Relevant bibliographies by topics / G2/M block

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Academic literature on the topic 'G2/M block'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "G2/M block"

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Bork, Ulrich, Wing-Kee Lee, Anna Kuchler, Thomas Dittmar, and Frank Thévenod. "Cadmium-induced DNA damage triggers G2/M arrest via chk1/2 and cdc2 in p53-deficient kidney proximal tubule cells." American Journal of Physiology-Renal Physiology 298, no. 2 (February 2010): F255—F265. http://dx.doi.org/10.1152/ajprenal.00273.2009.

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Carcinogenesis is a multistep process that is frequently associated with p53 inactivation. The class 1 carcinogen cadmium (Cd2+) causes renal cancer and is known to inactivate p53. G2/mitosis (M) arrest contributes to stabilization of p53-deficient mutated cells, but its role and regulation in Cd2+-exposed p53-deficient renal cells are unknown. In p53-inactivated kidney proximal tubule (PT) cells, comet assay experiments showed that Cd2+ (50–100 μM) induced DNA damage within 1–6 h. This was associated with peak formation of reactive oxygen species (ROS) at 1–3 h, measured with dihydrorhodamine 123, and G2/M cell cycle arrest at 6 h, which were abolished by the antioxidant α-tocopherol (100 μM). Cd2+-induced G2/M arrest was enhanced approximately twofold on release from cell synchronization (double thymidine block or nocodazole) and resulted in approximately twofold increase of apoptosis, indicating that G2/M arrest mirrors DNA damage and toxicity. The Chk1/2 kinase inhibitor UCN-01 (0.3 μM), which relieves G2/M transition block, abolished Cd2+-induced G2 arrest and increased apoptosis. This was accompanied by prevention of Cd2+-induced cyclin-dependent kinase cdc2 phosphorylation at tyrosine 15, as shown by immunofluorescence microscopy and immunoblotting. The data indicate that in p53-inactivated PT cells Cd2+-induced ROS formation and DNA damage trigger signaling of checkpoint activating kinases ataxia telangiectasia-mutated kinase (ATM) and ataxia telangiectasia and Rad3-related kinase (ATR) to cause G2/M arrest. This may promote survival of premalignant PT cells and Cd2+ carcinogenesis.
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Paris, J., P. Leplatois, and P. Nurse. "Study of the higher eukaryotic gene function CDK2 using fission yeast." Journal of Cell Science 107, no. 3 (March 1, 1994): 615–23. http://dx.doi.org/10.1242/jcs.107.3.615.

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In the fission yeast Schizosaccharomyces pombe, cdc2 function is required both in G1 to enter the cell cycle and in G2 to initiate mitosis. In higher eukaryotes, these functions appeared to be shared between several cdc2-like genes including CDK2. Temperature-sensitive mutations in S. pombe cdc2 that arrest the cell cycle in both G1 and G2 phases are not complemented by CDK2. We have used S. pombe to investigate what functions CDK2 can perform. We found that overexpression of the human homologue (HsCDK2) caused cell cycle arrest in G2/M showing that HsCDK2 interfered with mitotic events. Xenopus CDK2 (XlCDK2) overexpression did not cause cell cycle arrest and could rescue the G1 block but not the G2 block of a cdc2-M26 ts strain. A mutant XlCDK2-R33, which is inactive as a kinase, failed to rescue the G1 block, suggesting that the protein kinase activity of CDK2 is required to enter the cell cycle in these circumstances. We designed screens to select mutants that would require XlCDK2 expression for viability, hoping to isolate new gene functions interacting with, or that could be replaced by, XlCDK2 in G1, or new cdc2 mutants altered solely in their G1 role. From these screens several cell cycle mutants were selected that were XlCDK2-dependent. These were all cdc2 mutants altered only in their G2/M function. Therefore XlCDK2 can influence both the G1/S and G2/M transition points of cdc2 in S. pombe.
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Choudhuri, Tathagata, Subhash C. Verma, Ke Lan, Masanao Murakami, and Erle S. Robertson. "The ATM/ATR Signaling Effector Chk2 Is Targeted by Epstein-Barr Virus Nuclear Antigen 3C To Release the G2/M Cell Cycle Block." Journal of Virology 81, no. 12 (April 4, 2007): 6718–30. http://dx.doi.org/10.1128/jvi.00053-07.

