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Showing 1-30 of 33 results for "C9358" within Papers
Alessia Balestrini et al.
Molecular cancer research : MCR, 14(2), 185-195 (2015-11-06)
The Mre11 complex (Mre11, Rad50, and Nbs1) occupies a central node of the DNA damage response (DDR) network and is required for ATM activation in response to DNA damage. Hypomorphic alleles of MRE11 and NBS1 confer embryonic lethality in ATM-deficient
Human Endonuclease ANKLE1 Localizes at the Midbody and Processes Chromatin Bridges to Prevent DNA Damage and cGAS-STING Activation.
Jiang, et al.
Advanced science (Weinheim, Baden-Wurttemberg, Germany), 10, e2204388-e2204388 (2023)
Masami Nozaki et al.
Oncotarget, 10(10), 1014-1030 (2019-02-26)
Cancer stem cells (CSCs), which play important roles in tumor initiation and progression, are resistant to many types of therapies. However, the regulatory mechanisms underlying CSC-specific properties, including self-renewal, are poorly understood. Here, we found that LATS1/2, the core Hippo
Rose Boutros et al.
Cell cycle (Georgetown, Tex.), 7(3), 401-406 (2008-02-01)
The Cyclin-Dependent Kinase (CDK)-activating phosphatase CDC25B, localises to the centrosomes where its activity is both positively and negatively regulated by several kinases including Aurora A and CHK1. Our recent data also demonstrate a role for CDC25B in the centrosome duplication
Eleni Petsalaki et al.
The Journal of cell biology, 205(3), 339-356 (2014-05-07)
The spindle checkpoint delays exit from mitosis in cells with spindle defects. In this paper, we show that Chk2 is required to delay anaphase onset when microtubules are completely depolymerized but not in the presence of relatively few unattached kinetochores.
Joachim Bischof et al.
PloS one, 8(7), e68803-e68803 (2013-07-19)
CK1δ, a member of the casein kinase 1 family, is involved in the regulation of various cellular processes and has been associated with the pathophysiology of neurodegenerative diseases and cancer. Therefore recently, interest in generating highly specific inhibitors for personalized
Meelis Kadaja et al.
PLoS pathogens, 5(4), e1000397-e1000397 (2009-04-25)
In HPV-related cancers, the "high-risk" human papillomaviruses (HPVs) are frequently found integrated into the cellular genome. The integrated subgenomic HPV fragments express viral oncoproteins and carry an origin of DNA replication that is capable of initiating bidirectional DNA re-replication in
Y Sanchez et al.
Science (New York, N.Y.), 277(5331), 1497-1501 (1997-09-05)
In response to DNA damage, mammalian cells prevent cell cycle progression through the control of critical cell cycle regulators. A human gene was identified that encodes the protein Chk1, a homolog of the Schizosaccharomyces pombe Chk1 protein kinase, which is
Y Liu et al.
Cell death and differentiation, 18(5), 841-852 (2010-11-30)
Proapoptotic BH3 interacting domain death agonist (Bid), a BH3-only Bcl-2 family member, is situated at the interface between the DNA damage response and apoptosis, with roles in death receptor-induced apoptosis as well as cell cycle checkpoints following DNA damage.(1, 2
Sampada Kalan et al.
Frontiers in genetics, 4, 95-95 (2013-06-12)
LIM proteins constitute a superfamily characterized by the presence of a LIM domain, known to be involved in protein-protein interactions. Our previous work has implicated members of the Zyxin family of LIM proteins, namely TRIP6 and LPP, in the repression
Shriparna Sarbajna et al.
Genes & development, 28(10), 1124-1136 (2014-05-17)
The resolution of recombination intermediates containing Holliday junctions (HJs) is critical for genome maintenance and proper chromosome segregation. Three pathways for HJ processing exist in human cells and involve the following enzymes/complexes: BLM-TopoIIIα-RMI1-RMI2 (BTR complex), SLX1-SLX4-MUS81-EME1 (SLX-MUS complex), and GEN1.
C Lukas et al.
Cancer research, 61(13), 4990-4993 (2001-06-30)
The Chk2 kinase is a tumor suppressor and key transducer of DNA-damage checkpoints. We show that the human Chk2 protein is relatively stable, nuclear, and responding to gamma-radiation throughout the cell cycle. Contrary to the retinoblastoma protein-regulated, labile Chk1 kinase
A Blasina et al.
Current biology : CB, 9(1), 1-10 (1999-01-16)
In human cells, the mitosis-inducing kinase Cdc2 is inhibited by phosphorylation on Thr14 and Tyr15. Disruption of these phosphorylation sites abrogates checkpoint-mediated regulation of Cdc2 and renders cells highly sensitive to agents that damage DNA. Phosphorylation of these sites is
Zuzana Koledova et al.
Stem cells (Dayton, Ohio), 28(3), 450-461 (2010-01-28)
Cyclin-dependent kinase two (Cdk2) is the major regulator of the G1/S transition and the target of an activated G1 checkpoint in somatic cells. In the presence of DNA damage, Cdk2 kinase activity is abrogated by a deficiency of Cdc25A phosphatase
Ying Wai Chan et al.
