Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules.
Slender, cylindrical filaments found in the cytoskeleton of plant and animal cells. They are composed of the protein TUBULIN and are influenced by TUBULIN MODULATORS.
Agents that interact with TUBULIN to inhibit or promote polymerization of MICROTUBULES.
A major alkaloid from Colchicum autumnale L. and found also in other Colchicum species. Its primary therapeutic use is in the treatment of gout, but it has been used also in the therapy of familial Mediterranean fever (PERIODIC DISEASE).
A microtubule subunit protein found in large quantities in mammalian brain. It has also been isolated from SPERM FLAGELLUM; CILIA; and other sources. Structurally, the protein is a dimer with a molecular weight of approximately 120,000 and a sedimentation coefficient of 5.8S. It binds to COLCHICINE; VINCRISTINE; and VINBLASTINE.
An alkaloid isolated from Colchicum autumnale L. and used as an antineoplastic.
A fungal metabolite that blocks cytoplasmic cleavage by blocking formation of contractile microfilament structures resulting in multinucleated cell formation, reversible inhibition of cell movement, and the induction of cellular extrusion. Additional reported effects include the inhibition of actin polymerization, DNA synthesis, sperm motility, glucose transport, thyroid secretion, and growth hormone release.
A type of CELL NUCLEUS division by means of which the two daughter nuclei normally receive identical complements of the number of CHROMOSOMES of the somatic cells of the species.
A microtubule structure that forms during CELL DIVISION. It consists of two SPINDLE POLES, and sets of MICROTUBULES that may include the astral microtubules, the polar microtubules, and the kinetochore microtubules.
A cyclodecane isolated from the bark of the Pacific yew tree, TAXUS BREVIFOLIA. It stabilizes MICROTUBULES in their polymerized form leading to cell death.
Compounds with a BENZENE fused to IMIDAZOLES.
A fungal metabolite which is a macrocyclic lactone exhibiting a wide range of antibiotic activity.
The network of filaments, tubules, and interconnecting filamentous bridges which give shape, structure, and organization to the cytoplasm.
11- to 14-membered macrocyclic lactones with a fused isoindolone. Members with INDOLES attached at the C10 position are called chaetoglobosins. They are produced by various fungi. Some members interact with ACTIN and inhibit CYTOKINESIS.
A stack of flattened vesicles that functions in posttranslational processing and sorting of proteins, receiving them from the rough ENDOPLASMIC RETICULUM and directing them to secretory vesicles, LYSOSOMES, or the CELL MEMBRANE. The movement of proteins takes place by transfer vesicles that bud off from the rough endoplasmic reticulum or Golgi apparatus and fuse with the Golgi, lysosomes or cell membrane. (From Glick, Glossary of Biochemistry and Molecular Biology, 1990)
A family of Urodela consisting of 15 living genera and about 42 species and occurring in North America, Europe, Asia, and North Africa.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
The phase of cell nucleus division following PROMETAPHASE, in which the CHROMOSOMES line up across the equatorial plane of the SPINDLE APPARATUS prior to separation.
Large multiprotein complexes that bind the centromeres of the chromosomes to the microtubules of the mitotic spindle during metaphase in the cell cycle.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Established cell cultures that have the potential to propagate indefinitely.
Mad2 is a component of the spindle-assembly checkpoint apparatus. It binds to and inhibits the Cdc20 activator subunit of the anaphase-promoting complex, preventing the onset of anaphase until all chromosomes are properly aligned at the metaphase plate. Mad2 is required for proper microtubule capture at KINETOCHORES.
The cell center, consisting of a pair of CENTRIOLES surrounded by a cloud of amorphous material called the pericentriolar region. During interphase, the centrosome nucleates microtubule outgrowth. The centrosome duplicates and, during mitosis, separates to form the two poles of the mitotic spindle (MITOTIC SPINDLE APPARATUS).
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
The phase of cell nucleus division following PROPHASE, when the breakdown of the NUCLEAR ENVELOPE occurs and the MITOTIC SPINDLE APPARATUS enters the nuclear region and attaches to the KINETOCHORES.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
Filamentous proteins that are the main constituent of the thin filaments of muscle fibers. The filaments (known also as filamentous or F-actin) can be dissociated into their globular subunits; each subunit is composed of a single polypeptide 375 amino acids long. This is known as globular or G-actin. In conjunction with MYOSINS, actin is responsible for the contraction and relaxation of muscle.
Agents which affect CELL DIVISION and the MITOTIC SPINDLE APPARATUS resulting in the loss or gain of whole CHROMOSOMES, thereby inducing an ANEUPLOIDY.
A cytotoxic member of the CYTOCHALASINS.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
The chromosomal constitution of a cell containing multiples of the normal number of CHROMOSOMES; includes triploidy (symbol: 3N), tetraploidy (symbol: 4N), etc.
Organic nitrogenous bases. Many alkaloids of medical importance occur in the animal and vegetable kingdoms, and some have been synthesized. (Grant & Hackh's Chemical Dictionary, 5th ed)
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
Derivatives of carbamic acid, H2NC(=O)OH. Included under this heading are N-substituted and O-substituted carbamic acids. In general carbamate esters are referred to as urethanes, and polymers that include repeating units of carbamate are referred to as POLYURETHANES. Note however that polyurethanes are derived from the polymerization of ISOCYANATES and the singular term URETHANE refers to the ethyl ester of carbamic acid.
The phase of cell nucleus division following METAPHASE, in which the CHROMATIDS separate and migrate to opposite poles of the spindle.
A lignan (LIGNANS) found in PODOPHYLLIN resin from the roots of PODOPHYLLUM plants. It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Microscopy in which television cameras are used to brighten magnified images that are otherwise too dark to be seen with the naked eye. It is used frequently in TELEPATHOLOGY.
A cyclin B subtype that colocalizes with MICROTUBULES during INTERPHASE and is transported into the CELL NUCLEUS at the end of the G2 PHASE.
Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.)
Fibers composed of MICROFILAMENT PROTEINS, which are predominately ACTIN. They are the smallest of the cytoskeletal filaments.
A family of multisubunit cytoskeletal motor proteins that use the energy of ATP hydrolysis to power a variety of cellular functions. Dyneins fall into two major classes based upon structural and functional criteria.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
An antiprotozoal agent produced by Streptomyces cinnamonensis. It exerts its effect during the development of first-generation trophozoites into first-generation schizonts within the intestinal epithelial cells. It does not interfere with hosts' development of acquired immunity to the majority of coccidial species. Monensin is a sodium and proton selective ionophore and is widely used as such in biochemical studies.
A cyclin subtype that is transported into the CELL NUCLEUS at the end of the G2 PHASE. It stimulates the G2/M phase transition by activating CDC2 PROTEIN KINASE.
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Compounds that inhibit cell production of DNA or RNA.
The final phase of cell nucleus division following ANAPHASE, in which two daughter nuclei are formed, the CYTOPLASM completes division, and the CHROMOSOMES lose their distinctness and are transformed into CHROMATIN threads.
Phosphoprotein with protein kinase activity that functions in the G2/M phase transition of the CELL CYCLE. It is the catalytic subunit of the MATURATION-PROMOTING FACTOR and complexes with both CYCLIN A and CYCLIN B in mammalian cells. The maximal activity of cyclin-dependent kinase 1 is achieved when it is fully dephosphorylated.
A group of alicyclic hydrocarbons with the general formula R-C5H9.
Reduced (protonated) form of THIAZOLES. They can be oxidized to THIAZOLIDINEDIONES.
Self-replicating, short, fibrous, rod-shaped organelles. Each centriole is a short cylinder containing nine pairs of peripheral microtubules, arranged so as to form the wall of the cylinder.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Cellular uptake of extracellular materials within membrane-limited vacuoles or microvesicles. ENDOSOMES play a central role in endocytosis.

EB1, a protein which interacts with the APC tumour suppressor, is associated with the microtubule cytoskeleton throughout the cell cycle. (1/1483)

The characteristics of the adenomatous polyposis coli (APC) associated protein EB1 were examined in mammalian cells. By immunocytochemistry EB1 was shown to be closely associated with the microtubule cytoskeleton throughout the cell cycle. In interphase cells EB1 was associated with microtubules along their full length but was often particularly concentrated at their tips. During early mitosis, EB1 was localized to separating centrosomes and associated microtubules, while at metaphase it was associated with the spindle poles and associated microtubules. During cytokinesis EB1 was strongly associated with the midbody microtubules. Treatment with nocodazole caused a diffuse redistribution of EB1 immunoreactivity, whereas treatment with cytochalasin D had no effect. Interestingly, treatment with taxol abolished the EB1 association with microtubules. In nocodazole washout experiments EB1 rapidly became associated with the centrosome and repolymerizing microtubules. In taxol wash-out experiments EB1 rapidly re-associated with the microtubule cytoskeleton, resembling untreated control cells within 10 min. Immunostaining of SW480 cells, which contain truncated APC incapable of interaction with EB1, showed that the association of EB1 with microtubules throughout the cell cycle was not dependent upon an interaction with APC. These results suggest a role for EB1 in the control of microtubule dynamics in mammalian cells.  (+info)

Microtubule-dependent plus- and minus end-directed motilities are competing processes for nuclear targeting of adenovirus. (2/1483)

Adenovirus (Ad) enters target cells by receptor-mediated endocytosis, escapes to the cytosol, and then delivers its DNA genome into the nucleus. Here we analyzed the trafficking of fluorophore-tagged viruses in HeLa and TC7 cells by time-lapse microscopy. Our results show that native or taxol-stabilized microtubules (MTs) support alternating minus- and plus end-directed movements of cytosolic virus with elementary speeds up to 2.6 micrometer/s. No directed movement was observed in nocodazole-treated cells. Switching between plus- and minus end-directed elementary speeds at frequencies up to 1 Hz was observed in the periphery and near the MT organizing center (MTOC) after recovery from nocodazole treatment. MT-dependent motilities allowed virus accumulation near the MTOC at population speeds of 1-10 micrometer/min, depending on the cell type. Overexpression of p50/dynamitin, which is known to affect dynein-dependent minus end-directed vesicular transport, significantly reduced the extent and the frequency of minus end-directed migration of cytosolic virus, and increased the frequency, but not the extent of plus end-directed motility. The data imply that a single cytosolic Ad particle engages with two types of MT-dependent motor activities, the minus end- directed cytoplasmic dynein and an unknown plus end- directed activity.  (+info)

CLIP-170 highlights growing microtubule ends in vivo. (3/1483)

A chimera with the green fluorescent protein (GFP) has been constructed to visualize the dynamic properties of the endosome-microtubule linker protein CLIP170 (GFP-CLIP170). GFP-CLIP170 binds in stretches along a subset of microtubule ends. These fluorescent stretches appear to move with the growing tips of microtubules at 0.15-0.4 microm/s, comparable to microtubule elongation in vivo. Analysis of speckles along dynamic GFP-CLIP170 stretches suggests that CLIP170 treadmills on growing microtubule ends, rather than being continuously transported toward these ends. Drugs affecting microtubule dynamics rapidly inhibit movement of GFP-CLIP170 dashes. We propose that GFP-CLIP170 highlights growing microtubule ends by specifically recognizing the structure of a segment of newly polymerized tubulin.  (+info)

Distribution of 5-chloromethylfluorescein diacetate staining during meiotic maturation and fertilization in vitro of mouse oocytes. (4/1483)

