfamily protein 18A