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Journal articles on the topic 'G2/M checkpoint'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Xu, Bo, Seong-Tae Kim, Dae-Sik Lim, and Michael B. Kastan. "Two Molecularly Distinct G2/M Checkpoints Are Induced by Ionizing Irradiation." Molecular and Cellular Biology 22, no. 4 (2002): 1049–59. http://dx.doi.org/10.1128/mcb.22.4.1049-1059.2002.

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ABSTRACT Cell cycle checkpoints are among the multiple mechanisms that eukaryotic cells possess to maintain genomic integrity and minimize tumorigenesis. Ionizing irradiation (IR) induces measurable arrests in the G1, S, and G2 phases of the mammalian cell cycle, and the ATM (ataxia telangiectasia mutated) protein plays a role in initiating checkpoint pathways in all three of these cell cycle phases. However, cells lacking ATM function exhibit both a defective G2 checkpoint and a prolonged G2 arrest after IR, suggesting the existence of different types of G2 arrest. Two molecularly distinct G2

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2

Osman, Fekret, Irina R. Tsaneva, Matthew C. Whitby, and Claudette L. Doe. "UV Irradiation Causes the Loss of Viable Mitotic Recombinants in Schizosaccharomyces pombe Cells Lacking the G2/M DNA Damage Checkpoint." Genetics 160, no. 3 (2002): 891–908. http://dx.doi.org/10.1093/genetics/160.3.891.

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Abstract Elevated mitotic recombination and cell cycle delays are two of the cellular responses to UV-induced DNA damage. Cell cycle delays in response to DNA damage are mediated via checkpoint proteins. Two distinct DNA damage checkpoints have been characterized in Schizosaccharomyces pombe: an intra-S-phase checkpoint slows replication and a G2/M checkpoint stops cells passing from G2 into mitosis. In this study we have sought to determine whether UV damage-induced mitotic intrachromosomal recombination relies on damage-induced cell cycle delays. The spontaneous and UV-induced recombination

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3

Xu, Zhiheng, and David Norris. "The SFP1 Gene Product of Saccharomyces cerevisiae Regulates G2/M Transitions During the Mitotic Cell Cycle and DNA-Damage Response." Genetics 150, no. 4 (1998): 1419–28. http://dx.doi.org/10.1093/genetics/150.4.1419.

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Abstract In eukaryotic cells, checkpoint pathways arrest cell-cycle progression if a particular event has failed to complete appropriately or if an important intracellular structure is defective or damaged. Saccharomyces cerevisiae strains that lack the SFP1 gene fail to arrest at the G2 DNA-damage checkpoint in response to genomic injury, but maintain their ability to arrest at the replication and spindle-assembly checkpoints. sfp1Δ mutants are characterized by a premature entrance into mitosis during a normal (undamaged) cell cycle, while strains that overexpress Sfp1p exhibit delays in G2.

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4

Qiu, Ling, Andrew Burgess, David P. Fairlie, Helen Leonard, Peter G. Parsons, and Brian G. Gabrielli. "Histone Deacetylase Inhibitors Trigger a G2 Checkpoint in Normal Cells That Is Defective in Tumor Cells." Molecular Biology of the Cell 11, no. 6 (2000): 2069–83. http://dx.doi.org/10.1091/mbc.11.6.2069.

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Important aspects of cell cycle regulation are the checkpoints, which respond to a variety of cellular stresses to inhibit cell cycle progression and act as protective mechanisms to ensure genomic integrity. An increasing number of tumor suppressors are being demonstrated to have roles in checkpoint mechanisms, implying that checkpoint dysfunction is likely to be a common feature of cancers. Here we report that histone deacetylase inhibitors, in particular azelaic bishydroxamic acid, triggers a G2 phase cell cycle checkpoint response in normal human cells, and this checkpoint is defective in a

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5

Xu, Bo, Seong-tae Kim, and Michael B. Kastan. "Involvement of Brca1 in S-Phase and G2-Phase Checkpoints after Ionizing Irradiation." Molecular and Cellular Biology 21, no. 10 (2001): 3445–50. http://dx.doi.org/10.1128/mcb.21.10.3445-3450.2001.