The aim of this confocal microscopy study was to determine whether the pattern of CellTracker Green 5-chloromethylfluorescein diacetate (CMFDA) staining changes during meiotic maturation and fertilization in vitro of mouse oocytes. At different times during meiotic maturation and fertilization, oocytes, zygotes and two-cell embryos were stained with CMFDA to demonstrate intracellular glutathione S-transferase activity. After washing in CMFDA-free medium, most oocytes, zygotes and embryos were stained with dihydroethidium (HE) to visualize DNA structures. Meiotic maturation and fertilization in vitro of mouse oocytes were associated with changes in the pattern of intracellular CMFDA staining. In particular, accumulations of CMFDA-positive membranes were observed around the nucleus of germinal vesicle (GV) oocytes, overlaying the sperm nucleus as well as overlaying the first mitotic spindle if this approached the plasma membrane. Staining of oocytes and zygotes with the probes 3,3'-dihexyloxacarbocyanine iodine [DiOC6(3)], which stains all the intracellular membranes, and rhodamine 123, which stains active mitochondria, demonstrated that the intracellular structures evidenced by CMFDA staining did not correspond to accumulations of mitochondria. Exposure of oocytes and zygotes to the microtubule-disrupting agent nocodazole or the actin-depolymerizing drug cytochalasin D revealed an autonomous microfilament-dependent transport and relocation of CMFDA-positive membranes during meiotic maturation and fertilization. Such a transport of CMFDA-positive membranes may be envisaged as a protective shield built to prevent damage to DNA from endogenous and exogenous mutagen metabolites.  (+info)

Binding of Gal4p and bicoid to nucleosomal sites in yeast in the absence of replication. (5/1483)

The yeast transcriptional activator Gal4p can bind to sites in nucleosomal DNA in vivo which it is unable to access in vitro. One event which could allow proteins to bind to otherwise inaccessible sites in chromatin in living cells is DNA replication. To determine whether replication is required for Gal4p to bind to nucleosomal sites in yeast, we have used previously characterized chromatin reporters in which Gal4p binding sites are incorporated into nucleosomes. We find that Gal4p is able to perturb nucleosome positioning via nucleosomal binding sites in yeast arrested either in G1, with alpha-factor, or in G2/M, with nocodazole. Similar results were obtained whether Gal4p synthesis was induced from the endogenous promoter by growth in galactose medium or by an artificial, hormone-inducible system. We also examined binding of the Drosophila transcriptional activator Bicoid, which belongs to the homeodomain class of transcription factors. We show that Bicoid, like Gal4p, can bind to nucleosomal sites in SWI+ and swi1Delta yeast and in the absence of replication. Our results indicate that some feature of the intracellular environment other than DNA replication or the SWI-SNF complex permits factor access to nucleosomal sites.  (+info)

Intracellular trafficking pathways in the assembly of connexins into gap junctions. (6/1483)

Trafficking pathways underlying the assembly of connexins into gap junctions were examined using living COS-7 cells expressing a range of connexin-aequorin (Cx-Aeq) chimeras. By measuring the chemiluminescence of the aequorin fusion partner, the translocation of oligomerized connexins from intracellular stores to the plasma membrane was shown to occur at different rates that depended on the connexin isoform. Treatment of COS-7 cells expressing Cx32-Aeq and Cx43-Aeq with brefeldin A inhibited the movement of these chimera to the plasma membrane by 84 +/- 4 and 88 +/- 4%, respectively. Nocodazole treatment of the cells expressing Cx32-Aeq and Cx43-Aeq produced 29 +/- 16 and 4 +/- 7% inhibition, respectively. In contrast, the transport of Cx26 to the plasma membrane, studied using a construct (Cx26/43T-Aeq) in which the short cytoplasmic carboxyl-terminal tail of Cx26 was replaced with the extended carboxyl terminus of Cx43, was inhibited 89 +/- 5% by nocodazole and was minimally affected by exposure of cells to brefeldin A (17 +/-11%). The transfer of Lucifer yellow across gap junctions between cells expressing wild-type Cx32, Cx43, and the corresponding Cx32-Aeq and Cx43-Aeq chimeras was reduced by nocodazole treatment and abolished by brefeldin A treatment. However, the extent of dye coupling between cells expressing wild-type Cx26 or the Cx26/43T-Aeq chimeras was not significantly affected by brefeldin A treatment, but after nocodazole treatment, transfer of dye to neighboring cells was greatly reduced. These contrasting effects of brefeldin A and nocodazole on the trafficking properties and intercellular dye transfer are interpreted to suggest that two pathways contribute to the routing of connexins to the gap junction.  (+info)

The growth-related, translationally controlled protein P23 has properties of a tubulin binding protein and associates transiently with microtubules during the cell cycle. (7/1483)

The translationally controlled protein P23 was discovered by the early induction of its rate of synthesis after mitogenic stimulation of mouse fibroblasts. P23 is expressed in almost all mammalian tissues and it is highly conserved between animals, plants and yeast. Based on its amino acid sequence, P23 cannot be attributed to any known protein family, and its cellular function remains to be elucidated. Here, we present evidence that P23 has properties of a tubulin binding protein that associates with microtubules in a cell cycle-dependent manner. (1) P23 is a cytoplasmic protein that occurs in complexes of 100-150 kDa, and part of P23 can be immunoprecipitated from HeLa cell extracts with anti-tubulin antibodies. (2) In immunolocalisation experiments we find P23 associated with microtubules during G1, S, G2 and early M phase of the cell cycle. At metaphase, P23 is also bound to the mitotic spindle, and it is detached from the spindle during metaphase-anaphase transition. (3) A GST-P23 fusion protein interacts with alpha- and beta-tubulin, and recombinant P23 binds to taxol-stabilised microtubules in vitro. The tubulin binding domain of P23 was identified by mutational analysis; it shows similarity to part of the tubulin binding domain of the microtubule-associated protein MAP-1B. (4) Overexpression of P23 results in cell growth retardation and in alterations of cell morphology. Moreover, elevation of P23 levels leads to microtubule rearrangements and to an increase in microtubule mass and stability.  (+info)

Golgi structure correlates with transitional endoplasmic reticulum organization in Pichia pastoris and Saccharomyces cerevisiae. (8/1483)

Golgi stacks are often located near sites of "transitional ER" (tER), where COPII transport vesicles are produced. This juxtaposition may indicate that Golgi cisternae form at tER sites. To explore this idea, we examined two budding yeasts: Pichia pastoris, which has coherent Golgi stacks, and Saccharomyces cerevisiae, which has a dispersed Golgi. tER structures in the two yeasts were visualized using fusions between green fluorescent protein and COPII coat proteins. We also determined the localization of Sec12p, an ER membrane protein that initiates the COPII vesicle assembly pathway. In P. pastoris, Golgi stacks are adjacent to discrete tER sites that contain COPII coat proteins as well as Sec12p. This arrangement of the tER-Golgi system is independent of microtubules. In S. cerevisiae, COPII vesicles appear to be present throughout the cytoplasm and Sec12p is distributed throughout the ER, indicating that COPII vesicles bud from the entire ER network. We propose that P. pastoris has discrete tER sites and therefore generates coherent Golgi stacks, whereas S. cerevisiae has a delocalized tER and therefore generates a dispersed Golgi. These findings open the way for a molecular genetic analysis of tER sites.  (+info)