Nature cell biology, 20(1), 92-103 (2017-12-20)
The resolution of joint molecules that link recombining sister chromatids is essential for chromosome segregation. Here, we determine the fate of unresolved recombination intermediates arising in cells lacking two nucleases required for resolution (GEN1 -/- knockout cells depleted of MUS81).
B B Zhou et al.
Nature, 408(6811), 433-439 (2000-12-02)
The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development. Organisms respond to chromosomal insults by activating a complex damage response pathway. This pathway regulates known responses such as cell-cycle arrest
Identification of potential therapeutic targets in malignant mesothelioma using cell-cycle gene expression analysis
Romagnoli S, et al.
The American Journal of Pathology, 174(3), 762-770 (2009)
Solange Romagnoli et al.
The American journal of pathology, 174(3), 762-770 (2009-02-17)
Cell-cycle defects are responsible for cancer onset and growth. We studied the expression profile of 60 genes involved in cell cycle in a series of malignant mesotheliomas (MMs), normal pleural tissues, and MM cell cultures using a quantitative polymerase chain
Specific role of Chk1 phosphorylations in cell survival and checkpoint activation
Niida H, et al.
Molecular and Cellular Biology, 27(7), 2572-2581 (2007)
Kousuke Kasahara et al.
The EMBO journal, 29(16), 2802-2812 (2010-07-20)
14-3-3 proteins control various cellular processes, including cell cycle progression and DNA damage checkpoint. At the DNA damage checkpoint, some subtypes of 14-3-3 (beta and zeta isoforms in mammalian cells and Rad24 in fission yeast) bind to Ser345-phosphorylated Chk1 and
Hideaki Ogiwara et al.
PloS one, 7(12), e52810-e52810 (2013-01-04)
Histone acetylation at DNA double-strand break (DSB) sites by CBP and p300 histone acetyltransferases (HATs) is critical for the recruitment of DSB repair proteins to chromatin. Here, we show that CBP and p300 HATs also function in DSB repair by
Ryan D Beveridge et al.
Cell cycle (Georgetown, Tex.), 13(21), 3450-3459 (2014-12-09)
We previously identified and characterized TELO2 as a human protein that facilitates efficient DNA damage response (DDR) signaling. A subsequent yeast 2-hybrid screen identified LARG; Leukemia-Associated Rho Guanine Nucleotide Exchange Factor (also known as Arhgef12), as a potential novel TELO2
J A L Brown et al.
Oncogene, 29(40), 5537-5544 (2010-07-28)
Microcephalin (MCPH1/BRIT1) is a potential tumour suppressor that localizes to the centrosome, forms ionizing radiation-induced nuclear foci (IRIF) and is involved in the DNA damage checkpoints that ensure genome stability. Here, we report the impact of Mcph1 disruption in the
Hironori Abe et al.
Human molecular genetics, 27(7), 1136-1149 (2018-01-24)
The continuity of life depends on mechanisms in the germline that ensure the integrity of the genome. The DNA damage response/checkpoint kinases ATM and ATR are essential signaling factors in the germline. However, it remains unknown how a downstream transducer
Rachel Bayley et al.
Molecular cell, 82(10), 1924-1939 (2022-04-20)
The 53BP1-RIF1-shieldin pathway maintains genome stability by suppressing nucleolytic degradation of DNA ends at double-strand breaks (DSBs). Although RIF1 interacts with damaged chromatin via phospho-53BP1 and facilitates recruitment of the shieldin complex to DSBs, it is unclear whether other regulatory
Tsutomu Iwata et al.
PloS one, 12(5), e0178221-e0178221 (2017-05-31)
CBP-93872 suppresses maintenance of DNA double-stranded break-induced G2 checkpoint, by inhibiting the pathway between ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) activation. To examine the potential use of CBP-93872 for clinical applications, we analyzed the synergistic effects of platinum-containing
Yasunori Fukumoto et al.
The Journal of biological chemistry, 289(18), 12313-12329 (2014-03-19)
The DNA damage checkpoint arrests cell cycle progression to allow time for repair. Once DNA repair is completed, checkpoint signaling is terminated. Currently little is known about the mechanism by which checkpoint signaling is terminated, and the disappearance of DNA
Takuya Suzuki et al.
Oncology reports, 47(4) (2022-02-23)
The repair of DNA damage caused by chemotherapy in cancer cells occurs mainly at two cell cycle checkpoints (G1 and G2) and is a factor contributing to chemoresistance. Most colorectal cancers harbor mutations in p53, the main pathway involved in the G1
Shinnosuke Harata et al.
Oncology reports, 49(3) (2023-02-04)
Ataxia telangiectasia and Rad3‑related (ATR) is a kinase that repairs DNA damage. Although inhibitors that selectively target ATR have been developed, their effectiveness in colorectal cancer has not been widely reported. The present study hypothesized that anticancer agents that effectively
Hiroyuki Niida et al.
Molecular and cellular biology, 27(7), 2572-2581 (2007-01-24)
Chk1 is a multifunctional protein kinase that plays essential roles in cell survival and cell cycle checkpoints. Chk1 is phosphorylated at multiple sites by several protein kinases, but the precise effects of these phosphorylations are largely unknown. Using a knockout-knockin
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