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ABSTRACT Cell cycle arrests in the G1, S, and G2phases occur in mammalian cells after ionizing irradiation and appear to protect cells from permanent genetic damage and transformation. Though Brca1 clearly participates in cellular responses to ionizing radiation (IR), conflicting conclusions have been drawn about whether Brca1 plays a direct role in cell cycle checkpoints. Normal Nbs1 function is required for the IR-induced S-phase checkpoint, but whether Nbs1 has a definitive role in the G2/M checkpoint has not been established. Here we show that Atm and Brca1 are required for both the S-phas

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6

Dhar, Sonu, Jeremy A. Squire, M. Prakash Hande, Raymund J. Wellinger та Tej K. Pandita. "Inactivation of 14-3-3ς Influences Telomere Behavior and Ionizing Radiation-Induced Chromosomal Instability". Molecular and Cellular Biology 20, № 20 (2000): 7764–72. http://dx.doi.org/10.1128/mcb.20.20.7764-7772.2000.

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ABSTRACT Telomeres are complexes of repetitive DNA sequences and proteins constituting the ends of linear eukaryotic chromosomes. While these structures are thought to be associated with the nuclear matrix, they appear to be released from this matrix at the time when the cells exit from G2 and enter M phase. Checkpoints maintain the order and fidelity of the eukaryotic cell cycle, and defects in checkpoints contribute to genetic instability and cancer. The 14-3-3ς gene has been reported to be a checkpoint control gene, since it promotes G2 arrest following DNA damage. Here we demonstrate that

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7

Meng, Xiangbing, Jianling Bi, Yujun Li, et al. "AZD1775 Increases Sensitivity to Olaparib and Gemcitabine in Cancer Cells with p53 Mutations." Cancers 10, no. 5 (2018): 149. http://dx.doi.org/10.3390/cancers10050149.

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Tumor suppressor p53 is responsible for enforcing cell cycle checkpoints at G1/S and G2/M in response to DNA damage, thereby allowing both normal and tumor cells to repair DNA before entering S and M. However, tumor cells with absent or mutated p53 are able to activate alternative signaling pathways that maintain the G2/M checkpoint, which becomes uniquely critical for the survival of such tumor cells. We hypothesized that abrogation of the G2 checkpoint might preferentially sensitize p53-defective tumor cells to DNA-damaging agents and spare normal cells with intact p53 function. The tyrosine

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8

Kumar, Subodh, Srikanth Talluri, Mariateresa Fulciniti, Masood A. Shammas, and Nikhil C. Munshi. "Elevated APEX1 Disrupts G2/M Checkpoint, Contributing to Evolution and Survival of Myeloma Cells." Blood 126, no. 23 (2015): 2997. http://dx.doi.org/10.1182/blood.v126.23.2997.2997.

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Abstract Cell cycle checkpoints provide the cell with time to repair chromosomal DNA damage before its replication (G1) and also prior to its segregation (G2), thus ensuring integrity, maintenance and protection of genome. Although proper functioning of both checkpoints is essential, G2/M has a special significance as a potentially lethal double-strand break in DNA escape repair and persist from G2 into mitosis, it may recombine in G1 to produce gene rearrangements. Moreover, G2 is the phase where homologous recombination (HR) can utilize a sister chromatid as a template to provide error-free

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9

Naiki, Takahiro, Toshiyasu Shimomura, Tae Kondo, Kunihiro Matsumoto, and Katsunori Sugimoto. "Rfc5, in Cooperation with Rad24, Controls DNA Damage Checkpoints throughout the Cell Cycle inSaccharomyces cerevisiae." Molecular and Cellular Biology 20, no. 16 (2000): 5888–96. http://dx.doi.org/10.1128/mcb.20.16.5888-5896.2000.

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ABSTRACT RAD24 and RFC5 are required for DNA damage checkpoint control in the budding yeast Saccharomyces cerevisiae. Rad24 is structurally related to replication factor C (RFC) subunits and associates with RFC subunits Rfc2, Rfc3, Rfc4, and Rfc5. rad24Δ mutants are defective in all the G1-, S-, and G2/M-phase DNA damage checkpoints, whereas the rfc5-1 mutant is impaired only in the S-phase DNA damage checkpoint. Both the RFC subunits and Rad24 contain a consensus sequence for nucleoside triphosphate (NTP) binding. To determine whether the NTP-binding motif is important for Rad24 function, we

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10

Furnari, Beth, Alessandra Blasina, Michael N. Boddy, Clare H. McGowan, and Paul Russell. "Cdc25 Inhibited In Vivo and In Vitro by Checkpoint Kinases Cds1 and Chk1." Molecular Biology of the Cell 10, no. 4 (1999): 833–45. http://dx.doi.org/10.1091/mbc.10.4.833.