TY - JOUR. T1 - Dose-dependent effect of nocodazole on endothelial cell cytoskeleton. AU - Smurova, K. M.. AU - Birukova, A. A.. AU - Verin, A. D.. AU - Alieva, Irina B.. PY - 2008/6/1. Y1 - 2008/6/1. N2 - The endothelium lining the inner surface of blood vessels fulfils an important barrier function and specifically, it controls vascular membrane permeability as well as nutrient and metabolite exchange in circulating blood and tissue fluids. Disturbances in vascular endothelium barrier function (vascular endothelium dysfunction) are coupled to cytoskeleton rearrangements, actomyosin contractility, and as a consequence, formation of paracellular gaps between endothelial cells. Microtubules constitute the first effector link in the reaction cascade resulting in vascular endothelium dysfunction. Increased vascular permeability associated with many human diseases is also manifested as a side effect in anticancer mitosis-blocking therapy. The aim of this study was to examine the possibility of ...
Here we investigated microtubule dynamics and function during neutrophil migration in vivo. In accordance with reported in vitro findings, we found that microtubule disruption impairs neutrophil directed migration to wounds but induces cell motility and polarity in a PI(3)K-independent manner. We also found that Rho mediates nocodazole-induced neutrophil motility. These findings are consistent with previous findings in vitro, but further provide a physiological context for neutrophil migration. In addition, we elucidated two previously unidentified roles of microtubules during neutrophil motility in vivo. First, microtubule arrays nucleate in front of the nucleus and mainly radiate towards the uropod. Second, Rac is activated by microtubule depolymerization in primary human neutrophils and is necessary for nocodazole-induced neutrophil motility in vivo.. Leukocytes are often described as having the microtubule cytoskeleton and MTOC behind the nucleus at the uropod (Friedl and Weigelin, 2008; ...
CLIP-170 staining after nocodazole treatment. CLIP-170 appears in green and chromosomes in red. 10-15 optical sections were merged for the final images. Oocyt
A previous report has shown that microtubule depolymerization by nocodazole treatment arrests cell cycle extracts in M phase if containing very high densities of sperm nuclei. The use of MKP-1 further suggested that MAP kinase, the most likely target of MKP-1, may have a role in the spindle assembly checkpoint (20). However, whether classical MAP kinase is involved in the mitotic arrest remains to be determined. To address this question, we used MAP kinase-depleted extracts. We monitored the level of MPF as histone H1 kinase activity in the extracts supplemented with 9,000 sperm nuclei/μl. In the absence of nocodazole, the extracts returned to interphase after the first M phase, irrespective of whether MAP kinase was depleted or not (Fig. 3,A). In the presence of nocodazole, mock-treated extracts were arrested at the first M phase and the high MPF activity was sustained (Fig. 3,B, mock), whereas MAP kinase-depleted extracts returned to interphase after the first M phase (Fig. 3,B, αMAPK). In ...
Lasers have made the 21st century even more technologically advanced with the are not role models, implementation at the cellular level. How To. Confocal microscopy alternatively to ultraviolent mercury lamps, are higher in wavelength and are more detailed in illumination in regards to shapes of sport stars role anymore, organelles (Katula). In this experiment, using confocal microscopy, two organelles were visualized to history understand the drug effect of nocodazole on NIH3T3 cells. Using two fluorescent stains, Mitotracker Red (accumulates in mitochondria) and role Hoechst 33342 (accumulates in nuclei) were used to test what microtubules would look like resulting from the drug. Nocodazole is a drug that penetrates the microtubules to where it can be synchronized. Ap World Essay 2007. (Karbowski). Microtubules are made up of polarized tubulin that are important for cytoskeletal rigidity, mitotic division, and act as a branch in sport role models anymore transporting molecules to other parts ...
Figure 1. High‐throughput siRNA screen identifies kinases that regulate the ionizing‐radiation‐induced G2 checkpoint. (A) Schematic overview of the robot‐automated high‐throughput siRNA screen. p53 dominant‐negative U2OS (U2OS p53dneg) cells were reverse transfected and, after incubation for 2 days, treated with 6 Gy of IR and, 2 h later, with nocodazole for 8 h and subsequently stained with H3Ser10p antibody to stain mitotic cells, and Hoechst to stain the nuclei. (B) Flow cytometric analysis of U2OS p53dneg cells. Where indicated, cells were treated with IR (6 Gy) and 2 h later with nocodazole for 8 h. Cells were collected and stained with phospho H3ser10 (H3Ser10p) antibody and propidium iodide (PI). (C) CHK1 depletion abrogates the G2 checkpoint. U2OS p53dneg cells were transfected with CHK1 siRNA and treated with IR (6 Gy) and 2 h later with nocodazole for 8 h. Top panel: immunofluorescence microscopy images obtained from the robot‐automated screen. Bottom panel: cells were ...
Author(s): Breitfeld, PP; McKinnon, WC; Mostov, KE | Abstract: A polarized cell, to maintain distinct basolateral and apical membrane domains, must tightly regulate vesicular traffic terminating at either membrane domain. In this study we have examined the extent to which microtubules regulate such traffic in polarized cells. Using the polymeric immunoglobulin receptor expressed in polarized MDCK cells, we have examined the effects of nocodazole, a microtubule-disrupting agent, on three pathways that deliver proteins to the apical surface and two pathways that deliver proteins to the basolateral surface. The biosynthetic and transcytotic pathways to the apical surface are dramatically altered by nocodazole in that a portion of the protein traffic on each of these two pathways is misdirected to the basolateral surface. The apical recycling pathway is slowed in the presence of nocodazole but targeting is not disrupted. In contrast, the biosynthetic and recycling pathways to the basolateral surface are
Hypoparathyroidism, mental retardation and facial dysmorphism (HRD) is a fatal developmental disease caused by mutations in tubulin-specific chaperone E (TBCE). A mouse Tbce mutation causes progressive motor neuronopathy. To dissect the functions of TBCE and the pathogenesis of HRD, mutations were generated in Drosophila tbce, and its expression was manipulated in a tissue-specific manner. Drosophila tbce nulls are embryonic lethal. Tissue-specific knockdown and overexpression of tbce in the neuromusculature resulted in disrupted and increased microtubules, respectively. Alterations in TBCE expression also affected neuromuscular synapses. Genetic analyses revealed an antagonistic interaction between TBCE and the microtubule-severing protein Spastin. Moreover, treatment of muscles with the microtubule-depolymerizing drug nocodazole implicated TBCE as a tubulin polymerizing protein. Taken together, these results demonstrate that TBCE is required for the normal development and function of ...
The contributions of MT attachment and kinetochore tension in the SAC are still under investigation (Nicklas et al., 1995; Waters et al., 1998; King et al., 2000; Shannon et al., 2002; Pinsky and Biggins, 2005), so the importance of tension was tested using brief treatment with taxol. This approach maintains MT attachment but reduces tension at the kinetochores of aligned chromosomes (Waters et al., 1998). Interkinetochore distance measurements confirmed decreased tension but not the completely relaxed kinetochore state observed in nocodazole (Fig. S4). PT89 signal was retained at the kinetochores of taxol-treated cells (Fig. 6 A) at levels similar to nocodazole-treated cells. As in nocodazole-treated cells, the retention of PT89 was linked to the retention of BubR1. Together, these results suggest that effective dynein dephosphorylation requires both MT attachment and kinetochore tension.. The requirement for both MT attachment and tension was reminiscent of previous work on kinetochore ...
Abstract Background Many cloned animals have been created by transfer of differentiated cells at G0/G1 or M phase of the cell cycle into enucleated M II oocytes having high maturation/meiosis/mitosis-promoting factor activity. Because maturation/meiosis/mitosis-promoting factor activity during oocyte maturation is maximal at both M I and M II, M I oocytes may reprogram differentiated cell nuclei as well. The present study was conducted to examine the developmental ability in vitro of porcine embryos reconstructed by transferring somatic cells (ear fibroblasts) into enucleated M I or M II oocytes. Results Analysis of the cell cycle stages revealed that 91.2 ± 0.2% of confluent cells were at the G0/G1 phase and 54.1 ± 4.4% of nocodazole-treated cells were at the G2/M phase, respectively. At 6 h after activation, nuclear swelling was observed in 50.0-88.9% and 34.4-39.5% of embryos reconstituted with confluent cells and nocodazole-treated cells regardless of the recipient oocytes, ...
Tyrosine phosphorylation is implicated in the formation, maintenance and turnover of cell-matrix adhesions (Barry and Critchley, 1994; Ridley and Hall, 1994; Chrzanowska-Wodnicka and Burridge, 1994; Bershadsky et al., 1996; Retta et al., 1996; Ayalon and Geiger, 1997; Schneider et al., 1998), yet the mechanism underlying this involvement is still obscure. In this study, we addressed this issue by comparing local changes in PY levels to the recruitment of several FA proteins induced by the microtubule-disrupting drug nocodazole. For this purpose, we have combined quantitative immunofluorescence microscopy with a novel approach for monitoring kinetics of tyrosine phosphorylation in live cells.. FA assembly is a multistage process that involves the transformation of small, dot-like focal complexes into large FAs (see Geiger et al., 2001). Previous studies have shown that application of mechanical force to focal complexes, either by increasing cytoskeletal contractility or by external perturbation, ...
Apoptosis resistance is the major cause of chemotherapy failure in most kinds of cancers, including Burkitt lymphomas (BL). To elucidate molecular mechanisms regulating the development of apoptosis resistance, a panel of 15 BL cell lines was investigated for apoptosis induction upon treatment with microtubule inhibitors taxol, nocodazole and vincristine. Significant differences were observed in the extent of apoptosis induction among BL cell lines examined. Interestingly, cell lines exhibiting resistance to taxol- or nocodazole-induced apoptosis, showed development of polyploidy (,4N) and vice versa, displaying an inverse relationship between apoptosis and polyploidy induction. Further, in sensitive cell lines taxol-induced apoptosis was accompanied by caspase activation, Bid cleavage and Mcl-1 down-regulation. In contrast, most apoptosis resistant cell lines exhibited a loss of Bax and Bak expression and showed prolonged mitotic arrest with ,4N DNA content upon treatment. To gain mechanistic ...
We hypothesized that the effects of Centrin2 inactivation could be associated with transient microtubule disruption. In support of this idea, we found that the treatment of freshly isolated E16 mouse neurons with the microtubule-destabilizing agent nocodazole (6 μm, 2 h) lead to disruption of the cytoplasmic polarity, as evidenced by the dispersion of the Golgi apparatus and late endosomes (see supplemental Fig. 3C,D, available at www.jneurosci.org as supplemental material) (n = 90 cells from 3 brains) as well as neurite retraction (data not shown) (de Anda et al., 2005). To confirm the specificity of the Centrin2 inactivation using CALI, we imaged neurons in irradiated slices that did not express the Centrin2-KR and found normal neuronal differentiation with the polarized cytoplasm oriented toward the medial/apical neurite (Fig. 3C,D) (8 h) that would become the axon (Fig. 3D, 42 h, black arrowheads and Inset 1) (for the whole time-lapse sequence and detailed z-stack analysis of the L1 ...
Initially, MTs in the vegetal shear zone are disorganized and short, but as cortical rotation progresses, they lengthen into parallel bundles, which have their plus-ends oriented away from the site of sperm entry (Fig. 2C,F) (Houliston and Elinson, 1991a). The subcortical MTs depolymerize near the end of the first cell cycle, ending the process of cortical rotation (Schroeder and Gard, 1992; Marrari et al., 2003). During rotation, the cortex (and the dorsalizing activity) moves towards the plus-ends of the MTs, explaining why the direction of cortical rotation depends on the site of fertilization and why the dorsal organizer forms on the side of the embryo opposite the sperm entry point (reviewed by Houliston and Elinson, 1992).. The proper formation of the MT array is crucial for the development of the dorsal axis. If MT polymerization is blocked during the first cell cycle by exposure to UV irradiation or to the MT-depolymerizing drug nocodazole, or with inhibitory antibodies to the ...
