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KIF11 encodes a motor protein that belongs to the kinesin-like protein family. Additionally we are shipping KIF11 Antibodies (94) and KIF11 Kits (5) and many more products for this protein.
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Patients with KIF11 mutations show a specific ocular phenotype with variable expressivity and intrafamilial variability. Macular atrophy and dysfunction have not been consistently documented before.
This stuidy demonstrated that overexpression of Eg5 associates with high-grade astrocytic neoplasm.
Data show that kinesin spindle protein Eg5 inhibitor LY2523355 has broad target-mediated anticancer activity in vitro and in vivo.
Data show there was no significant change in Eg5 protein inhibitor treatment.
the levels and distribution of TPX2 are likely to be determinants of when and where kinesin-5 acts in neurons.
Targeting KIF11 also hit the other arm of the "go or grow" cell fate decision by reducing glioma cell invasion.
Identification of mutations in 8.3% patients suggests KIF11 mutations as a common cause of familial exudative vitreoretinopathy (FEVR (show NDP Proteins)).
This report, therefore, further expands the clinical and molecular spectrum of KIF11-associated microcephaly.
Data show that kinesin spindle protein (KSP) inhibition sensitized chronic myeloid leukemia (CML) cells to imatinib-induced apoptosis.
All inherited cases, and 50% of sporadic cases of MCLMR are due to germline KIF11 mutations. It is possible that mosaic KIF11 mutations cause the remainder of sporadic case
Data suggest that poleward transport of TPX2, which requires dynein and Eg5, down-regulates its microtubule nucleating activity near kinetochores and links microtubules to dynein for incorporation into the spindle.
Data suggest that amyloid-beta (here, Abeta 1-42) induces acute and chronic synaptic dysfunction in part through inhibition of Eg5 (kinesin-5) in hippocampal neurons.
Disruption of the in vivo interaction of KIF11 with ZBP1 (show ZBP1 Proteins) delocalizes beta-actin (show ACTB Proteins) mRNA and affects cell migration.
These results suggest that 4-(N-(2-(N-acetylcysteine-S-yl) acetyl) amino)-4'- (N-(2-(N-(triphenylmethyl)amino)acetyl)amino)azobenzene could be used as photochromic inhibitor of Eg5 to achieve photocontrol of living cells.
incorporation of photochromic molecules into the key region of loop L5 facilitates the photocontrol of the function of kinesin Eg5.
Finally, when kinesin spindle protein (KSP) siRNA was encapsulated in lipid nanoparticles containing a modest amount of PEG (show PAEP Proteins), the proliferation of endothelial cells was inhibited due to the efficient knock down of KSP mRNA.
These results show that intratumoral electro-transfer of siRNA is feasible and kinesin spindle protein (KSP)-specific siRNA may provide a novel strategy for therapeutic intervention.
observations explain the poleward accumulation of Eg5 in early mitosis and its redistribution in anaphase. Inhibition of dynein blocked Eg5 movement on microtubules, whereas depletion of the Eg5-binding protein TPX2 (show DAZL Proteins) resulted in end-directed Eg5 movement.
Observations further support the conclusion that Eg5 is essential for cell division early in mouse development.
Results indicate that Eg5 overexpression disrupts the unique balance of forces associated with normal spindle assembly and function, and thereby leads to the development of spindle defects, genetic instability, and tumors.
Eg5 is essential during early mouse development and cannot be compensated by another molecular motor (show MYO1B Proteins).
This gene encodes a motor protein that belongs to the kinesin-like protein family. Members of this protein family are known to be involved in various kinds of spindle dynamics. The function of this gene product includes chromosome positioning, centrosome separation and establishing a bipolar spindle during cell mitosis.
TR-interacting protein 5
, kinesin-like protein 1
, kinesin-like protein KIF11
, kinesin-like spindle protein HKSP
, kinesin-related motor protein Eg5
, thyroid receptor-interacting protein 5
, kinesin 11
, kinesin-like 1