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In the fission yeast Schizosaccharomyces pombe, the protein kinase Cds1 is activated by the S–M replication checkpoint that prevents mitosis when DNA is incompletely replicated. Cds1 is proposed to regulate Wee1 and Mik1, two tyrosine kinases that inhibit the mitotic kinase Cdc2. Here, we present evidence from in vivo and in vitro studies, which indicates that Cds1 also inhibits Cdc25, the phosphatase that activates Cdc2. In an in vivo assay that measures the rate at which Cdc25 catalyzes mitosis, Cds1 contributed to a mitotic delay imposed by the S–M replication checkpoint. Cds1 also inhibite

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11

Hayashi, S. "A Cdc2 dependent checkpoint maintains diploidy in Drosophila." Development 122, no. 4 (1996): 1051–58. http://dx.doi.org/10.1242/dev.122.4.1051.

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DNA replication in G2 does not normally occur due to the checkpoint control. To elucidate its mechanism, the functions of the escargot and Dmcdc2 genes of Drosophila were studied. When escargot function was eliminated, diploid imaginal cells that were arrested in G2 lost Cyclin A, a regulatory subunit of G2/M cdk, and entered an endocycle. escargot genetically interacted with Dmcdc2 which encodes a catalytic subunit of G2/M cdk. The mutant phenotypes of Dmcdc2 itself was similar to those of escargot: many diploid cells in imaginal discs, salivary glands and the central nervous system entered a

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12

Forbes, Kristi Chrispell, Timothy Humphrey, and Tamar Enoch. "Suppressors of Cdc25p Overexpression Identify Two Pathways That Influence the G2/M Checkpoint in Fission Yeast." Genetics 150, no. 4 (1998): 1361–75. http://dx.doi.org/10.1093/genetics/150.4.1361.

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Abstract Checkpoints maintain the order of cell-cycle events. At G2/M, a checkpoint blocks mitosis in response to damaged or unreplicated DNA. There are significant differences in the checkpoint responses to damaged DNA and unreplicated DNA, although many of the same genes are involved in both responses. To identify new genes that function specifically in the DNA replication checkpoint pathway, we searched for high-copy suppressors of overproducer of Cdc25p (OPcdc25+), which lacks a DNA replication checkpoint. Two classes of suppressors were isolated. One class includes a new gene encoding a p

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13

Deckbar, Dorothee, Julie Birraux, Andrea Krempler, et al. "Chromosome breakage after G2 checkpoint release." Journal of Cell Biology 176, no. 6 (2007): 749–55. http://dx.doi.org/10.1083/jcb.200612047.

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DNA double-strand break (DSB) repair and checkpoint control represent distinct mechanisms to reduce chromosomal instability. Ataxia telangiectasia (A-T) cells have checkpoint arrest and DSB repair defects. We examine the efficiency and interplay of ATM's G2 checkpoint and repair functions. Artemis cells manifest a repair defect identical and epistatic to A-T but show proficient checkpoint responses. Only a few G2 cells enter mitosis within 4 h after irradiation with 1 Gy but manifest multiple chromosome breaks. Most checkpoint-proficient cells arrest at the G2/M checkpoint, with the length of

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14

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 (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

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15

Poggioli, George J., Roberta L. DeBiasi, Ryan Bickel, et al. "Reovirus-Induced Alterations in Gene Expression Related to Cell Cycle Regulation." Journal of Virology 76, no. 6 (2002): 2585–94. http://dx.doi.org/10.1128/jvi.76.6.2585-2594.2002.

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ABSTRACT Mammalian reovirus infection results in perturbation of host cell cycle progression. Since reovirus infection is known to activate cellular transcription factors, we investigated alterations in cell cycle-related gene expression following HEK293 cell infection by using the Affymetrix U95A microarray. Serotype 3 reovirus infection results in differential expression of 10 genes classified as encoding proteins that function at the G1-to-S transition, 11 genes classified as encoding proteins that function at G2-to-M transition, and 4 genes classified as encoding proteins that function at

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16

Moser, Bettina A., Jean-Marc Brondello, Beth Baber-Furnari, and Paul Russell. "Mechanism of Caffeine-Induced Checkpoint Override in Fission Yeast." Molecular and Cellular Biology 20, no. 12 (2000): 4288–94. http://dx.doi.org/10.1128/mcb.20.12.4288-4294.2000.

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ABSTRACT Mitotic checkpoints restrain the onset of mitosis (M) when DNA is incompletely replicated or damaged. These checkpoints are conserved between the fission yeast Schizosaccharomyces pombe and mammals. In both types of organisms, the methylxanthine caffeine overrides the synthesis (S)-M checkpoint that couples mitosis to completion of DNA S phase. The molecular target of caffeine was sought in fission yeast. Caffeine prevented activation of Cds1 and phosphorylation of Chk1, two protein kinases that enforce the S-M checkpoint triggered by hydroxyurea. Caffeine did not inhibit these kinase

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17

Sánchez-Molina, Sara, Oliver Mortusewicz, Béatrice Bieber, et al. "Role for hACF1 in the G2/M damage checkpoint." Nucleic Acids Research 39, no. 19 (2011): 8445–56. http://dx.doi.org/10.1093/nar/gkr435.