Stabilization of microtubules through the expression of Syk. (A)MDA-MB-231 cells lacking Syk (−Syk) or expressing Syk (+Syk)and treated with nocodazole were s
Spindle checkpoint proteins monitor the interaction of the spindle apparatus with the kinetochores, halting anaphase even if the microtubule attachment of only a single chromosome is altered. In this study, we show that Bub3p of Saccharomyces cerevisiae, an evolutionarily conserved spindle checkpoint protein, exhibits distinct interactions with an altered or defective kinetochore(s). We show for the first time that green fluorescent protein-tagged S. cerevisiae Bub3p (Bub3-GFP) exhibits not only a diffuse nuclear localization pattern but also forms distinct nuclear foci in unperturbed growing and G2/M-arrested cells. As Bub3-GFP foci overlap only a subset of kinetochores, we tested a model in which alterations or defects in kinetochore or spindle integrity lead to the distinct enrichment of Bub3p at these structures. In support of our model, kinetochore-associated Bub3-GFP is enriched upon activation of the spindle checkpoint due to nocodazole-induced spindle disassembly, overexpression of the
Here, we report that a centrosomal protein FOR20 [FOP (FGFR1 (fibroblast growth factor receptor 1) oncogene protein)-like protein of molecular mass of 20 kDa; also named as C16orf63, FLJ31153 or PHSECRG2] can regulate the assembly and stability of microtubules. Both FOR20 IgG antibody and GST (glutathione S-transferase)-tagged FOR20 could precipitate tubulin from the HeLa cell extract, indicating a possible interaction between FOR20 and tubulin. FOR20 was also detected in goat brain tissue extract and it cycled with microtubule-associated proteins. Furthermore, FOR20 bound to purified tubulin and inhibited the assembly of tubulin in vitro. The overexpression of FOR20 depolymerized interphase microtubules and the depletion of FOR20 prevented nocodazole-induced depolymerization of microtubules in HeLa cells. In addition, the depletion of FOR20 suppressed the dynamics of individual microtubules in live HeLa cells. FOR20-depleted MDA-MB-231 cells displayed zigzag motion and migrated at a slower rate ...
KCNH2 encodes the Kv11.1 α-subunit that underlies the rapidly activating delayed-rectifier K+ current in the heart. Loss-of-function KCNH2 mutations cause long QT syndrome type 2 (LQT2), and most LQT2-linked missense mutations inhibit the trafficking of Kv11.1 channel protein to the cell surface membrane. Several trafficking-deficient LQT2 mutations (e.g., G601S) generate Kv11.1 proteins that are sequestered in a microtubule-dependent quality control (QC) compartment in the transitional endoplasmic reticulum (ER). We tested the hypothesis that the QC mechanisms that regulate LQT2-linked Kv11.1 protein trafficking are mutation-specific. Confocal imaging analyses of HEK293 cells stably expressing the trafficking-deficient LQT2 mutation F805C showed that, unlike G601S-Kv11.1 protein, F805C-Kv11.1 protein was concentrated in several transitional ER subcompartments. The microtubule depolymerizing drug nocodazole differentially affected G601S- and F805C-Kv11.1 protein immunostaining. Nocodazole caused G601S
In addition to direct tumor cell cytotoxicity, chemotherapy can mediate tumor reduction through immune modulation of the tumor microenvironment to promote anti-tumor immunity. Mature dendritic cells (DCs) play key roles in priming robust immune responses in tumor-bearing hosts. Here, we screened a p …
Analysis and theory development in cognitive psychology and science education study remain mainly isolated. AP biology programs in high school and accomplished a score of 4 or 5 5 on the AP Biology examination. These college students participated as part of their normal classroom activities. The nonmajors group (= 68) was composed of students enrolled …Read More. ...
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Fluorescence images of control and Si-RNA transfected HeLa cells treated with nocodazole and allowed to recover. Mitotic cells were stained for alpha-...
Cytoskeleton inhibitors were used to study morphogenesis in the pathogenic and dimorphic fungus Candida albicans Nocodazole is a specific microtubule inhibitor and chloropropham (CIPC), at high concentrations, is an inhibitor of microtubules and microfilaments. Distribution of microtubules and microfilaments was studied by immunofluorescence techniques using anti-tubulin antibody with FITC-conjugated secondary antibody, and by staining with Rh-phalloidin. Nocodazole did not arrest apical cell elongation at a concentration (20 µg ml−1) that inhibited nuclear division and migration. Cytoplasmic and nuclear microtubules disappeared within 30 min in filamentous cells under these conditions. However, the Rh-phalloidin-stained actin granules which were localized in the tips of filamentous cells, and the microfilaments, were arranged normally at this concentration of nocodazole. Growth, and normal distribution of microtubules and microfilaments, were inhibited by a high concentration (200 µg ml−1) of
The IPL1 gene is required for high-fidelity chromosome segregation in the budding yeast Saccharomyces cerevisiae. Conditional ipl1ts mutants missegregate chromosomes severely at 37 degrees C. Here, we report that IPL1 encodes an essential putative protein kinase whose function is required during the later part of each cell cycle. At 26 degrees C, the permissive growth temperature, ipl1 mutant cells are defective in the recovery from a transient G2/M-phase arrest caused by the antimicrotubule drug nocodazole. In an effort to identify additional gene products that participate with the Ipl1 protein kinase in regulating chromosome segregation in yeast, a truncated version of the previously identified DIS2S1/GLC7 gene was isolated as a dosage-dependent suppressor of ipl1ts mutations. DIS2S1/GLC7 is predicted to encode a catalytic subunit (PP1C) of type 1 protein phosphatase. Overexpression of the full-length DIS2S1/GLC7 gene results in chromosome missegregation in wild-type cells and exacerbates the ...
We have examined the cortex of Caenorhabditis elegans eggs during pseudocleavage (PC), a period of the first cell cycle which is important for the generation of asymmetry at first cleavage (Strome, S. 1989. Int. Rev. Cytol. 114: 81-123). We have found that directed, actin dependent, cytoplasmic, and cortical flow occurs during this period coincident with a rearrangement of the cortical actin cytoskeleton (Strome, S. 1986. J. Cell Biol. 103: 2241-2252). The flow velocity (4-7 microns/min) is similar to previously determined particle movements driven by cortical actin flows in motile cells. We show that directed flows occur in one of the daughters of the first division that itself divides asymmetrically, but not in its sister that divides symmetrically. The cortical and cytoplasmic events of PC can be mimicked in other cells during cytokinesis by displacing the mitotic apparatus with the microtubule polymerization inhibitor nocodazole. In all cases, the polarity of the resulting cortical and ...
We constructed complexes between isolated chromosomes and microtubules made from purified tubulin to study the movement of chromosomes towards the minus end of microtubules in vitro, a process analogous to the movement of chromosomes towards the pole of the spindle at anaphase of mitosis. Our results show that the energy for this movement is derived solely from microtubule depolymerization, and indicate that anaphase movement of chromosomes is both powered and regulated by microtubule depolymerization at the kinetochore ...
Subsets of microtubules enriched in posttranslationally detyrosinated (Gundersen, G. G., M. H. Kalnoski, and J. C. Bulinski. 1984. Cell. 38:779) or acetylated (Piperno, G., M. Le Dizet, and X. Chang. 1987. J. Cell Biol. 104:298), alpha tubulin have previously been described in interphase cultured cells. In this study an immunofluorescence comparison of these minor populations of microtubules revealed that, in African green monkey kidney epithelial cells (TC-7 line), the population of microtubules enriched in detyrosinated tubulin was virtually coincident with the population enriched in acetylated alpha tubulin. In some cell types, however, such as human HeLa or marsupial PtK-2 cells, only one posttranslationally modified form of tubulin, i.e., acetylated or detyrosinated, respectively, was detectable in microtubules. In TC-7 cells, although both modifications were present, dissimilar patterns and kinetics of reappearance of microtubules enriched in detyrosinated and acetylated tubulin were ...
Although mitochondria are known to move actively in plant cells, little is known about how they move. In higher plants, actin filaments have been reported to be involved in the movement of organelles, such as chloroplasts, peroxisomes, endoplasmic reticulum and Golgi apparatus. Mitochondria were visualized in living ,i,Arabidopsis thaliana,/i, plants using fluorescent proteins fused to a mitochondria targeting signal. To compare the movement of mitochondria to the movements of another organelle, we also examined peroxisomes because of their similarity in size. Velocities of individual mitochondria and peroxisomes, as measured by time-lapse laser scanning microscopy, varied, although the average velocities of the two organelles were similar. Latrunculin B, an actin-depolymerizing drug, stopped movement of mitochondria and peroxisomes, demonstrating that movement of these organelles depends on actin filaments. On the other hand, propyzamide, a microtubule-depolymerizing drug, did not affect the ...
Similar to that described in previous studies (6, 7), our examination into cell cycle-dependent regulation of homologous recombination was undertaken by α-factor treatment to induce G1 arrest and nocodazole treatment to induce G2/M arrest. It has been reported that activation of homologous recombination is also observed in the S phase in S. cerevisiae (1, 20). Because replication stress is a major source of DSBs, DNA damage repair by homologous recombination is critically required to maintain genome stability in the S phase. Thus, it is reasonable to assume that a mechanism exists whereby homologous recombination is also activated in the S phase. In this study, we found that the phosphorylation of Rad51 and Rad52 for the progression of homologous recombination is catalyzed by Cdc28 combined with either Clb2 or Clb3. Given that Clb2 and Clb3 are redundantly expressed in the S and G2/M phases (fig. S2D), it is presumable that Cdc28 combined with either Clb2 or Clb3 induces Rad51 and Rad52 to ...
Based on these findings, we believe that microtubules are a critical target of PD environmental toxins such as rotenone, said Feng. Since many microtubule-depolymerizing agents are compounds naturally produced in many plants, our research points to the need to examine their possible link to Parkinsons disease. In addition, PD has a higher incidence in rural areas and is associated with pesticides and insecticides frequently used in farming practices ...
El nostre treball demostra que el 2ME2 inhibeix langiogènesis tumoral mitjançant la inhibició dels nivells proteics del factor HIF-1 així com la seva activitat transcripcional, incloent la transcripció del VEGF, en diverses línies cel.lulars. El 2ME2 no indueix la degradació proteica a través del proteosoma ni tampoc redueix els nivells dARNm del HIF-1, sinó que més aviat inhibeix la síntesi proteica de novo. Notablement, hem mostrat que el 2ME2 inhibeix el factor HIF-1 amb posterioritat a la disrupció del citoesquelet de microtúbuls aportant sòlides proves que afavoreixen una relació funcional entre els efectes anti-angiogènics i la disrupció dels microtúbuls. Aquests efectes no són una propietat única del 2ME2 sinó que és compartida per altres agents que actuen sobre els microtúbuls, com ara el taxol i la vincristina, suggerint un mecanisme dacció semblant per a tots aquests agents. Finalment, la nostra investigació demostra per primera vegada que el 2ME2 ...
Immunocompromisation is a major cause of opportunistic infections, activation of latent viruses, and the development of certain carcinomas such as Kaposis sarcoma (1, 2). This is particularly evident in many diseases that weaken the immune surveillance system, including AIDS and various cancer treatment modalities (e.g., radiation therapy, chemotherapy, and, in particular, antimicrotubule therapy), primarily because of severe myelosuppression and immunosuppression (3, 4). Finally, the resolution of these infections is dependent on the treatment modality of the malignancy and the ability of the host to mount an adequate immune response to fight off the infection (2).. Although antimicrotubule drugs constitute an important major class of anticancer drugs mainly typified by agents that either overpolymerize or bundle microtubules (such as the taxane family, ref. 5) or those that depolymerize them (such as the vincas; ref. 6, recently reviewed in refs. 7, 8), these agents, due to their gross ...