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ABSTRACT Epstein-Barr virus (EBV) infects most of the human population and persists in B lymphocytes for the lifetime of the host. The establishment of latent infection by EBV requires the expression of a unique repertoire of genes. The product of one of these viral genes, the EBV nuclear antigen 3C (EBNA3C), is essential for the growth transformation of primary B lymphocytes in vitro and can regulate the transcription of a number of viral and cellular genes important for the immortalization process. This study demonstrates an associated function of EBNA3C which involves the disruption of the G2/M cell cycle checkpoint. We show that EBNA3C-expressing lymphoblastoid cell lines treated with the drug nocodazole, which is known to block cells at the G2/M transition, did not show a G2/M-specific checkpoint arrest. Analyses of the cell cycles of cells expressing EBNA3C demonstrated that the expression of this essential EBV nuclear antigen is capable of releasing the G2/M checkpoint arrest induced by nocodazole. This G2/M arrest in response to nocodazole was also abolished by caffeine, suggesting an involvement of the ATM/ATR signaling pathway in the regulation of this cell cycle checkpoint. Importantly, we show that the direct interaction of EBNA3C with Chk2, the ATM/ATR signaling effector, is responsible for the release of this nocodazole-induced G2/M arrest and that this interaction leads to the serine 216 phosphorylation of Cdc25c, which is sequestered in the cytoplasm by 14-3-3. Overall, our data suggest that EBNA3C can directly regulate the G2/M component of the host cell cycle machinery, allowing for the release of the checkpoint block.
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Liu, Chang, Jing Nie, Rensheng Wang, and Weidong Mao. "The Cell Cycle G2/M Block Is an Indicator of Cellular Radiosensitivity." Dose-Response 17, no. 4 (October 1, 2019): 155932581989100. http://dx.doi.org/10.1177/1559325819891008.

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Background: Determination of the radiosensitivity of a specific tumor is essential to its precision tumor radiotherapy, but the measurement of cellular radiosensitivity with a routine colony forming assay is both labor- and time-consuming. An alternative option allowing rapid and precise prediction of radiosensitivity is necessary. Methods: In this study, we exposed 4 in vitro cultured cell lines to various doses of X-rays or carbon ions and then measured their radiosensitivities with a routine colony-forming assay, and monitored the kinetics of cell cycle distribution with routine propidium iodine staining and flow cytometry. Results: Based on the results, we correlated cellular radiosensitivity with a dynamic assay of cell cycle distribution, specifically, the negative correlation of cellular radiosensitivity with the accumulated G2/M arrested cells at 48 hours after exposure. The higher the proportion of accumulated G2/M arrested cells at 48 hours after exposure, the lower the radiosensitivity of the cell line, that is, the higher radioresistance of the cell line. Conclusion: These findings provide an optional application of regular cell cycle analysis for the prediction of tumor radiosensitivity.
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Kiang, Lee, Christian Heichinger, Stephen Watt, Jürg Bähler, and Paul Nurse. "Cyclin-Dependent Kinase Inhibits Reinitiation of a Normal S-Phase Program during G2 in Fission Yeast." Molecular and Cellular Biology 29, no. 15 (June 1, 2009): 4025–32. http://dx.doi.org/10.1128/mcb.00185-09.

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ABSTRACT To achieve faithful replication of the genome once in each cell cycle, reinitiation of S phase is prevented in G2 and origins are restricted from refiring within S phase. We have investigated the block to rereplication during G2 in fission yeast. The DNA synthesis that occurs when G2/M cyclin-dependent kinase (CDK) activity is depleted has been assumed to be repeated rounds of S phase without mitosis, but this has not been demonstrated to be the case. We show here that on G2/M CDK depletion in G2, repeated S phases are induced, which are correlated with normal G1/S transcription and attainment of doublings in cell size. Mostly normal mitotic S-phase origins are utilized, although at different efficiencies, and replication is essentially equal across the genome. We conclude that CDK inhibits reinitiation of S phase during G2, and if G2/M CDK is depleted, replication results from induction of a largely normal S-phase program with only small differences in origin usage and efficiency.
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Bolton, Diane L., and Michael J. Lenardo. "Vpr Cytopathicity Independent of G2/M Cell Cycle Arrest in Human Immunodeficiency Virus Type 1-Infected CD4+ T Cells." Journal of Virology 81, no. 17 (June 6, 2007): 8878–90. http://dx.doi.org/10.1128/jvi.00122-07.