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18

Sheppard, Karen E., Richard B. Pearson, and Ross D. Hannan. "Unexpected role of CDK4 in a G2/M checkpoint." Cell Cycle 14, no. 9 (2015): 1351–52. http://dx.doi.org/10.1080/15384101.2015.1022060.

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19

Rabouille, Catherine, and Vangelis Kondylis. "Golgi Ribbon Unlinking: An Organelle-Based G2/M Checkpoint." Cell Cycle 6, no. 22 (2007): 2723–29. http://dx.doi.org/10.4161/cc.6.22.4896.

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20

Hasthorpe, Suzanne, Kellie Tainton, Melissa Peart, et al. "G2/M checkpoint gene expression in developing germ cells." Molecular Reproduction and Development 74, no. 5 (2007): 531–38. http://dx.doi.org/10.1002/mrd.20549.

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21

Wang, X. W., Q. Zhan, J. D. Coursen, et al. "GADD45 induction of a G2/M cell cycle checkpoint." Proceedings of the National Academy of Sciences 96, no. 7 (1999): 3706–11. http://dx.doi.org/10.1073/pnas.96.7.3706.

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22

Mikhailov, Alexei, Mio Shinohara, and Conly L. Rieder. "Topoisomerase II and histone deacetylase inhibitors delay the G2/M transition by triggering the p38 MAPK checkpoint pathway." Journal of Cell Biology 166, no. 4 (2004): 517–26. http://dx.doi.org/10.1083/jcb.200405167.

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When early prophase PtK1 or Indian muntjac cells are exposed to topoisomerase II (topo II) inhibitors that induce little if any DNA damage, they are delayed from entering mitosis. We show that this delay is overridden by inhibiting the p38, but not the ATM, kinase. Treating early prophase cells with hyperosmotic medium or a histone deacetylase inhibitor similarly delays entry into mitosis, and this delay can also be prevented by inhibiting p38. Together, these results reveal that agents or stresses that induce global changes in chromatin topology during G2 delay entry into mitosis, independent

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23

Zhu, Wenge, and Anindya Dutta. "An ATR- and BRCA1-Mediated Fanconi Anemia Pathway Is Required for Activating the G2/M Checkpoint and DNA Damage Repair upon Rereplication." Molecular and Cellular Biology 26, no. 12 (2006): 4601–11. http://dx.doi.org/10.1128/mcb.02141-05.

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ABSTRACT The timely assembly of prereplicative complexes at replication origins is tightly controlled to ensure that genomic DNA is replicated once per cell cycle. The loss of geminin, a DNA replication inhibitor, causes rereplication that activates a G2/M checkpoint in human cancer cells. Fanconi anemia (FA) is an autosomal recessive and X-linked disorder associated with cancer susceptibility. Here we show that rereplication activates the FA pathway both for the activation of a G2/M checkpoint and for repair processes, like recruitment of RAD51. Both ATR and BRCA1 are required to activate the

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24

Hoffmann, Michèle J., Sarah Meneceur, Katrin Hommel, Wolfgang A. Schulz, and Günter Niegisch. "Downregulation of Cell Cycle and Checkpoint Genes by Class I HDAC Inhibitors Limits Synergism with G2/M Checkpoint Inhibitor MK-1775 in Bladder Cancer Cells." Genes 12, no. 2 (2021): 260. http://dx.doi.org/10.3390/genes12020260.

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Since genes encoding epigenetic regulators are often mutated or deregulated in urothelial carcinoma (UC), they represent promising therapeutic targets. Specifically, inhibition of Class-I histone deacetylase (HDAC) isoenzymes induces cell death in UC cell lines (UCC) and, in contrast to other cancer types, cell cycle arrest in G2/M. Here, we investigated whether mutations in cell cycle genes contribute to G2/M rather than G1 arrest, identified the precise point of arrest and clarified the function of individual HDAC Class-I isoenzymes. Database analyses of UC tissues and cell lines revealed mu

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Shibata, Atsushi, Olivia Barton, Angela T. Noon, et al. "Role of ATM and the Damage Response Mediator Proteins 53BP1 and MDC1 in the Maintenance of G2/M Checkpoint Arrest." Molecular and Cellular Biology 30, no. 13 (2010): 3371–83. http://dx.doi.org/10.1128/mcb.01644-09.