マウス・モノクローナル抗体 ab56676 交差種: Rat,Rb,Hu 適用: WB,IHC-P,Flow Cyt…Tubulin抗体一覧…画像、プロトコール、文献などWeb上の情報が満載のアブカムの Antibody 製品。国内在庫と品質保証制度も充実。
The incidence and mortality of breast cancer have increased throughout the world (Althuis et al., 2005), and it remains the most common cancer in women (Murray et al., 2012). In recent years, more and more drugs explored in clinical trials have provided promising advances in breast cancer treatments. Microtubule-binding agents are among the efficacious chemotherapeutic drugs that are commonly used for the treatment of breast cancer. Although antimicrotubule drugs, such as PTX and docetaxel, have been successfully applied in the clinic, drug resistance often occurred (Kavallaris, 2010) and acted as an obstacle for first-line chemotherapy. Augmented efflux transporters and diverse β-tubulin isotypes were involved in the development of drug resistance (Dumontet and Sikic, 1999). Thus, there is a pressing need to develop new microtubule inhibitors that can escape from the efflux of transporters related to MDR.. As a promising microtubule inhibitor candidate, DPT possesses various pharmacologic ...
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Lipid droplets (LDs) are intracellular organelles that provide fatty acids (FAs) to cellular processes including synthesis of membranes and production of metabolic energy. While known to move bidirectionally along microtubules (MTs), the role of LD motion and whether it facilitates interaction with other organelles are unclear. Here we show that during nutrient starvation, LDs and mitochondria relocate on detyrosinated MT from the cell centre to adopt a dispersed distribution. In the cell periphery, LD-mitochondria interactions increase and LDs efficiently supply FAs for mitochondrial beta-oxidation. This cellular adaptation requires the activation of the energy sensor AMPK, which in response to starvation simultaneously increases LD motion, reorganizes the network of detyrosinated MTs and activates mitochondria. In conclusion, we describe the existence of a specialized cellular network connecting the cellular energetic status and MT dynamics to coordinate the functioning of LDs and mitochondria ...
Biological activities of the 1,4-benzoquinone derivatives 5-O-ethylembelin (1) and 5-O-methylembelin (2) were investigated. Both of them showed anti proliferative activity against a panel of human tumor cell lines upon comparison to normal marsupial kidney cells (PtK2). They arrested HL-60 cells in the G(0)/G(1) phase of the cell cycle in a dose- and time-dependent manner. In HeLa cells, exposure to 100 mu M of 1 or 2 for 6 h induced a complete disassembly of the microtubule network and an increased number of cells blocked in mitotic stages. Treatment with 10 mu M of 1 and 2 for 24 h induced apoptosis in HL-60 cells. This evidence suggests that both 1 and 2 are promising novel antimitotic and anticancer molecules targeting microtubular proteins. ...
SID-530 is an intravenous formulation containing docetaxel, a semi-synthetic, second-generation taxane derived from a compound found in the European yew tree, Taxus baccata, with potential antineoplastic activity. Taxol analogue SID 530 binds to and stabilizes tubulin, inhibiting microtubule disassembly, which results in cell-cycle arrest at the G2/M phase and cell death. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus) (last updated: 6/23/2015)
SMCC-DM1 (DM1-SMCC) is a drug-linker conjugate composed of a potent microtubule-disrupting agent DM1 and a linker SMCC to make antibody drug conjugate (ADC). - Mechanism of Action & Protocol.
Motor proteins in the kinesin-8 family depolymerize microtubules in a length-dependent manner that may be crucial for controlling the length of organelles
Order Dynamitin ELISA Kits for many Reactivities. Human, Mouse, Rat and more. Compare Dynamitin ELISA Kits and find the right product on antibodies-online.com.
for 8 hours (by this time most MCF-7 cells had not yet accumulated in mitosis and thus remained adherent), fixed, stained with anti-α-tubulin, and visualized by fluorescence microscopy ...
Rudiger, M., Wehland, J., Weber, K. (1994). „The carboxy-terminal peptide of detyrosinated α tubulin provides a minimal system to study the substrate specificity of tubulin-tyrosine ligase. Eur. J. Biochem. 220: 309-320. PMID 7510228 ...
It is well known that c-Jun N-terminal kinase (JNK) plays pivotal roles in various mitotic events, but its function in mammalian oocyte meiosis remains unknown. In this study, we found that no specific JNK2 signal was detected in germinal vesicle stage. JNK2 was associated with the spindles especially the spindle poles and cytoplasmic microtubule organizing centers at prometaphase I, metaphase I, and metaphase II stages. JNK2 became diffusely distributed and associated with the midbody at telophase I stage. Injection of myc-tagged JNK2α1 mRNA into oocytes also revealed its localization on spindle poles. The association of JNK2 with spindle poles was further confirmed by colocalization with the centrosomal proteins, γ-tubulin and Plk1. Nocodazole treatment showed that JNK2 may interact with Plk1 to regulate the spindle assembly. Then we investigated the possible function of JNK2 by JNK2 antibody microinjection and JNK specific inhibitor SP600125 treatment. These two manipulations caused ...
Eribulin mesylate (eribulin), an analogue of the marine natural product halichondrin B, is a microtubule-depolymerizing drug that has utility in the treatment of patients with breast cancer. Clinical trial results have demonstrated that eribulin treatment provides a survival advantage to patients with metastatic or locally advanced breast cancer previously treated with an anthracycline and a taxane. Furthermore, a pooled analysis of two pivotal phase III trials has demonstrated that eribulin also improves overall survival in several patient subgroups, including in women with HER2-negative disease and triple-negative breast cancer. This review covers the preclinical research that led to the clinical testing and approval of eribulin, as well as subsequent research that was prompted by distinct and unexpected effects of eribulin in the clinic. Initial studies with halichondrin B demonstrated unique effects on tubulin binding that resulted in distinct microtubule-dependent events and antitumor ...
The trafficking of the adenomatous polyposis coli (APC) tumour suppressor protein in mammalian cells is a perennially controversial topic. Immunostaining evidence for an actin-associated APC localisation at intercellular junctions has been previously presented, though live imaging of mammalian junctional APC has not been documented. Using live imaging of transfected COS-7 cells we observed intercellular junction-associated pools of GFP-APC in addition to previously documented microtubule-associated GFP-APC and a variety of minor localisations. Although both microtubule and junction-associated populations could co-exist within individual cells, they differed in their subcellular location, dynamic behaviour and sensitivity to cytoskeletal poisons. GFP-APC deletion mutant analysis indicated that a protein truncated immediately after the APC armadillo repeat domain retained the ability to localise to adhesive membranes in transfected cells. Supporting this, we also observed junctional APC immunostaining in
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To determine whether TRF function was required to maintain cohesion, we examined cohesion in the trf4-ts trf5double mutant. If TRF function were required to maintain cohesion, then cells arrested with nocodazole at a permissive temperature and then shifted to the nonpermissive temperature should show an increased cohesion defect. After nocodazole arrest at the permissive temperature of 30°C, the trf4-ts trf5double mutant was able to maintain cohesion as monitored by the GFP-marked chromosome assay. However, when mutant cells were shifted to 37°C for 3 hours, a marked increase in cohesion-defective cells was observed (Fig. 3B). This demonstrates that TRF function is indeed required to maintain cohesion.. The ability of cells lacking TRF function to duplicate the genome was then examined as follows. Synchronous populations of either wild-type or otherwise isogenic trf4-ts trf5double-mutant G1 daughter cells were obtained by centrifugal elutriation. Wild-type and mutant cells were then released ...
4SC-207 is a novel microtubule inhibitor, which shows strong anti-proliferative activity in a large panel of tumor cell lines with an average GI50 of 11 nM. In particular, 4SC-207 is active in multi-drug resistant cell lines, such as HCT-15 and ACHN, suggesting that it is a poor substrate for drug efflux pumps. 4SC-207 inhibits microtubule growth in vitro and in vivo and promotes, in a dose dependent manner, a mitotic delay/arrest, followed by apoptosis or aberrant divisions due to chromosome alignment defects and formation of multi-polar spindles. Furthermore, preliminary data from preclinical studies suggest low propensity towards bone marrow toxicities at concentrations that inhibit tumor growth in paclitaxel-resistant xenograft models. 4SC-207 may be a potential anti-cancer agent.
TY - JOUR. T1 - Organization of non-centrosomal microtubules in epithelial cells. AU - Toya, Mika. AU - Takeichi, Masatoshi. PY - 2016/1/1. Y1 - 2016/1/1. N2 - Polarized epithelial cells contain a characteristic array of microtubules in which non-centrosomal microtubules are aligned along the apical-to-basal axis of the cell with their minus ends oriented towards the apical pole. Although this unique orientation of microtubules was discovered in the late 1980s, how this orientation is established remains unresolved partly because of limited information about molecular factors that regulate the minus ends of non-centrosomal microtubules. Recent studies, however, identified novel minus end- associated proteins, revealing mechanisms by which the polarized arrays of microtubules are established in epithelial cells. These studies have also demonstrated the importance of apico-basally orientated microtubules in intra-structural organization of cells. This review focuses on recent progress of our ...
The cytoskeleton is responsible for cell shape, motility (movement) of the cell as a whole, and motility of organelles within a cell. There are three types of filaments in the cytoplasm of most vertebrate cells: microfilaments, microtubules, and intermediate filaments.. filament systems are able to lengthen or shorten very rapidly. This dynamic nature of the cytoskeleton is necessary for cells to be able to change shape, complete cell division, or migrate.. The microfilament system is a network of filaments 6 nanometers (nm) in diameter that are important for anchoring plasma membrane proteins, for producing cell movement, and for cell division. The base filament is composed of a protein called actin.. Microtubules are the largest of the cytoskeletal filaments with a diameter of 25 nm. There are many parallels between the microfilament cytoskeletal system and the microtubule system. Like microfilaments, microtubules are produced by the self-assembly of a subunit, which in the case of ...
MLN0264 is an investigational antibody-drug conjugate (ADC) that consists of the human anti-guanylyl cyclase C (GCC) antibody linked to a microtubule-disrupting agent (monomethyl auristatin). As ADCs have a very long clearance half-life, the potential exists for a highly infrequent dosing schedule. A quantitative understanding of the relationship between exposure and preclinical antitumor biological activity is thus applied to support dose schedule selection in the clinic.. In this study, we develop a pharmacokinetic/efficacy (PK/E) relationship in xenograft models to evaluate the predictive contributions of exposure and xenograft characteristics to MLN0264 biological activity. Single dose pharmacokinetic (PK) data were obtained for a range of time points, and a linear two-compartment PK model was built. Xenograft biological activity studies were conducted in which MLN0264 was administered at various dose levels and dosing schedules to mice bearing one of six different xenograft models. We used ...
Mitotic spindle position defines the cell cleavage site during cytokinesis. cortex. In elongating cells asymmetrically, dynein-dependent spindle anchoring at the fixed cell cortex guarantees correct spindle setting. Our outcomes reveal the anaphase-specific spindle centering systems that obtain equal-sized cell department. syncytial embryos (Silverman-Gavrila et al., 2008). To evaluate the contribution of chromosome-derived Ran-GTP indicators in mammalian cells, we utilized tsBN2 cells, which include a heat range delicate mutation in RCC1 that stops the formation of Ran-GTP at the restricted heat range (Nishitani et al., 1991). In nocodazole treated tsBN2 cells, Anillin was decreased from the cell cortex in the location of the chromosome herd at the permissive heat range (Fig. 7A, still left) equivalent to HeLa cells (Fig. 6E). Nevertheless, at the restricted heat range, Anillin localised to the cell cortex also in the location of chromosomes (Fig. 7A, correct). The heat range change do not ...
