Disease relevance of R 17934

• Finally, T47D, a human breast tumor cell line that is sensitive to taxol and nocodazole, had reduced MAD2 expression and failed to arrest in mitosis after nocodazole treatment [1].
• Toxicities of various microtubule inhibitors, namely, colchicine, podophyllotoxin, maytansine, vinblastine, nocodazole, griseofulvin, and steganacine, toward numerous independently established cell lines from three different species, namely, human, mouse, and Chinese hamster, were examined [2].
• Expression of DVL-1 protects stable microtubules from depolymerization by nocodazole in both dividing cells and differentiated neuroblastoma cells [3].
• The polarized delivery of membrane proteins to the cell surface and the initial secretion of lysosomal proteins into the culture medium were studied in the polarized human intestinal adenocarcinoma cell line Caco-2 in the presence or absence of the microtubule-active drug nocodazole [4].
• We describe here a monogenic nuclear recessive mutation, crochu1 (cro1), resulting in abnormal cell shape and cortical pattern and hypersensitivity to nocodazole [5].

Psychiatry related information on R 17934

• This redistribution was disrupted by nocodazole, implicating an underlying plus end-directed microtubule motor activity [6].

High impact information on R 17934

• Fragmentation of the Golgi apparatus by nocodazole or Brefeldin A treatment prior to or post microinjection of the anti-GRASP65 antibody alleviated the block in mitotic entry [7].
• The percent of centromeres with microtubule-binding activity is 7- to 10-fold higher in lysates made from nocodazole-arrested G2-M cells than from alpha factor G1 cells, suggesting that this centromere activity is regulated during the cell cycle [8].
• In mutant zygotes with abnormal spindle orientations and in wild-type zygotes treated with the microtubule inhibitors nocodazole, colcemid, vinblastine, and griseofulvin, both P-granule segregation to the posterior pole and the concomitant pseudocleavage occur apparently normally, but the normally concurrent migration of the pronuclei is inhibited [9].
• Cells with neurites are incubated with the microtubule-depolymerizing drug Nocodazole [10].
• In the presence of the gamma-tubulin antibody, microtubules fail to regrow into cytoplasmic arrays after depolymerization induced by nocodazole or cold [11].

Chemical compound and disease context of R 17934

• In this study it is demonstrated that the extent of phosphorylation of serine 209 in the beta subunit is significantly increased relative to phosphorylation of the autophosphorylation site when chicken bursal lymphoma BK3A cells are arrested at mitosis by nocodazole treatment [12].
• Infection of Balb/MK cells with an ODC retrovirus to elevate ODC and polyamine levels increased overall protein phosphorylation as well as CK2 protein levels and enzyme activity in mimosine- or nocodazole- arrested cells [13].
• Expression of de-N-acetyl-gangliosides in human melanoma cells is induced by genistein or nocodazole [14].
• The tubular/vesicular clusters were dispersed throughout the cytoplasm upon treatment with the microtubule-depolymerizing agent nocodazole and were accessible to endocytosed transferrin, but not exocytic cargo (vesicular stomatitis virus glycoprotein) [15].
• The effect of colchicine, Nocodazole, and dibucaine on the assembly of Semliki Forest virus was investigated [16].

Biological context of R 17934

• The kinase p38, but not MAPK or JNK, was activated in mammalian cultured cells when the cells were arrested in M phase by disruption of the spindle with nocodazole [17].
• XMAD2 protein associated with unattached kinetochores in prometaphase and in nocodazole-treated cells and disappeared from kinetochores at metaphase in untreated cells, suggesting that XMAD2 plays a role in the activation of the checkpoint by unattached kinetochores [18].
• Abrogation of Lats2 promotes accumulation of polyploid cells upon exposure to nocodazole, which can be prevented by direct activation of p53 [19].
• Destabilization of the MT network by nocodazole, colchicine, or a tubulin mutant disrupts the complex between Smads and MTs and increases TGF beta-induced Smad2 phosphorylation and transcriptional response in CCL64 cells [20].
• Exposure of murine and human macrophages and human umbilical vein endothelial cells to micromolar concentrations of five microtubule (MT)-depolymerizing agents (colchicine, nocodazole, podophyllotoxin, vincristine, and vinblastine) resulted in a loss of binding sites for iodinated TNF-alpha [21].