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ABSTRACT ATM-dependent initiation of the radiation-induced G2/M checkpoint arrest is well established. Recent results have shown that the majority of DNA double-strand breaks (DSBs) in G2 phase are repaired by DNA nonhomologous end joining (NHEJ), while ∼15% of DSBs are slowly repaired by homologous recombination. Here, we evaluate how the G2/M checkpoint is maintained in irradiated G2 cells, in light of our current understanding of G2 phase DSB repair. We show that ATM-dependent resection at a subset of DSBs leads to ATR-dependent Chk1 activation. ATR-Seckel syndrome cells, which fail to effi

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26

Sturgeon, Christopher M., and Michel Roberge. "G2 Checkpoint Kinase Inhibitors Exert Their Radiosensitizing Effects Prior to the G2/M Transition." Cell Cycle 6, no. 5 (2007): 572–75. http://dx.doi.org/10.4161/cc.6.5.3926.

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27

Scott, Kenneth L., and Sharon E. Plon. "Loss of Sin3/Rpd3 Histone Deacetylase Restores the DNA Damage Response in Checkpoint-Deficient Strains of Saccharomyces cerevisiae." Molecular and Cellular Biology 23, no. 13 (2003): 4522–31. http://dx.doi.org/10.1128/mcb.23.13.4522-4531.2003.

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ABSTRACT We previously reported that expression of the human forkhead/winged helix transcription factor, CHES1 (checkpoint suppressor 1; FOXN3), suppresses sensitivity to DNA damage and restores damage-induced G2/M arrest in checkpoint-deficient strains of Saccharomyces cerevisiae. We find that a functional glutathione S-transferase-Ches1 fusion protein binds in vivo to Sin3, a component of the S. cerevisiae Sin3/Rpd3 histone deacetylase complex. Checkpoint mutant strains with SIN3 deleted show increased resistance to UV irradiation, which is not further enhanced by CHES1 expression. Conversel

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Yasutis, Kimberly, Marissa Vignali, Matthew Ryder, et al. "Zds2p Regulates Swe1p-dependent Polarized Cell Growth inSaccharomyces cerevisiaevia a Novel Cdc55p Interaction Domain." Molecular Biology of the Cell 21, no. 24 (2010): 4373–86. http://dx.doi.org/10.1091/mbc.e10-04-0326.

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Deletion of the paralogs ZDS1 and ZDS2 in the budding yeast Saccharomyces cerevisiae causes a mis-regulation of polarized cell growth. Here we show a function for these genes as regulators of the Swe1p (Wee1p) kinase–dependent G2/M checkpoint. We identified a conserved domain in the C-terminus of Zds2p consisting of amino acids 813–912 (hereafter referred to as ZH4 for Zds homology 4) that is required for regulation of Swe1p-dependent polarized bud growth. ZH4 is shown by protein affinity assays to be necessary and sufficient for interaction with Cdc55p, a regulatory subunit of protein phospha

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Liu, Li-Li, Ji-Min Zhu, Xiang-Nan Yu, et al. "UBE2T promotes proliferation via G2/M checkpoint in hepatocellular carcinoma." Cancer Management and Research Volume 11 (September 2019): 8359–70. http://dx.doi.org/10.2147/cmar.s202631.

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Chung, Jon H., and Fred Bunz. "Cdk2 Is Required for p53-Independent G2/M Checkpoint Control." PLoS Genetics 6, no. 2 (2010): e1000863. http://dx.doi.org/10.1371/journal.pgen.1000863.

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Yan, Y., C. P. Black, and K. H. Cowan. "Irradiation-induced G2/M checkpoint response requires ERK1/2 activation." Oncogene 26, no. 32 (2007): 4689–98. http://dx.doi.org/10.1038/sj.onc.1210268.

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Busch, Corinna, Olivia Barton, Eberhard Morgenstern, et al. "The G2/M checkpoint phosphatase cdc25C is located within centrosomes." International Journal of Biochemistry & Cell Biology 39, no. 9 (2007): 1707–13. http://dx.doi.org/10.1016/j.biocel.2007.04.022.

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Shinohara, Mio, Alexei V. Mikhailov, Julio A. Aguirre-Ghiso, and Conly L. Rieder. "Extracellular Signal-regulated Kinase 1/2 Activity Is Not Required in Mammalian Cells during Late G2 for Timely Entry into or Exit from Mitosis." Molecular Biology of the Cell 17, no. 12 (2006): 5227–40. http://dx.doi.org/10.1091/mbc.e06-04-0284.