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ABSTRACT The mechanism of CD4+ T-cell depletion in human immunodeficiency virus type 1 (HIV-1)-infected individuals remains unknown, although mounting evidence suggests that direct viral cytopathicity contributes to this loss. The HIV-1 Vpr accessory protein causes cell death and arrests cells in the G2/M phase; however, the molecular mechanism underlying these properties is not clear. Mutation of hydrophobic residues on the surface of its third alpha-helix disrupted Vpr toxicity, G2/M arrest induction, nuclear localization, and self-association, implicating this region in multiple Vpr functions. Cytopathicity by virion-delivered mutant Vpr protein correlated with G2/M arrest induction but not nuclear localization or self-association. However, infection with whole virus encoding these Vpr mutants did not abrogate HIV-1-induced cell killing. Rather, mutant Vpr proteins that are impaired for G2/M block still prevented infected cell proliferation, and this property correlated with the death of infected cells. Chemical agents that inhibit infected cells from entering G2/M also did not reduce HIV-1 cytopathicity. Combined, these data implicate Vpr in HIV-1 killing through a mechanism involving inhibiting cell division but not necessarily in G2/M. Thus, the hydrophobic region of the third alpha-helix of Vpr is crucial for mediating G2/M arrest, nuclear localization, and self-association but dispensable for HIV-1 cytopathicity due to residual cell proliferation blockade mediated by a separate region of the protein.
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Bielaszewska, Martina, Bhanu Sinha, Thorsten Kuczius, and Helge Karch. "Cytolethal Distending Toxin from Shiga Toxin-Producing Escherichia coli O157 Causes Irreversible G2/M Arrest, Inhibition of Proliferation, and Death of Human Endothelial Cells." Infection and Immunity 73, no. 1 (January 2005): 552–62. http://dx.doi.org/10.1128/iai.73.1.552-562.2005.

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ABSTRACT Recently, cytolethal distending toxin V (CDT-V), a new member of the CDT family, was identified in Shiga toxin-producing Escherichia coli (STEC) O157 and particular non-O157 serotypes. Here we investigated the biological effects of CDT-V from STEC O157:H− (strain 493/89) on human endothelial cells, which are believed to be major pathogenetic targets in severe STEC-mediated diseases. CDT-V caused dose-dependent G2/M cell cycle arrest leading to distension, inhibition of proliferation, and death in primary human umbilical vein endothelial cells (HUVEC) and two endothelial cell lines, EA.hy 926 cells (HUVEC derived) and human brain microvascular endothelial cells (HBMEC). The cell cycle effects of CDT-V were cell type specific. In HUVEC and EA.hy 926 cells, CDT-V caused a slowly developing but persistent G2/M block which resulted in delayed nonapoptotic cell death. In contrast, in HBMEC, CDT-V induced a rapidly evolving but transient G2/M block which was followed by progressive, mostly apoptotic cell death. In both HBMEC and EA.hy 926 cells, G2/M arrest was preceded by the early accumulation of a phosphorylated inactive form of cdc2 kinase. Significant G2/M arrest and inhibition of proliferation in both HUVEC and each of the endothelial cell lines were induced by 2 to 15 min of exposure to CDT-V, indicating that the effects of the toxin are irreversible. CDT-V-treated HBMEC and EA.hy 926 cells displayed fragmented nuclei and expressed phosphorylated histone protein H2AX, indicative of DNA damage followed by a DNA repair response. Our data demonstrate that CDT-V causes irreversible damage to human endothelial cells and thus may contribute to the pathogenesis of STEC-mediated diseases.
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Trielli, M. O., P. R. Andreassen, F. B. Lacroix, and R. L. Margolis. "Differential Taxol-dependent arrest of transformed and nontransformed cells in the G1 phase of the cell cycle, and specific-related mortality of transformed cells." Journal of Cell Biology 135, no. 3 (November 1, 1996): 689–700. http://dx.doi.org/10.1083/jcb.135.3.689.

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Taxol (paclitaxel) induces a microtubule hyperassembled state, and effectively blocks cells in mitosis. Here we report that Taxol also induces a stable late-G1 block in nontransformed REF-52 and WI-38 mammalian fibroblast cells, but not in T antigen-transformed cells of the same parental lineage. G1 arrest is characterized by partially dephosphorylated pRb, and inactive cdk2 kinase. Nontransformed cells recover normally from Taxol arrest. In contrast, T antigen transformed cells continue inappropriately past both G1 and G2-M in the presence of Taxol, and undergo a rapid death upon release. These results demonstrate a microtubule sensitive step in G1 regulation of nontransformed fibroblast cells. Also, Taxol selectively induces death of transformed cells, possibly because they slip the Taxol-dependent G1 arrest, as well as G2/M arrest, which are both specific to nontransformed cells.
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Whitehouse, Chris A., Paul B. Balbo, Everett C. Pesci, Daniel L. Cottle, Peter M. Mirabito, and Carol L. Pickett. "Campylobacter jejuni Cytolethal Distending Toxin Causes a G2-Phase Cell Cycle Block." Infection and Immunity 66, no. 5 (May 1, 1998): 1934–40. http://dx.doi.org/10.1128/iai.66.5.1934-1940.1998.