Mitotic spindle position defines the cell cleavage site during cytokinesis. cortex. In elongating cells asymmetrically, dynein-dependent spindle anchoring at the fixed cell cortex guarantees correct spindle setting. Our outcomes reveal the anaphase-specific spindle centering systems that obtain equal-sized cell department. syncytial embryos (Silverman-Gavrila et al., 2008). To evaluate the contribution of chromosome-derived Ran-GTP indicators in mammalian cells, we utilized tsBN2 cells, which include a heat range delicate mutation in RCC1 that stops the formation of Ran-GTP at the restricted heat range (Nishitani et al., 1991). In nocodazole treated tsBN2 cells, Anillin was decreased from the cell cortex in the location of the chromosome herd at the permissive heat range (Fig. 7A, still left) equivalent to HeLa cells (Fig. 6E). Nevertheless, at the restricted heat range, Anillin localised to the cell cortex also in the location of chromosomes (Fig. 7A, correct). The heat range change do not ...
Subcellular distribution of mass can be analyzed by a technique that involves culturing cells on interferometers and digitizing their interference contours. Contour sampling resulted in 102 variables per cell, which were predictors of oncogenic transformation. Cell phenotypes can be deconstructed by use of latent factors, which represent the covariance of the real variables. The reversal of the cancertype phenotype by a combination of microtubule- stabilizing and -depolymerizing agents was described previously. The implications of these results have been explored by clinicians who treated patients with the combination of docetaxel and vinorelbine (Navelbine®). The current study was performed to determine the effects of different combinations on phenotype and in phases of the cell cycle other than mitosis. Combinations of paclitaxel with either colchicine, podophyllotoxin, nocodazole, or vinblastine caused phenotype reversal. Paclitaxel analogue, 7-deoxytaxol, by itself caused reversal. Factors #4,
The table lists cell cycle regulated chromatin remodeling genes. Five transcriptome data sets, in which the genes that are periodically expressed in at least one data set, and one ribosomal profiling (translationally regulated) data set are included. Periodically expressed genes are indicated with cell cycle phase in which they show the highest expression level. Gene sets in which a given gene is not significantly cell cycle regulated is indicated as NR (not transcriptionally regulated in the cell cycle) or NTR (not translationally regulated in the cell cycle) in transcriptome and ribosomal profiling data sets, respectively. Four experiments are supplemented with expression profiles which can be found by clicking the gene name. Synchronization methods are abbreviated as: SS=serum starvation, TT= double thymidine block, NZ=nocodazole, MS=mitotic shake-off ...
Nocodazole is a chemical agent that interferes with the polymerization of microtubules. Cells treated with nocodazole arrest ... Taxol works in the opposite way of nocodazole, instead stabilizing the microtubule polymer and preventing it from disassembly. ... Xu K, Schwarz PM, Ludueña RF (Feb 2002). "Interaction of nocodazole with tubulin isotypes". Drug Development Research. 55 (2): ... Kuhn M (March 1998). "The microtubule depolymerizing drugs nocodazole and colchicine inhibit the uptake of Listeria ...
Fenbendazole Oxfendazole Nocodazole "Farnam Pet Press Release. TRUSTED D-WORM offers product for tapeworm management". Farnam ...
Experiments using nocodazole and taxol support this observation. Taxol, which stabilized microtubules, forced a significant ... Moreover, disruption of microtubule polymerization with nocodazole, and of actin polymerization with cytochalisin B, shows the ... Moreover, embryos treated with nocodazole, which sequesters tubulin dimers and promotes microtubule depolymerization, similarly ...
Oxfendazole Nocodazole Praziquantel Plumb's Veterinary Drug Handbook, Fifth Edition, 2005. Junquera, P. (2015-07-26). " ...
Cells will remain arrested until the nocodazole has been washed out. Nocodazole does not appear to disrupt interphase ... "Production of large numbers of mitotic mammalian cells by use of the reversible microtubule inhibitor Nocodazole: Nocodazole ... Nocodazole is a rapidly-reversible inhibitor of microtubule polymerization that can be used to arrest cells before Anaphase at ... Because microtubules are vital in other cellular functions, sustained use of nocodazole can result in disruption of those ...
However, nocodazole also blocks formation of aggresomes, complicating interpretation of these observations. Partial inhibition ... Inhibition of microtubule polymerization with nocodazole blocks formation of the purinosome macrobodies, and reduces the flux ...
Vasquez RJ, Howell B, Yvon AM, Wadsworth P, Cassimeris L (June 1997). "Nanomolar concentrations of nocodazole alter microtubule ...
Vinorelbine, Nocodazole, vincristine, and colchicine have the opposite effect, blocking the polymerization of tubulin into ... microtubule dynamics and lamellipodium formation revealed by direct imaging of microtubules in cells treated with nocodazole or ...
2005). "Overexpression of DRG2 increases G2/M phase cells and decreases sensitivity to nocodazole-induced apoptosis". J. ...
Nocodazole, for example, has been used in biological research for synchronization, although some evidence suggests it may lack ... 2006). "Nocodazole does not synchronize cells: implications for cell-cycle control and whole-culture synchronization" (PDF). ...
Microtubule-disruptive drugs like vinblastine, colcemid, and nocodazole have been reported to act by two mechanisms. At very ...
Effects of substances interacting with microtubular function and axonal flow [nocodazole, taxol and erythro-9-3-(2-hydroxynonyl ...
Using drugs such as nocodazole and colchicine, the mitotic spindle disassembles and the cell cycle is blocked at the metaphase- ... Wang Y, Burke DJ (December 1995). "Checkpoint genes required to delay cell division in response to nocodazole respond to ... laevis meiosis II extracts without the addition of sperm of nuclei and nocodazole to prevent spindle assembly. The leading ...
This hypothesis is based on the fact that disruption of microtubules with the chemical nocodazole blocks the appearance of the ...
When cells overexpressing Aurora C were treated with nocodazole to turn on the SAC, Aurora B protein stability and activity ...
Microtubule inhibitors, such as nocodazole, are used to arrest the oocyte in M phase, during which its nuclear membrane is ...
In fact, when metaphase mammalian cells are treated with the spindle-depolymerizing agent nocodazole, Mad2 proteins become ... it was essential to execute a block in the metaphase-to-anaphase transition in response to the microtubule poison nocodazole. ...
... cells and its localization at the apical junctional complex is perturbed by treatment with the microtubule drug nocodazole. ...
Accordingly, studies of HT-29 cells have shown induced differentation as a result of forskolin, Colchicine, nocodazole, and ...
Treating embryos with the microtubule depolymerizing agent nocodazole completely blocks epiboly of the YSL and partially blocks ...
... nocodazole MeSH D03.438.103.675 - omeprazole MeSH D03.438.103.732 - pimozide MeSH D03.438.103.850 - thiabendazole MeSH D03.438. ...
... nocodazole (INN) nofecainide (INN) nogalamycin (INN) Nogenic HC nolatrexed (INN) nolinium bromide (INN) nolpitantium besilate ( ...
They found that when the cells were released and concurrently treated with nocodazole, a G2/M phase cell cycle inhibitor, ...
As nocodazole affects the cytoskeleton, it is often used in cell biology experiments as a control: for example, some dominant ... Cells treated with nocodazole arrest with a G2- or M-phase DNA content when analyzed by flow cytometry. Microscopy of ... Nocodazole is an antineoplastic agent which exerts its effect in cells by interfering with the polymerization of microtubules. ... Nocodazole has been shown to decrease the oncogenic potential of cancer cells via another microtubules-independent mechanisms. ...
As nocodazole affects the cytoskeleton, it is often used in cell biology experiments as a control: for example, some dominant ... Cells treated with nocodazole arrest with a G2- or M-phase DNA content when analyzed by flow cytometry. Microscopy of ... Nocodazole is an antineoplastic agent which exerts its effect in cells by interfering with the polymerization of microtubules. ... Nocodazole has been shown to decrease the oncogenic potential of cancer cells via another microtubules-independent mechanisms. ...
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Nocodazole is an anti-mitotic agent that reversibly interferes with the polymerization of microtubules. ... Nocodazole is an anti-mitotic agent that reversibly interferes with the polymerization of microtubules (De Brabander et al.). ... Internal Search Keywords: nocodazole,74072,74074,31430-18-9,oncodazole,Nocodazolum,Nocidazole,Nocodazol,NSC 238159,NSC-238159, ... Nocodazole binds to beta-tubulin and disrupts microtubule assembly/disassembly dynamics, impairing formation of the metaphase ...
... is an antineoplastic microtubule polymerization inhibitor. It is frequently used to synchronize cell cycling and ...
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B) Arrest in G2 after exposure to medium containing 100 nM nocodazole for 2 h. (C) The removal of nocodazole and exposure to ... 2C). The nocodazole treatment could then be repeated, and the cells arrested in G2/M again (Fig. 2D). Using drugs to reversibly ... Arrest of Giardia cell cycle with aphidicolin and nocodazole. (A and B) Subjecting a control culture with a 5:1 ratio of G2 to ... Arrest of Giardia cell cycle with nocodazole and aphidicolin. (A) Starting culture with a 5:1 ratio of G2 to G1 cells. ( ...
It is shown here that nocodazole at concentrations as low as 100 nM caused the GA to disperse in treated fibro-blasts that ... Antibody-blocking analysis of Mts after injection of biotin-tubulin into the HSFs was used to show that nocodazole at low ... These data demonstrate that the dispersal of GA in the cytoplasm of nocodazole-treated HSFs is a kinesin-driven process with ... The GA in different cell types undergoes fragmentation and dispersal throughout the cytoplasm upon treatment with nocodazole. ...
Previously, we showed that low concentrations (,200 nM) of nocodazole or taxol reduced the rate of locomotion of NRK ... The percent time MTs were inactive (i.e., paused) increased greater than twofold in nocodazole- and taxol-treated cells, while ... In support of the latter hypothesis, when all MTs were rapidly depolymerized by 20 microM nocodazole, we detected the rapid ... Previously, we showed that low concentrations (,200 nM) of nocodazole or taxol reduced the rate of locomotion of NRK ...
Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the ... Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the ... Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the ... Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the ...
Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics ... Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics ... Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics ... Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. Implications for the role of microtubule dynamics ...
The impact of the microtubule-disrupting drug nocodazole on renal tubular s ... Nocodazole inhibition of organic anion secretion in teleost renal proximal tubules.: ... Nocodazole inhibition of organic anion secretion in teleost renal proximal tubules.. Authors * Miller, D S ... Nocodazole reversibly inhibited 20-30% of the tubular accumulation of two model organic anions, p-aminohippurate and ...
The biosynthetic and transcytotic pathways to the apical surface are dramatically altered by nocodazole in that a portion of ... The apical recycling pathway is slowed in the presence of nocodazole but targeting is not disrupted. In contrast, the ... Using the polymeric immunoglobulin receptor expressed in polarized MDCK cells, we have examined the effects of nocodazole, a ... biosynthetic and recycling pathways to the basolateral surface are less affected by nocodazole and therefore appear to be more ...