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Extracellular signal-regulated kinase (ERK)1/2 activity is reported to be required in mammalian cells for timely entry into and exit from mitosis (i.e., the G2-mitosis [G2/M] and metaphase-anaphase [M/A] transitions). However, it is unclear whether this involvement reflects a direct requirement for ERK1/2 activity during these transitions or for activating gene transcription programs at earlier stages of the cell cycle. To examine these possibilities, we followed live cells in which ERK1/2 activity was inhibited through late G2 and mitosis. We find that acute inhibition of ERK1/2 during late G

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Yamada, Ayumi, Brad Duffy, Jennifer A. Perry, and Sally Kornbluth. "DNA replication checkpoint control of Wee1 stability by vertebrate Hsl7." Journal of Cell Biology 167, no. 5 (2004): 841–49. http://dx.doi.org/10.1083/jcb.200406048.

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G2/M checkpoints prevent mitotic entry upon DNA damage or replication inhibition by targeting the Cdc2 regulators Cdc25 and Wee1. Although Wee1 protein stability is regulated by DNA-responsive checkpoints, the vertebrate pathways controlling Wee1 degradation have not been elucidated. In budding yeast, stability of the Wee1 homologue, Swe1, is controlled by a regulatory module consisting of the proteins Hsl1 and Hsl7 (histone synthetic lethal 1 and 7), which are targeted by the morphogenesis checkpoint to prevent Swe1 degradation when budding is inhibited. We report here the identification of X

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35

Lynch, Katherine N., Joyce F. Liu, Nikolas Kesten, et al. "Enhanced Efficacy of Aurora Kinase Inhibitors in G2/M Checkpoint Deficient TP53 Mutant Uterine Carcinomas Is Linked to the Summation of LKB1–AKT–p53 Interactions." Cancers 13, no. 9 (2021): 2195. http://dx.doi.org/10.3390/cancers13092195.

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Uterine carcinoma (UC) is the most common gynecologic malignancy in the United States. TP53 mutant UCs cause a disproportionate number of deaths due to limited therapies for these tumors and the lack of mechanistic understanding of their fundamental vulnerabilities. Here we sought to understand the functional and therapeutic relevance of TP53 mutations in UC. We functionally profiled targetable TP53 dependent DNA damage repair and cell cycle control pathways in a panel of TP53 mutant UC cell lines and patient-derived organoids. There were no consistent defects in DNA damage repair pathways. Ra

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Adamson, Aaron W., Dillon I. Beardsley, Wan-Ju Kim, Yajuan Gao, R. Baskaran, and Kevin D. Brown. "Methylator-induced, Mismatch Repair-dependent G2 Arrest Is Activated through Chk1 and Chk2." Molecular Biology of the Cell 16, no. 3 (2005): 1513–26. http://dx.doi.org/10.1091/mbc.e04-02-0089.

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SN1 DNA methylating agents such as the nitrosourea N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) elicit a G2/M checkpoint response via a mismatch repair (MMR) system-dependent mechanism; however, the exact nature of the mechanism governing MNNG-induced G2/M arrest and how MMR mechanistically participates in this process are unknown. Here, we show that MNNG exposure results in activation of the cell cycle checkpoint kinases ATM, Chk1, and Chk2, each of which has been implicated in the triggering of the G2/M checkpoint response. We document that MNNG induces a robust, dose-dependent G2 arrest in M

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Ödborn Jönsson, Linnéa, Maryam Sahi, Ximena Lopez-Lorenzo, et al. "Heterogeneities in Cell Cycle Checkpoint Activation Following Doxorubicin Treatment Reveal Targetable Vulnerabilities in TP53 Mutated Ultra High-Risk Neuroblastoma Cell Lines." International Journal of Molecular Sciences 22, no. 7 (2021): 3664. http://dx.doi.org/10.3390/ijms22073664.

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Most chemotherapeutics target DNA integrity and thereby trigger tumour cell death through activation of DNA damage responses that are tightly coupled to the cell cycle. Disturbances in cell cycle regulation can therefore lead to treatment resistance. Here, a comprehensive analysis of cell cycle checkpoint activation following doxorubicin (doxo) treatment was performed using flow cytometry, immunofluorescence and live-cell imaging in a panel of TP53 mutated ultra high-risk neuroblastoma (NB) cell lines, SK-N-DZ, Kelly, SK-N-AS, SK-N-FI, and BE(2)-C. Following treatment, a dose-dependent accumul

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Yu, Xiaochun, and Junjie Chen. "DNA Damage-Induced Cell Cycle Checkpoint Control Requires CtIP, a Phosphorylation-Dependent Binding Partner of BRCA1 C-Terminal Domains." Molecular and Cellular Biology 24, no. 21 (2004): 9478–86. http://dx.doi.org/10.1128/mcb.24.21.9478-9486.2004.