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ABSTRACT Cytolethal distending toxin (CDT) from the diarrheagenic bacteriumCampylobacter jejuni was shown to cause a rapid and specific cell cycle arrest in HeLa and Caco-2 cells. Within 24 h of treatment, CDT caused HeLa cells to arrest with a 4N DNA content, indicative of cells in G2 or early M phase. Immunofluorescence studies indicated that the arrested cells had not entered M phase, since no evidence of tubulin reorganization or chromatin condensation was visible. CDT treatment was also shown to cause HeLa cells to accumulate the inactive, tyrosine-phosphorylated form of CDC2. These results indicated that CDT treatment results in a failure to activate CDC2, which leads to cell cycle arrest in G2. This mechanism of action is novel for a bacterial toxin and provides a model for the generation of diarrheal disease byC. jejuni and other diarrheagenic bacteria that produce CDT.
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Muratori, M., I. Nicoletti, G. B. Vannelli, M. Luconi, E. Macorsini, M. Serio, G. Forti, and M. Maggi. "Genistein induces a G2/M block and apoptosis in human uterine adenocarcinoma cell lines." Endocrine Related Cancer 4, no. 2 (June 1, 1997): 203–18. http://dx.doi.org/10.1677/erc.0.0040203.

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Dissertations / Theses on the topic "G2/M block"

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Sigglekow, Nicholas David Garvan Institute of Medical Research Faculty of Medicine UNSW. "Mutated in colorectal cancer (MCC): a putative tumour suppressor gene in colorectal cancer." Publisher:University of New South Wales. Garvan Institute of Medical Research, 2009. http://handle.unsw.edu.au/1959.4/43617.

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Colorectal cancer (CRC) remains a significant burden in contemporary society due to an aging population, unhealthy dietary choices and an increasingly sedentary lifestyle. While the underlying defects for many hereditary forms of CRC have been determined, many genetic and epigenetic changes promoting common sporadic CRCs have yet to be identified. The Mutated in Colorectal Cancer (MCC) gene, identified in 1991, was initially thought to be responsible for the hereditary form of CRC, familial adenomatous polyposis, before the discovery of the susceptibility gene Adenomatous Polyposis Coli (APC), which then became the focus of intense research. Recent data, however, suggests that MCC may also be important in the development of CRC. I have investigated the mechanism of MCC gene silencing, the putative structure, and multiple functions of MCC. MCC was frequently silenced by promoter hypermethylation in CRC cell lines and primary tumours. MCC methylation showed strong molecular and clinicopathological associations with hallmarks of the serrated neoplasia pathway. Furthermore, MCC methylation was more frequent in serrated precursor lesions compared with adenomas, thus occurring early during carcinogenesis. MCC is highly conserved in complex multicellular organisms. Re-introduction of MCC in CRC cell lines resulted in partial G1 to S phase, and G2/M phase cell cycle blocks, potentially by upregulating cell cycle inhibitor gene transcription and interfering with the process of mitotic checkpoints and division, respectively. Changes in MCC levels also modulated NF?B pathway signalling, the pathway required for maintaining cell viability and proliferation in colonic epithelial cells. In particular, MCC overexpression suppressed both TNF? and LPS-induced NF?B activation, decreasing both the magnitude and rate of cellular responses. Overexpression also resulted in downregulation of proteins involved in canonical NF?B pathway signalling, while increasing the transcription of non-canonical NF?B genes. Therefore, MCC may direct activation of this pathway to a specific subset of NF?B-regulated genes. These data provide a molecular basis for the role of MCC as a tumour suppressor gene in CRC. MCC may have multiple functions, regulating cell cycle progression and modulating NF?B pathway signalling, either through direct involvement in pathway signalling cascades, or by providing a scaffold on which signalling events can occur.
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Book chapters on the topic "G2/M block"

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Böhm, L., T. Theron, and A. Binder. "Pentoxifylline Inhibits the Irradiation Induced G2/M Block and Alters DNA Synthesis in P53 Mutant and Repair Deficient Cells." In Fundamentals for the Assessment of Risks from Environmental Radiation, 305–10. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4585-5_39.

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Mowat, Michael R. A., and Nancy Stewart. "Mechanisms of Cell Cycle Blocks at the G2/M Transition and Their Role in Differentiation and Development." In Inhibitors of Cell Growth, 73–100. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72149-6_5.

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Conference papers on the topic "G2/M block"

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Biskup, E., O. Niazi, V. Pless, and R. Gniadecki. "PO-044 Possible involvement of G2/M block defects in cell sensitivity towards ATR inhibitors." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.88.

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