Since nocodazole has been used as a chemotherapy reagent in cancer treatment, it will be beneficial to re-evaluate the ... In this work, nocodazole, a microtubule destabilizer, was used to treat HeLa cells with different concentrations. The results ... It suggested that nocodazole may inhibit cell growth through an alternative impacting effect other than destabilizing ... Whereas, at concentration of 1 mM, nocodazole induced significant alterations of F-actin structure in HeLa cells. It indicated ...
Tag: order Nocodazole. Analysis and theory development in cognitive psychology and science education study. Posted on December ...
The effect of nocodazole on endothelial cell cytoskeleton was found to be dose-dependent. Nocodazole in micromolar ... The effect of nocodazole on endothelial cell cytoskeleton was found to be dose-dependent. Nocodazole in micromolar ... The effect of nocodazole on endothelial cell cytoskeleton was found to be dose-dependent. Nocodazole in micromolar ... The effect of nocodazole on endothelial cell cytoskeleton was found to be dose-dependent. Nocodazole in micromolar ...
Cell Lysis and Nocodazole Treatment.. Cells grown in 25-cm2 flasks were harvested as follows. The medium was removed, and the ... 4A), treatment with nocodazole resulted in an increased phosphorylation of both histone H1 and the GST-ICP0 20-241 fusion ... The cdc2 kinase was immune-precipitated from HEp-2 cells treated with nocodazole for 20 h and reacted with roscovitine before ... GST-ICP0 543-768 fusion protein served as a negative control and was not phosphorylated by the nocodazole-induced kinase ...
To ensure the feasibility of this model, we treated labeled zebrafish with nocodazole and demonstrated that nocodazole could ... To ensure the feasibility of this model, we treated labeled zebrafish with nocodazole and demonstrated that nocodazole could ... Nocodazole Treatment. Nocodazole is a typical inhibitor of microtubule polymerization that can effectively restrict ... noco: 74.9 ± 7.0%, n = 8 fish, Students two-tailed t-test, p = 0.607; Figure 2C). Mitochondrial speed in the nocodazole group ...
Nocodazole is a microtubule depolymerizing agent. There is one binding site for nocodazole per tubulin monomer, and nocodazole ... Steroids counteract nocodazole effects. (a) Inhibition of microtubule polymerization by nocodazole and partial protection by ... 30 μM nocodazole was added for 15 min. In control cultures, nocodazole induced a prominent retraction of neurites from an ... was achieved with 10 μM nocodazole (14). Then, microtubule assembly was monitored in the presence of both nocodazole and either ...
While in ITGB2 a position to catch the Nocodazole novel inhibtior fundamental Nocodazole novel inhibtior behavior of the ... of mass actions based versions that accurately explain the root biochemistry is normally restricted to little Nocodazole novel ...
40)Nocodazole suppresses construction the forskolin induced neurite-like structure. - Duration: 29 seconds.. *67 views ...
CLIP-170 staining after nocodazole treatment. CLIP-170 appears in green and chromosomes in red. 10-15 optical sections were ... Oocytes were cultured in the presence of 10 μg/ml nocodazole from 3 to 5 h after GVBD and fixed 2 h after removal of the drug ( ... Oocytes were cultured in the presence of 10 μg/ml nocodazole from 3 to 5 h after GVBD and fixed 2 h after removal of the drug ( ... Mentions: This result was reinforced by live observation of chromosome movements after nocodazole treatment. In the NZ/3h-5h ...
View our 40 Mitosis-Related Compounds products for your research including Mitosis-Related Compounds Small Molecules and Mitosis-Related Compounds Peptides.
... washed twice with 0.3 μM nocodazole ( Aldrich Chemical Co., Milwaukee, WI) in PBS, exposed to 0.3 μM nocodazole in M-199 medium ... Nocodazole.. The prevalence of posttranslationally modified α-tubulin in cardiocyte microtubules was used as the primary ... Resistance to nocodazole- induced microtubule depolymerization was used as one of two additional measures of microtubule ... Of interest, after 90 min of nocodazole exposure the majority of the residual microtubules of RV but not LV cardiocytes was ...
Nocodazole. Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl, Abl( ... Nocodazole. Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl, Abl( ... A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). Total cell lysates ... A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). Total cell lysates ...
Nocodazole washout assay. Cells were incubated in a low concentration of nocodazole (30 ng/ml) in growth medium for 2-3 h to ... To remove nocodazole, cells were washed three times with fresh L15 medium. The time of the first wash was recorded as time zero ... After removal of nocodazole, we imaged the cells during recovery as tension was established (Fig. S5). In control cells, sensor ... We found that GFP-PP1α and GFP-PP1γ levels at kinetochores are low in early prometaphase or in nocodazole-treated cells, but ...
A) Wild-type embryo grown without nocodazole, (B) grown in 10 μg/ml nocodazole for 1 hour, starting at late gastrulation or (C ... to nocodazole (5 or 10 μg/ml) starting at midgastrulation or at YPC, continuing 1 or 2 hours. We found that 5 μg/ml nocodazole ... 5D) nocodazole-treated (n=7) compared with control (n=7) embryos. These results support the notion that intact MTs are required ... Pk and nocodazole experiments. Embryos were injected with RNAs coding for RFP-CAAX (Jason Jessen, Vanderbilt University Medical ...
Noc, nocodazole; "washout" indicates removal of nocodazole. (B, C) Unsynchronized T. annulata-transformed cells undergoing ... A) T. annulata-transformed cells were synchronized in prometaphase by treatment with nocodazole. Upon nocodazole washout, ... of nocodazole. Control cells were released from nocodazole block in the presence of DMSO (control). Data represent the mean of ... A) T. annulata-transformed cells were arrested in prometaphase by treatment with nocodazole (Noc; top panels). Upon removal of ...
Nocodazole Treatment Increases the Ca2+ Influx Following GPN Treatment. Mitochondrial movement on cytoskeletal elements to Ca2+ ... nocodazole treatment of T lymphocytes from control rats resulted in a substantial decrease in TG-induced Ca2+ influx through ... Nocodazole was obtained from Calbiochem. R73 (anti-rat TCR), H57 (anti-mouse TCR), and IP36 (anti-human TCR) monoclonal ... These observations complement our previous report that addition of nocodazole prevented mitochondrial Ca2+ uptake in T ...
Within the nocodazole experiment, the doses were injected at varying time intervals before and after mating. On day seventeen ... The Teratogenic Effects of Nocodazole and Acrylamide in Mus Musculus Description: In two separate experiments, weight adjusted ... Nocodazole induced a significant increase in reproductive pathology per total implants when administered one hour after mating ... doses of nocodazole and acrylamide were injected intraperitoneally at various time intervals into twelve week old female mice. ...
  • It is shown here that nocodazole at concentrations as low as 100 nM caused the GA to disperse in treated fibro-blasts that still contained a fairly high amount of Mts. (biologists.org)
  • Antibody-blocking analysis of Mts after injection of biotin-tubulin into the HSFs was used to show that nocodazole at low concentrations induced the stabilization of the remaining Mts. (biologists.org)
  • In this paper, we directly measured the dynamics of MTs in migrating NRK cells injected with rhodamine tubulin and treated with low concentrations of nocodazole or taxol. (nih.gov)
  • Finally, immunohistochemistry with an anti-tubulin antibody showed that the concentrations of nocodazole used in the above experiments reversibly disrupted microtubules within renal epithelial cells. (mysciencework.com)
  • In this work, nocodazole, a microtubule destabilizer, was used to treat HeLa cells with different concentrations. (sciencepublishinggroup.com)
  • Nanomolar concentrations of nocodazole alter microtubule dynamic instability in vivo and in vitro. (sciencepublishinggroup.com)
  • Nocodazole in micromolar concentrations not only irreversibly changed the barrier function, but also upset the viability of endothelial cells and induced their death. (elsevier.com)
  • At high concentrations, Nocodazole rapidly depolymerizes microtubules in cells, while low concentrations of Nocodazole inhibit microtubule dynamic instability. (invivochem.com)
  • Mitotic cells incubated with different concentrations of Paclitaxel are inhibited from progressing to G1 phase 6 hours after release from the Nocodazole block, with a median inhibitory concentration of 4 nM. (invivochem.com)
  • Further experiments revealed that the type B cells exhibited a biphasic dose-response curve, with mitotic arrest at low drug concentrations (100 nM nocodazole or 6 nM vincristine) that failed to depolymerize microtubules and a p53-independent p21 waf1/cip1 -associated G 1 and G 2 arrest at higher concentrations (1 μM nocodazole or 100 nM vincristine) that depolymerized microtubules. (pubmedcentralcanada.ca)
  • 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 μM for 3 hours) induces numerous Golgi elements to form adjacent to ER exit sites. (wikipedia.org)
  • Nocodazole, a microtubule-disrupting agent, induces a major retraction of neurites in control cultures, but pretreatment with PREG/MePREG is protective. (pnas.org)
  • Nocodazole induces apoptosis . (selleckchem.com)
  • Nocodazole induces apoptosis in chronic lymphocytic leukemia cells. (invivochem.com)
  • Prolonged arrest of cells in mitosis due to nocodazole treatment typically results in cell death by apoptosis. (wikipedia.org)
  • Nocodazole decreases apoptosis in some human colon carcinoma cells. (invivochem.com)
  • Nocodazole-induced p53-dependent c-Jun N-terminal kinase activation reduces apoptosis in human colon carcinoma HCT116 cells. (wikipathways.org)
  • 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 polymerise. (wikipedia.org)
  • A brief nocodazole treatment resulted in cells arrested early in mitosis or at the end of G 2 , presumably by the activation of a mitotic spindle checkpoint ( 22 ). (asm.org)
  • Nocodazole is a potent Tubulin production inhibitor, anti-neoplastic agent, and inhibitor of mitosis. (scbt.com)
  • After treatment with 1 μM nocodazole, seven of ten breast cancer lines (type A cells) arrested in mitosis, whereas the other three (type B cells) did not. (pubmedcentralcanada.ca)
  • These actions are useful in cell synchronization studies, where brief exposures to nocodazole are routinely used to reversibly arrest cells in mitosis ( 4 , 5 ). (pubmedcentralcanada.ca)
  • We additionally investigated whether cells were able to enter M phase after γ irradiation by treatment with nocodazole, a microtubule-disrupting agent that traps cells in mitosis ( 8 , 9 ). (sciencemag.org)
  • In the absence of γ irradiation, about 35% of cells of both genotypes were trapped in mitosis after 12 hours of nocodazole treatment ( Fig. 1 D). When cells were subjected to γ irradiation with nocodazole treatment, cells of both genotypes arrested in G 2 for 12 hours ( Fig. 1 D). However, after 18 hours, significantly more Chk2 −/− cells entered mitosis. (sciencemag.org)
  • Nocodazole is an antineoplastic microtubule polymerization inhibitor. (peprotech.com)
  • Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule polymerization, also inhibits Abl , Abl(E255K) and Abl(T315I) with IC50 of 0.21 μM, 0.53 μM and 0.64 μM in cell-free assays, respectively. (selleckchem.com)
  • G 2 arrest using nocodazole was combined with G 1 arrest using aphidicolin, a drug that presumably acts through the inhibition of polymerase-dependent DNA synthesis ( 8 , 12 , 14 , 25 ). (asm.org)
  • Micro-injection of the well-characterized HD antibody against kinesin but not the preimmune IgG caused inhibition of GA dispersal in HSFs by nocodazole. (biologists.org)
  • Nocodazole inhibition of organic anion secretion in teleost re. (mysciencework.com)
  • Nocodazole inhibition of organic anion secretion in teleost renal proximal tubules. (mysciencework.com)
  • Nocodazole-Induced Expression and Phosphorylation of Anillin and Other Mitotic Proteins Are Decreased in DNA-Dependent Protein Kinase Catalytic Subunit-Deficient Cells and Rescued by Inhibition of the Anaphase-Promoting Complex/Cyclosome with proTAME but Not Apcin. (kettenbachlab.org)
  • Furthermore, stabilization and inhibition of MTs by low doses of taxol and nocodazole enhance and impair spine formation elicited by BDNF (brain-derived neurotrophic factor), respectively. (jneurosci.org)
  • Applications of 5-hydroxyindole and nocodazole, a microtubule disruptor, significantly slowed 5-HT 3A receptor desensitization and reduced the magnitude of AEA inhibition. (aspetjournals.org)
  • Effects of vinblastine, podophyllotoxin and nocodazole on mitotic spindles. (biologists.org)