Anatomical context of R 17934

• Embryonic chick lens epithelial cells cultured in serum-supplemented medium elongated in the absence of microtubules after treatment with the antimicrotubule drug nocodazole [22].
• Treatment of NIH 3T3 cells with a specific inhibitor of p38 suppressed activation of the checkpoint by nocodazole [17].
• Nocodazole, a microtubule poison that provokes centrosome/mitotic apparatus dysfunction, induces Lats2 translocation from centrosomes to the nucleus and p53 accumulation [19].
• Second, both rM-CSF- and PMA-stimulated LY accumulation could be inhibited by treatment of cells with the cytoskeleton destabilizing drugs nocodazole, colchicine, or cytochalasin D [23].
• After treatment with 1 microM nocodazole, seven of ten breast cancer lines (type A cells) arrested in mitosis, whereas the other three (type B cells) did not [24].

Associations of R 17934 with other chemical compounds

• Phagosome-phagosome fusion required bacterial protein synthesis and intact host microtubules, and both chloramphenicol and nocodazole increased killing of intracellular H. pylori [25].
• Constitutive IGF-II-expressing cells actively incorporated thymidine and showed an increase in the proportion of cells with >4N DNA ploidy in the presence of nocodazole [26].
• METHODS: Confocal microscopy and image analysis were performed to quantitatively assess changes in secretory capacity and vesicle targeting in isolated rat hepatocyte couplets that had been exposed to fluorescent bile acid after pretreatment with dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP) and/or nocodazole [27].
• Glu tubulin injected into nocodazole-treated cells was converted to Tyr tubulin by a putative tubulin/tyrosine ligase activity [28].
• Finally, we have found that expression of human gamma-tubulin or overexpression of S. pombe gamma-tubulin causes no significant alteration of resistance to the antimicrotubule agents benomyl, thiabendazole and nocodazole [29].

Gene context of R 17934

• We find that upon spindle checkpoint activation by microtubule inhibitors benomyl or nocodazole, wild-type Saccharomyces cerevisiae contains less Cdc20p than spindle checkpoint mutants do, whereas their CDC20 mRNA levels are similar [30].
• Antibodies that recognize the MDF-2 protein localize to nuclei of the cleaving embryo in a cell-cycle-dependent manner. mdf-1, a gene encoding a product that interacts with MDF-2, is required for cell-cycle arrest and proper chromosome segregation in premeiotic germ cells treated with nocodazole, a microtubule-depolymerizing agent [31].
• Depolymerization of some of the cellular microtubules with nocodazole preferentially retained the microtubule localization of both cyclin B and MAP4 [32].
• Nocodazole treatment of cells results in an extensive BICD2-dynactin-dynein co-localization [33].
• Furthermore, spc24-2 cells showed a mitotic checkpoint defect when microtubules were depolymerized with nocodazole, indicating that Spc24p has a function in checkpoint control [34].

Analytical, diagnostic and therapeutic context of R 17934

• The reversibility of the anti-invasive effect of 4-day treatment with Nocodazole (1 microgram/ml) was demonstrated in shaker cocultures with the use of fluid medium [35].
• We used the inhibitor nocodazole in conjunction with immunofluorescence and electron microscopy to investigate microtubule function in the yeast cell cycle [36].
• Electron microscopy of nocodazole-treated mitotic wild-type cells revealed stretches of rough endoplasmic reticulum, strongly fenestrated Golgi cisternae and clusters of vesicles with the diameter of 30-90 nm [37].
• By indirect immunofluorescence, E2 and E1 were localized to the Golgi region of all three cell types, and their distribution was disrupted by treatment with BFA or nocodazole [38].
• Immunoblotting of extracts from synchronized cultures reveals that Myf5 undergoes periodic fluctuations during the cell cycle and is absent from cells blocked early in mitosis by use of nocodazole [39].

References