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ABSTRACT The BRCA1 C-terminal (BRCT) domain has recently been implicated as a phospho-protein binding domain. We demonstrate here that a CTBP-interacting protein CtIP interacts with BRCA1 BRCT domains in a phosphorylation-dependent manner. The CtIP/BRCA1 complex only exists in G2 phase and is required for DNA damage-induced Chk1 phosphorylation and the G2/M transition checkpoint. However, the CtIP/BRCA1 complex is not required for the damage-induced G2 accumulation checkpoint, which is controlled by a separate BRCA1/BACH1 complex. Taken together, these data not only implicate CtIP as a critica

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Saldivar, Joshua C., Stephan Hamperl, Michael J. Bocek, et al. "An intrinsic S/G2 checkpoint enforced by ATR." Science 361, no. 6404 (2018): 806–10. http://dx.doi.org/10.1126/science.aap9346.

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The cell cycle is strictly ordered to ensure faithful genome duplication and chromosome segregation. Control mechanisms establish this order by dictating when a cell transitions from one phase to the next. Much is known about the control of the G1/S, G2/M, and metaphase/anaphase transitions, but thus far, no control mechanism has been identified for the S/G2 transition. Here we show that cells transactivate the mitotic gene network as they exit the S phase through a CDK1 (cyclin-dependent kinase 1)–directed FOXM1 phosphorylation switch. During normal DNA replication, the checkpoint kinase ATR

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Wade, Mark, and Martin J. Allday. "Epstein-Barr Virus Suppresses a G2/M Checkpoint Activated by Genotoxins." Molecular and Cellular Biology 20, no. 4 (2000): 1344–60. http://dx.doi.org/10.1128/mcb.20.4.1344-1360.2000.

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ABSTRACT Several Epstein-Barr virus (EBV)-negative Burkitt lymphoma-derived cell lines (for example, BL41 and Ramos) are extremely sensitive to genotoxic drugs despite being functionally null for the tumor suppressor p53. They rapidly undergo apoptosis, largely from G2/M of the cell cycle. 5-Bromo-2′-deoxyuridine labeling experiments showed that although the treated cells can pass through S phase, they are unable to complete cell division, suggesting that a G2/M checkpoint is activated. Surprisingly, latent infection of these genotoxin-sensitive cells with EBV protects them from both apoptosis

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Simhadri, Srilatha, Gabriele Vincelli, Yanying Huo, et al. "PALB2 connects BRCA1 and BRCA2 in the G2/M checkpoint response." Oncogene 38, no. 10 (2018): 1585–96. http://dx.doi.org/10.1038/s41388-018-0535-2.

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Erson, Ayse E., and Elizabeth M. Petty. "CHFR-associated early G2/M checkpoint defects in breast cancer cells." Molecular Carcinogenesis 39, no. 1 (2003): 26–33. http://dx.doi.org/10.1002/mc.10161.

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Krauer, Kenia G., Andrew Burgess, Marion Buck, James Flanagan, Tom B. Sculley, and Brian Gabrielli. "The EBNA- 3 gene family proteins disrupt the G2/M checkpoint." Oncogene 23, no. 7 (2003): 1342–53. http://dx.doi.org/10.1038/sj.onc.1207253.

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Melixetian, Marina, Ditte Kjærsgaard Klein, Claus Storgaard Sørensen, and Kristian Helin. "NEK11 regulates CDC25A degradation and the IR-induced G2/M checkpoint." Nature Cell Biology 11, no. 10 (2009): 1247–53. http://dx.doi.org/10.1038/ncb1969.

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Funk, J. O., T. Herzinger, K. Hillmer, D. A. Wolf, D. Eick, and P. Kind. "Mechanisms of G2/M-checkpoint control in ultraviolet B-irradiated keratinocytes." Journal of Cancer Research and Clinical Oncology 121, S1 (1995): A10. http://dx.doi.org/10.1007/bf02572004.

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Gotoh, Tetsuya, Keita Ohsumi, Tomoko Matsui, Haruhiko Takisawa, and Takeo Kishimoto. "Inactivation of the checkpoint kinase Cds1 is dependent on cyclin B-Cdc2 kinase activation at the meiotic G2/M-phase transition in Xenopus oocytes." Journal of Cell Science 114, no. 18 (2001): 3397–406. http://dx.doi.org/10.1242/jcs.114.18.3397.

