Nocodazole - CAS 31430-18-9
Catalog number: 31430-18-9
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Nocodazole, also called Oncodazole, reversibly inhibits microtubule polymerization so it has anti-neoplastic effect. It is inhibitor of Abl (IC50= 0.21 μM), Abl(E255K) (IC50= 0.53 μM)and Abl(T315I) (IC50= 0.53 μM). in vitro: a high-affinity ligand for Abl phosphorylated (Kd= 0.091 μM), c-Kit (Kd= 1.6 μM), BRAF (Kd= 1.8 μM), and MEK (Kd= 1.6 μM) in vivo: combined with Ketoconazole strongly enhances apoptosis of COLO 205 tumor xenografts
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Brife Description:
Reversibly inhibits microtubule polymerization
Pale beige solid
methyl N-[6-(thiophene-2-carbonyl)-1H-benzimidazol-2-yl]carbamate; nocodazole; Oncodazole; 31430-18-9; R 17934; Nocodazolum; Nocidazole; Nocodazol; NSC 238159; Methyl N-(5-thenoyl-2-benzimidazolyl)carbamate; Methyl [5-(2-thienylcarbonyl)-1H-benzimidazol-2-yl]carbamate; NSC-238159; R-17934; R 17,934; C14H11N3O3S; Methyl 5-(2-thenoyl)-2-benzimidazolecarbamate; Nocodazole [USAN:INN]
Soluble to 50 mM in DMSO
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -63℃ for long term (months to years).
Canonical SMILES:
1.Promotion of Functional Nerve Regeneration by Inhibition of Microtubule Detyrosination.
Gobrecht P1, Andreadaki A1, Diekmann H1, Heskamp A1, Leibinger M1, Fischer D2. J Neurosci. 2016 Apr 6;36(14):3890-902. doi: 10.1523/JNEUROSCI.4486-15.2016.
Functional recovery of injured peripheral neurons often remains incomplete, but the clinical outcome can be improved by increasing the axonal growth rate. Adult transgenic GSK3α(S/A)/β(S/A)knock-in mice with sustained GSK3 activity show markedly accelerated sciatic nerve regeneration. Here, we unraveled the molecular mechanism underlying this phenomenon, which led to a novel pharmacological approach for the promotion of functional recovery after nerve injury.In vitroandin vivoanalysis of GSK3 single knock-in mice revealed the unexpected contribution of GSK3α in addition to GSK3β, as both GSK3(S/A)knock-ins improved axon regeneration. Moreover, growth stimulation depended on overall GSK3 activity, correlating with increased phosphorylation of microtubule-associated protein 1B and reduced microtubule detyrosination in axonal tips. Pharmacological inhibition of detyrosination by parthenolide or cnicin mimicked this axon growth promotion in wild-type animals, although it had no effect in GSK3α(S/A)/β(S/A)mice.
2.Targeting of tubulin polymerization and induction of mitotic blockage by Methyl 2-(5-fluoro-2-hydroxyphenyl)-1H-benzo[d]imidazole-5-carboxylate (MBIC) in human cervical cancer HeLa cell.
Hasanpourghadi M1, Karthikeyan C2, Pandurangan AK1, Looi CY1, Trivedi P2, Kobayashi K3, Tanaka K3, Wong WF4, Mustafa MR5. J Exp Clin Cancer Res. 2016 Mar 31;35(1):58. doi: 10.1186/s13046-016-0332-0.
BACKGROUND: Microtubule Targeting Agents (MTAs) including paclitaxel, colchicine and vinca alkaloids are widely used in the treatment of various cancers. As with most chemotherapeutic agents, adverse effects and drug resistance are commonly associated with the clinical use of these agents. Methyl 2-(5-fluoro-2-hydroxyphenyl)-1H- benzo[d]imidazole-5-carboxylate (MBIC), a benzimidazole derivative displays greater toxicity against various cancer compared to normal human cell lines. The present study, focused on the cytotoxic effects of MBIC against HeLa cervical cancer cells and possible actions on the microtubule assembly.
3.Microtubules Are Essential for Mitochondrial Dynamics-Fission, Fusion, and Motility-in Dictyostelium discoideum.
Woods LC1, Berbusse GW2, Naylor K1. Front Cell Dev Biol. 2016 Mar 22;4:19. doi: 10.3389/fcell.2016.00019. eCollection 2016.
Mitochondrial function is dependent upon mitochondrial structure which is in turn dependent upon mitochondrial dynamics, including fission, fusion, and motility. Here we examined the relationship between mitochondrial dynamics and the cytoskeleton in Dictyostelium discoideum. Using time-lapse analysis, we quantified mitochondrial fission, fusion, and motility in the presence of cytoskeleton disrupting pharmaceuticals and the absence of the potential mitochondria-cytoskeleton linker protein, CluA. Our results indicate that microtubules are essential for mitochondrial movement, as well as fission and fusion; actin plays a less significant role, perhaps selecting the mitochondria for transport. We also suggest that CluA is not a linker protein but plays an unidentified role in mitochondrial fission and fusion. The significance of our work is to gain further insight into the role the cytoskeleton plays in mitochondrial dynamics and function.
4.Centlein, a novel microtubule-associated protein stabilizing microtubules and involved in neurite formation.
Jing Z1, Yin H2, Wang P3, Gao J4, Yuan L5. Biochem Biophys Res Commun. 2016 Apr 1;472(2):360-5. doi: 10.1016/j.bbrc.2016.02.079. Epub 2016 Feb 23.
We have previously reported that the centriolar protein centlein functions as a molecular link between C-Nap1 and Cep68 to maintain centrosome cohesion [1]. In this study, we identified centlein as a novel microtubule-associated protein (MAP), directly binding to purified microtubules (MTs) via its longest coiled-coil domain. Overexpression of centlein caused profound nocodazole- and cold-resistant MT bundles, which also relied on its MT-binding domain. siRNA-mediated centlein depletion resulted in a significant reduction in tubulin acetylation level and overall fluorescence intensity of cytoplasmic MT acetylation. Centlein was further characterized in neurons. We found that centlein overexpression inhibited neurite formation in retinoic acid (RA)-induced SH-SY5Y and N2a cells. Taken together, we propose that centlein is involved in MT stability and neuritogenesis in vivo.
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CAS 31430-18-9 Nocodazole

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