Kinesin
Kinesins are a family of molecular motors that use the energy of ATP hydrolysis to move along the surface of, or destabilize, microtubule filaments. The kinesin motor protein family consists of 14 distinct subclasses and 45 kinesin proteins in humans. A large number of these proteins, or their orthologues, have been shown to possess essential function(s) in both the mitotic and the meiotic cell cycle. Kinesins also can be classified into three groups based on the position of their motor domains: N-terminal, C-terminal and internal kinesins. Conventional kinesin operates as a dimer, walking in a co-ordinated, hand-over-hand fashion along a microtubule protofilament.
Kinesins have important roles in chromosome separation, microtubule dynamics, spindle formation, cytokinesis and cell cycle progression. Roles of kinesins in diseases typically involve defective transport of cell components, transport of pathogens, or cell division.
Alle Kinesin Isoform-spezifische Produkte anzeigen
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Kinesin Verwandte Produkte (111)
Verwandte Produkte (111)
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Antibodies (15)
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Kinesin Isoform Comparison
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S-Trityl-L-cysteine
0 ImagesSynonyms: NSC 83265; S-Tritylcysteine; 3-Tritylthio-L-alanineS-Trityl-L-cysteine (NSC 83265) is a selective and allosteric kinesin Eg5 inhibitor with an IC50 of 1 μM for the inhibition of basal ATPase activity and 140 nM for the microtubule-activated ATPase activity. S-Trityl-L-cysteine has antitumor activities.
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ALN-12115 sodium scrambled negative control
0 ImagesArt. -Nr.: HY-177613BALN-12115 sodium scrambled negative control is the sequence scrambled negative control of ALN-12115 sodium.
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Kolaflavanone
0 ImagesArt. -Nr.: HY-121816CAS. Nr.: 68705-66-8Kolaflavanone is an biflavonoid allosteric inhibitor of Eg5. Kolaflavanone inhibits the ATPase and tyrosinase activities of Eg5 under both basal and microtubule-activated conditions, suppresses microtubule sliding activity, binds to the L5/α2/α3 allosteric pocket of Eg5, induces conformational changes of Eg5 and microtubule dissociation, interacts with aldehyde dehydrogenase, inhibits the ATPase activity of kinesin-1, and binds to HSA via pH-dependent forces. Kolaflavanone exhibits antihepatotoxic activity and can be used in studies related to Phalloidin (HY-P0028)-induced liver injury.
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SeSA-HCPT
0 ImagesArt. -Nr.: HY-181694SeSA-HCPT is an orally active dual-target inhibitor integrating Topo I and HDAC inhibition. SeSA-HCPT induces potent DNA damage, apoptosis, S-phase arrest in prostate cancer cells. SeSA-HCPT inhibits cancer cells proliferation and migration. SeSA-HCPT impairs homologous recombination by suppressing KIF4A-RAD51 signaling. SeSA-HCPT markedly inhibits CRPC tumor growth with minimal systemic toxicity.
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AZ82
0 ImagesAZ82 is a selective kinesin-like protein KIFC1 (HSET/KIFC1) inhibitor, with a Ki of 43 nM and an IC50 of 300 nM for KIFC1.
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KIF18A-IN-6
0 ImagesKIF18A-IN-6 (Compound 134) is an orally active KIF18A inhibitor with an IC50 of 0.016 μM against KIF18A microtubule-dependent ATPase activity.
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VLS-1272
0 ImagesSynonyms: KIF18A-IN-7VLS-1272 (Compound 22) is an orally active KIF18A inhibitor that binds to the KIF18A-microtubule complex in an ATP-noncompetitive manner (IC50 = 41 nM), blocking its ATPase activity and inhibiting microtubule translocation. This leads to abnormal accumulation of KIF18A at spindle poles, disrupting chromosome alignment and inducing mitotic arrest and apoptosis in CINHigh tumor cells (e.g., ovarian cancer OVCAR-3, breast cancer JIMT-1). VLS-1272 is a promising candidate for anti-tumor research.
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MK-0731
0 ImagesMK-0731 is a selective, non-competitive and allosteric kinesin spindle protein (KSP) inhibitor with an IC50 of 2.2 nM and a pKa of 7.6. MK-0731 is >20,000 fold selectivity against other kinesins. MK-0731 induces mitotic arrest and induces apoptosis in tumors. MK-0731 provides significant antitumor efficacy.
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UMK57
0 ImagesUMK57 is a MCAK activator and kinetochore-microtubule destabilizer. UMK57 enhances MCAK-dependent microtubule depolymerization, increases kinetochore-microtubule turnover, reduces chromosome mis-segregation and lagging chromosomes, and inhibits cancer cell proliferation. UMK57 triggers adaptive resistance in Aurora B cancer cells via reversible Aurora B signaling pathway alterations. UMK57 can be used for the research of solid tumors.