  • Collectively, these observations provide evidence for coupling of premitotic cell-cycle progression to microtubule integrity in some breast cancer cell lines (representing a possible "microtubule integrity checkpoint") and suggest a potential explanation for the recently reported failure of some cancer cell lines to undergo nocodazole-induced mitotic arrest despite intact mitotic checkpoint proteins. (pubmedcentralcanada.ca)
  • Nocodazole stimulates the expression of LATS2 which potently inhibits the Wnt signaling pathway by abrogating the interaction between the Wnt-dependent transcriptional co-factors beta-catenin and BCL9. (wikipedia.org)
  • Nocodazole inhibits insulin-stimulated glucose transport. (invivochem.com)
  • Cells were also released into media containing 15 μg/ml of nocodazole to activate the SAC ( Figure 1, B and D ). Pds1 was stabilized by SAC activation (compare Figure 1, A and B ), since nocodazole treatment inhibits both APC Cdc20 and APC Cdh1 . (genetics.org)
  • The results showed that nocodazole was able to inhibit HeLa cell's growth rate significantly at the concentration of 100 nM. (sciencepublishinggroup.com)
  • It suggested that nocodazole may inhibit cell growth through an alternative impacting effect other than destabilizing microtubules, since the effect of nocodazole destabilizing microtubule is usually not seen at micromolar range. (sciencepublishinggroup.com)
  • 200 nM) of nocodazole or taxol reduced the rate of locomotion of NRK fibroblasts over 60% without altering MT polymer level [Liao et al. (nih.gov)
  • The percent time MTs were inactive (i.e., paused) increased greater than twofold in nocodazole- and taxol-treated cells, while the percent time growing was substantially reduced. (nih.gov)
  • A, HeLa cells were treated with DMSO, Taxol (100 nM for 16 h), or Nocodazole (Noco, 100 ng/ml for 16 h). (selleckchem.com)
  • Recombinant human brain-derived neurotrophic factor (BDNF) was purchased from Peprotech, and taxol and nocodazole were from Sigma. (jneurosci.org)
  • Nocodazole binds to beta-tubulin and disrupts microtubule assembly/disassembly dynamics, impairing formation of the metaphase spindles during the cell division cycle. (stemcell.com)
  • Nocodazole disrupts microtubules by binding to β-tubulin. (invivochem.com)
  • Nocodazole-pretreated cells exposed to Paclitaxel in the absence of Nocodazole only form free-floating microtubules, whereas pretreated cells exposed to Paclitaxel in the presence of Nocodazole-assembled centrosome organize microtubules. (invivochem.com)
  • It was found that nocodazole could have better anticancer effect than paclitaxel. (spandidos-publications.com)
  • Using the polymeric immunoglobulin receptor expressed in polarized MDCK cells, we have examined the effects of nocodazole, a microtubule-disrupting agent, on three pathways that deliver proteins to the apical surface and two pathways that deliver proteins to the basolateral surface. (escholarship.org)
  • Reduced localization of UNC-43, TIR-1 and NSY-1 proteins in the AWC axons strongly correlates with the 2AWC ON phenotype in nocodazole-treated animals. (biologists.org)
  • Whereas, at concentration of 1 mM, nocodazole induced significant alterations of F-actin structure in HeLa cells. (sciencepublishinggroup.com)
  • The impact of the microtubule-disrupting drug nocodazole on renal tubular secretion of organic anions was examined in vitro using proximal tubular masses from teleost fish. (mysciencework.com)
  • In vitro activity: Nocodazole is a high-affinity ligand for the cancer-related kinases including Abl phosphorylated, c-Kit, BRAF, and MEK with Kd of 0.091 μM, 1.6 μM, 1.8 μM and 1.6 μM, respectively. (invivochem.com)
  • Several drugs including vincristine and colcemid are similar to nocodazole in that they interfere with microtubule polymerization. (wikipedia.org)
  • Nocodazole, vincristine, and colchicine are structurally diverse agents that disrupt microtubule function by binding to various sites on β-tubulin and suppressing microtubule dynamics or inducing microtubule depolymerization ( 1 - 3 ). (pubmedcentralcanada.ca)
  • Effect of nocodazole on vesicular traffic to the apical and basolateral surfaces of polarized MDCK cells. (escholarship.org)
  • Here we report that both apical and basolateral transport is inhibited by nocodazole treatment. (nih.gov)
  • Another standard cell biological application of nocodazole is to induce the formation of Golgi ministacks in eukaryotic cells. (wikipedia.org)
  • However, at nanomolar concentration, nocodazole was not able to induce any changes in F-actin structure. (sciencepublishinggroup.com)
  • This hypothesis was validated in this study, in which nocodazole was used to induce vascular endothelium dysfunction in lung endothelial cells. (elsevier.com)
  • Nocodazole in a dose of 100 ng/ml was used to induce polyploidization in a breast cancer cell line MDA-MB-231 cells. (bvsalud.org)
  • The complete disruption of Mts by the incubation of HSFs at 0 degrees C prevented the dispersal of GA from the perinuclear area when the cells were subsequently warmed to 37 degrees C in the presence of nocodazole. (biologists.org)
  • In contrast, the biosynthetic and recycling pathways to the basolateral surface are less affected by nocodazole and therefore appear to be more resistant to microtubule disruption. (escholarship.org)
  • At 100 nM, nocodazole induced partial disruption of the microtubule network near the cell margin without any appreciable effect on acetylated microtubules and actin filaments. (elsevier.com)
  • Similar to unc-43, tir-1 and nsy-1 loss-of-function mutants, specific disruption of microtubules in AWC by nocodazole generates two AWC ON neurons. (biologists.org)
  • To define the role of MEKK1 in activation of the JNK pathway by different extracellular inputs, we exposed MEKK1 −/− and MEKK1 +/+ cells to several different stress stimuli, including microtubule disruption by nocodazole, cold shock, hyperosmolarity, ultraviolet (UV) irradiation, anisomycin, and heat shock ( Fig. 2 , A to D) ( 14 ). (sciencemag.org)
  • The biosynthetic and transcytotic pathways to the apical surface are dramatically altered by nocodazole in that a portion of the protein traffic on each of these two pathways is misdirected to the basolateral surface. (escholarship.org)
  • The GA in different cell types undergoes fragmentation and dispersal throughout the cytoplasm upon treatment with nocodazole. (biologists.org)
  • Since nocodazole has been used as a chemotherapy reagent in cancer treatment, it will be beneficial to re-evaluate the effective concentration in terms of cancer treatment. (sciencepublishinggroup.com)
  • CLIP-170 staining after nocodazole treatment. (nih.gov)
  • This result was reinforced by live observation of chromosome movements after nocodazole treatment. (nih.gov)
  • B) Cells arrested in prometaphase by treatment with nocodazole (left panels) or monastrol (right panels) and analyzed by IFM using antibodies to Plk1, TaSP1 and α-tubulin. (nih.gov)
  • Over-expression of RNP-1 protected microtubules from nocodazole treatment. (missouristate.edu)
  • Nocodazole is an antineoplastic agent which exerts its effect in cells by interfering with the polymerization of microtubules. (wikipedia.org)
  • Nocodazole has been shown to decrease the oncogenic potential of cancer cells via another microtubules-independent mechanisms. (wikipedia.org)
  • Cells treated with nocodazole arrest with a G2- or M-phase DNA content when analyzed by flow cytometry. (wikipedia.org)
  • Nocodazole impairs the morphology and directionality of migrating medial gan-glionic eminence cells. (invivochem.com)
  • Methods: The growth rates and the microtubule networks of Dictyostelium cells were assessed with or without nocodazole (10 μmol/L) in suspension culture. (missouristate.edu)
  • Our results indicate that polyploid tumor cells induced by spindle poison Nocodazole are more resistant to most of chemotherapeutic drugs. (bvsalud.org)
  • Cells were treated with etoposide (5 μmol/L), actinomycin D (5 nmol/L), nocodazole (50 ng/mL), and 5-aza-cytidine (5 μmol/L) for the indicated duration. (aacrjournals.org)
  • 2012) Global detection of protein kinase D-dependent phosphorylation events in nocodazole-treated human cells. (phosphosite.org)
  • Cells lacking Cdc20 and treated with nocodazole stabilized both Clb5 and Pds1 ( Figure 1D ). (genetics.org)
  • Cells were then released into media with Raff/Gal (A), Raff/Gal with nocodazole (B), glucose (C), or glucose with nocodazole (D). α-Factor was added back to the media after cells had budded to restrict the analysis to a single cell cycle. (genetics.org)
  • Where indicated, cells were synchronized in G 0 /G 1 phase by incubation in Dulbecco's modified Eagle's medium supplemented with 0.5% fetal calf serum for 24 h, in S phase with 2 mM hydroxyurea (Sigma), and in M phase with 0.2 μg/ml nocodazole (Sigma). (asm.org)
  • Upon removal of nocodazole, MT polymerization was monitored by immunofluorescence microscopy (IFM) for up to 120 min. (nih.gov)
  • These functional Golgi ministacks remain distributed about the cell, unable to track forward to form a perinuclear Golgi since nocodazole has depolymerized the microtubules. (wikipedia.org)
  • These data demonstrate that the dispersal of GA in the cytoplasm of nocodazole-treated HSFs is a kinesin-driven process with stable Mts serving as tracks. (biologists.org)
  • As nocodazole affects the cytoskeleton, it is often used 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. (wikipedia.org)
  • Nocodazole reversibly inhibited 20-30% of the tubular accumulation of two model organic anions, p-aminohippurate and fluorescein (FL), by winter flounder tubular masses. (mysciencework.com)
  • In addition, the Kd of Nocodazole for Abl(E255K) phosphorylated, Abl(T315I) phosphorylated, BRAF(V600E) and PI3Kγ is 0.12 μM, 0.17 μM, 1.1 μM and 1.5 μM, respectively. (invivochem.com)
  • The effect of nocodazole on endothelial cell cytoskeleton was found to be dose-dependent. (elsevier.com)
  • Instead, epifluorescence video microscopy and digital image analysis of killifish tubules showed that nocodazole greatly reduced luminal accumulation of FL and had a smaller effect on cellular dye accumulation. (mysciencework.com)
  • For cell synchronization experiments, nocodazole is usually used at a concentration of 40-100 ng/mL of culture medium for a duration of 12-18 hours. (wikipedia.org)
  • In this study experiments were performed on human skin fibroblasts (HSFs) and rat fibroblasts (REF 52) to determine whether the dispersal of GA in HSFs treated with nocodazole is dependent on Mts that show the higher resistance to this Mt-depolymerizing drug. (biologists.org)
  • This work demonstrates successful cell cycle arrest by using nocodazole, a microtubule-destabilizing drug that leads to the depolymerization of spindle microtubules in Giardia ( 6 , 20 ). (asm.org)
  • 40)Nocodazole suppresses construction the forskolin induced neurite-like structure. (youtube.com)
  • Journal Article] αB-crystallin-coated MAP microtubule resists nocodazole and calcium-induced disassembly. (nii.ac.jp)
  • Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the yeast Saccharomyces cerevisiae. (asm.org)
  • In support of the latter hypothesis, when all MTs were rapidly depolymerized by 20 microM nocodazole, we detected the rapid formation of exaggerated protrusions from the leading edge of the cell. (nih.gov)
  • An RNA-binding protein, RNP-1, protects microtubules from nocodazole a" by Thu Ngo, Xin Miao et al. (missouristate.edu)
  • In this study, we analyzed the functions of the protein RNP-1, which was previously discovered in a genetic selection screen for nocodazole suppression. (missouristate.edu)
  • The mRNA and protein levels of cyclin D1, CDK4, CDK6, (p)Rb and P16 consistently demonstrated a reverse trend with the levels in the chondrocytes treated with nocodazole. (ingentaconnect.com)
  • METH-induced cell death is significantly decreased by Nocodazole pretreatment in comparison to METH alone. (invivochem.com)
  • Results: Over-expression of RNP-1 rescued the growth defects caused by the microtubule-destabilizing agent nocodazole. (missouristate.edu)
  • At 200 nM, nocodazole exerted a pronounced effect on the system of dynamic (but not acetylated) microtubules and increased the population of actin filaments in the central region of the cell. (elsevier.com)
  • Nocodazole suppress METH-induced cell death and lysosomal dysfunction. (invivochem.com)
  • The apical recycling pathway is slowed in the presence of nocodazole but targeting is not disrupted. (escholarship.org)
  • Oocytes were cultured in the presence of 10 μg/ml nocodazole from 3 to 5 h after GVBD and fixed 2 h after removal of the drug (A). Oocytes were cultured in the presence of 10 μg/ml nocodazole from 6 to 8 h after GVBD and fixed 15 (B) and 30 min (C) after removal of the drug. (nih.gov)
  • Nocodazole prevents the formation of one of the two interchain disulfide linkages. (invivochem.com)
  • Nocodazole is frequently used in cell biology laboratories to synchronize the cell division cycle. (wikipedia.org)