Nocodazole is an anti-neoplastic agent which exerts its effect in cells by interfering with the polymerization of microtubules (tubulin). Several drugs including vincristine and colcemid are similar to Nocodazole in that they interfere with microtubule polymerization. As Nocodazole affects the cytoskeleton, it is often employed in cell biology experiments as a control: for example, some dominant negative Rho small GTPases cause a similar effect as Nocodazole, and constitutively activated mutants often reverse or negate the effect. Nocodazole is frequently employed in cell biology laboratories to synchronize the cell division cycle. Cells treated with Nocodazole arrest with a G2- or M-phase DNA content when analyzed by flow cytometry. Nocodazole binds to the same site as colchinine on beta-tubulin to inhibit microtubule polymerization. But, unlike colchicine, the effects of Nocodazole are reversible. Microscopy of Nocodazole-treated cells shows that they do enter mitosis but cannot form metaphase spindles because microtubules (of which the spindles are made) cannot polymerize. The absence of microtubule attachment to kinetochores activates the spindle assembly checkpoint, causing the cell to arrest in prometaphase. For cell synchronization experiments, Nocodazole is usually employed at a concentration of 40-100 ng/mL of culture medium for a duration of 12-18 hours. Prolonged arrest of cells in mitosis due to Nocodazole treatment typically results in apoptosis. Another standard cell biological application of Nocodazole is to induce the formation of Golgi ministacks in eukaryotic cells. The perinuclear structural organization of the Golgi apparatus in eukaryotes is dependent on microtubule trafficking, but disrupting the trafficking of Golgi elements from the endoplasmic reticulum treatment with Nocodazole (33 uM for 3 hours works) induces numerous Golgi elements to form adjacent to ER exit sites. These functional Golgi ministacks remain distributed about the cell, unable to track forward to form a perinuclear Golgi since Nocodazole has depolymerized the microtubules. Nocodazole is also known as Oncodazole, NSC 238159, R 17934, and Methyl-[5-(2-thienylcarbonyl)-1H-benzimidazol-2-yl]-carbamate.
|Appearance||Off white solid|
Exp. Date: 11/29/2027
Visualizar com outras pessoas usaram Nocodazole (CAS 31430-18-9). Clique em PubMed para ver .
PMID: 36721160 | Folylpolyglutamate synthetase mRNA G-quadruplexes regulate its cell protrusion localization and enhance a cancer cell invasive phenotype upon folate repletion. | Stark, M. et al. 2023. BMC Biol. 21: 13.
PMID: 35858563 | Adherens junctions stimulate and spatially guide integrin activation and extracellular matrix deposition. | Hadjisavva, R. et al. 2022. Cell Rep. 40: 111091.
PMID: 35947950 | Nano-organization of spontaneous GABAergic transmission directs its autonomous function in neuronal signaling. | Guzikowski, NJ. et al. 2022. Cell Rep. 40: 111172.
PMID: 34910909 | YTHDC2 is essential for pachytene progression and prevents aberrant microtubule-driven telomere clustering in male meiosis. | Liu, R. et al. 2021. Cell Rep. 37: 110110.
PMID: 33493514 | G protein βγ translocation to the Golgi apparatus activates MAPK via p110γ-p101 heterodimers. | Khater, M. et al. 2021. J Biol Chem. 100325.
PMID: 34378349 | Profiling the physiological pitfalls of anti-hepatitis C direct-acting agents in budding yeast. | Yahya, G. et al. 2021. Microb Biotechnol. 14: 2199-2213.
PMID: 34689556 | Delivery of Ultrasmall Nanoparticles to the Cytosolic Compartment of Pyroptotic J774A.1 Macrophages via GSDMDNterm Membrane Pores. | Wu, D. et al. 2021. ACS Appl Mater Interfaces.
PMID: 31321035 | DLGAP1 directs megakaryocytic growth and differentiation in an MPL dependent manner in hematopoietic cells. | Kwiatkowski, BA. et al. 2019. Biomark Res. 7: 13.
PMID: 31427565 | NudC-like protein 2 restrains centriole amplification by stabilizing HERC2. | Li, M. et al. 2019. Cell Death Dis. 10: 628.
PMID: 29093022 | Giantin knockout models reveal a feedback loop between Golgi function and glycosyltransferase expression. | Stevenson, NL. et al. 2017. J. Cell. Sci.