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Checkpoint controls ensure chromosomal integrity through the cell cycle. Chk1 and Cds1/Chk2 are effector kinases in the G2-phase checkpoint activated by damaged or unreplicated DNA, and they prevent entry into M-phase through inhibition of cyclin B-Cdc2 kinase activation. However, little is known about how the effector kinases are regulated when the checkpoint is attenuated. Recent studies indicate that Chk1 is also involved in the physiological G2-phase arrest of immature Xenopus oocytes via direct phosphorylation and inhibition of Cdc25C, the activator of cyclin B-Cdc2 kinase. Bearing in min

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Lottersberger, Francisca, Fabio Rubert, Veronica Baldo, Giovanna Lucchini, and Maria Pia Longhese. "Functions of Saccharomyces cerevisiae 14-3-3 Proteins in Response to DNA Damage and to DNA Replication Stress." Genetics 165, no. 4 (2003): 1717–32. http://dx.doi.org/10.1093/genetics/165.4.1717.

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Abstract Two members of the 14-3-3 protein family, involved in key biological processes in different eukaryotes, are encoded by the functionally redundant Saccharomyces cerevisiae BMH1 and BMH2 genes. We produced and characterized 12 independent bmh1 mutant alleles, whose presence in the cell as the sole 14-3-3 source causes hypersensitivity to genotoxic agents, indicating that Bmh proteins are required for proper response to DNA damage. In particular, the bmh1-103 and bmh1-266 mutant alleles cause defects in G1/S and G2/M DNA damage checkpoints, whereas only the G2/M checkpoint is altered by

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Kandel, Eugene S., Jennifer Skeen, Nathan Majewski, et al. "Activation of Akt/Protein Kinase B Overcomes a G2/M Cell Cycle Checkpoint Induced by DNA Damage." Molecular and Cellular Biology 22, no. 22 (2002): 7831–41. http://dx.doi.org/10.1128/mcb.22.22.7831-7841.2002.

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ABSTRACT Activation of Akt, or protein kinase B, is frequently observed in human cancers. Here we report that Akt activation via overexpression of a constitutively active form or via the loss of PTEN can overcome a G2/M cell cycle checkpoint that is induced by DNA damage. Activated Akt also alleviates the reduction in CDC2 activity and mitotic index upon exposure to DNA damage. In addition, we found that PTEN null embryonic stem (ES) cells transit faster from the G2/M to the G1 phase of the cell cycle when compared to wild-type ES cells and that inhibition of phosphoinositol-3-kinase (PI3K) in

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Balcer-Kubiczek, Elizabeth K., Mona Attarpour, Jian Z. Wang, and William F. Regine. "The Effect of Docetaxel (Taxotere®) on Human Gastric Cancer Cells Exhibiting Low-Dose Radiation Hypersensitivity." Clinical medicine. Oncology 2 (January 2008): CMO.S463. http://dx.doi.org/10.4137/cmo.s463.

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Low-dose radiation hypersensitivity (HRS) describes a phenomenon of excessive sensitivity to X ray doses <0.5 Gy. Docetaxel is a taxane shown to arrest cells in the G2/M phase of the cell cycle. Some previous studies suggested that HRS might result from the abrogation of the early G2 checkpoint arrest. First we tested whether HRS occurs in gastric cancer—derived cells, and whether pre-treatment of cells with low docetaxel concentrations can enhance the magnitude of HRS in gastric cancer cells. The results demonstrated HRS at ~0.3 Gy and the synergy between 0.3 Gy and docetaxel (3 nM for 24

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Pike, Brietta L., Suganya Yongkiettrakul, Ming-Daw Tsai, and Jörg Heierhorst. "Mdt1, a Novel Rad53 FHA1 Domain-Interacting Protein, Modulates DNA Damage Tolerance and G2/M Cell Cycle Progression in Saccharomycescerevisiae." Molecular and Cellular Biology 24, no. 7 (2004): 2779–88. http://dx.doi.org/10.1128/mcb.24.7.2779-2788.2004.

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ABSTRACT The Rad53 kinase plays a central role in yeast DNA damage checkpoints. Rad53 contains two FHA phosphothreonine-binding domains that are required for Rad53 activation and possibly downstream signaling. Here we show that the N-terminal Rad53 FHA1 domain interacts with the RNA recognition motif, coiled-coil, and SQ/TQ cluster domain-containing protein Mdt1 (YBl051C). The interaction of Rad53 and Mdt1 depends on the structural integrity of the FHA1 phosphothreonine-binding site as well as threonine-305 of Mdt1. Mdt1 is constitutively threonine phosphorylated and hyperphosphorylated in res

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