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Jeffrey Patterson-Fortin et al.
The Journal of biological chemistry, 285(40), 30971-30981 (2010-07-27)
BRCC36 is a JAMM (JAB1/MPN/Mov34 metalloenzyme) domain, lysine 63-ubiquitin (K63-Ub)-specific deubiquitinating enzyme (DUB) and a member of two protein complexes: the DNA damage-responsive BRCA1-RAP80 complex, and the cytoplasmic BRCC36 isopeptidase complex (BRISC). The presence of several identical constituents in both
Chao Liu et al.
The EMBO journal, 40(13), e106864-e106864 (2021-05-13)
Current understanding holds that Klinefelter syndrome (KS) is not inherited, but arises randomly during meiosis. Whether there is any genetic basis for the origin of KS is unknown. Here, guided by our identification of some USP26 variations apparently associated with
Double-strand break-induced transcriptional silencing is associated with loss of tri-methylation at H3K4.
Doris M Seiler,Jacques Rouquette,Volker J Schmid,Hilmar Strickfaden,Christian Ottmann et al.
Chromosome Research null
Wen-Hsing Cheng et al.
FEBS letters, 579(6), 1350-1356 (2005-03-01)
The WRN protein is mutated in the chromosomally unstable Werner syndrome (WS) and the Nbs1 protein is mutated in Nijmegen breakage syndrome (NBS). The Nbs1 protein is an integral component of the M/R/N complex. Although WRN is known to interact
Telma Roque et al.
Stem cells (Dayton, Ohio), 30(3), 537-547 (2011-12-14)
The cyclin-dependent kinase inhibitor p21(waf1/cip) mediates the p53-dependent G1/S checkpoint, which is generally considered to be a critical requirement to maintain genomic stability after DNA damage. We used staggered 5-ethynyl-2'deoxyuridine/5-bromo-2'-deoxyuridine double-labeling in vivo to investigate the cell cycle progression and
Bryan A Castaño et al.
Nucleic acids research, 52(7), 3740-3760 (2024-02-07)
It is well-established that, through canonical functions in transcription and DNA repair, the tumor suppressor p53 plays a central role in safeguarding cells from the consequences of DNA damage. Recent data retrieved in tumor and stem cells demonstrated that p53
Yong Wang et al.
Free radical biology & medicine, 48(2), 348-356 (2009-11-21)
Ionizing radiation (IR) and/or chemotherapy causes not only acute tissue damage but also late effects including long-term (or residual) bone marrow (BM) injury. The induction of residual BM injury is primarily attributable to the induction of hematopoietic stem cell (HSC)
Somaira Nowsheen et al.
Nature communications, 9(1), 2736-2736 (2018-07-18)
Cells respond to cytotoxic DNA double-strand breaks by recruiting repair proteins to the damaged site. Phosphorylation of the histone variant H2AX at S139 and Y142 modulate its interaction with downstream DNA repair proteins and their recruitment to DNA lesions. Here
Anna K Uryga et al.
Communications biology, 4(1), 611-611 (2021-05-23)
Accumulation of vascular smooth muscle cells (VSMCs) is a hallmark of multiple vascular pathologies, including following neointimal formation after injury and atherosclerosis. However, human VSMCs in advanced atherosclerotic lesions show reduced cell proliferation, extensive and persistent DNA damage, and features
Irene Sanchez-Lopez et al.
Nucleic acids research, 52(5), 2389-2415 (2024-01-15)
DNA damage represents a challenge for cells, as this damage must be eliminated to preserve cell viability and the transmission of genetic information. To reduce or eliminate unscheduled chemical modifications in genomic DNA, an extensive signaling network, known as the
Jose F Moruno-Manchon et al.
Aging, 9(9), 1957-1970 (2017-09-15)
The G-quadruplex is a non-canonical DNA secondary structure formed by four DNA strands containing multiple runs of guanines. G-quadruplexes play important roles in DNA recombination, replication, telomere maintenance, and regulation of transcription. Small molecules that stabilize the G-quadruplexes alter gene
Mei Hua Jin et al.
Cancer research and treatment : official journal of Korean Cancer Association, 52(1), 149-166 (2019-07-12)
Pancreatic cancer (PC) is one of the most lethal cancers worldwide, but there are currently no effective treatments. The DNA damage response (DDR) is under investigation for the development of novel anti-cancer drugs. Since DNA repair pathway alterations have been
Stefan J Kempf et al.
Molecular neurodegeneration, 9, 57-57 (2014-12-18)
Epidemiological evidence suggests that low doses of ionising radiation (≤1.0 Gy) produce persistent alterations in cognition if the exposure occurs at a young age. The mechanisms underlying such alterations are unknown. We investigated the long-term effects of low doses of total
Wenwen Liu et al.
Autophagy, 19(2), 644-659 (2022-07-06)
Primary ovarian insufficiency (POI), also known as premature ovarian failure, is an ovarian defect in humans characterized by the premature depletion of ovarian follicles before the age of 40. However, the mechanisms underlying POI remain largely unknown. Here, we show
Saniya Fayzullina et al.
PloS one, 9(3), e93329-e93329 (2014-03-29)
Spinal Muscular Atrophy (SMA) is a hereditary childhood disease that causes paralysis by progressive degeneration of skeletal muscles and spinal motor neurons. SMA is associated with reduced levels of full-length Survival of Motor Neuron (SMN) protein, due to mutations in
Benoit Miotto et al.
Nucleic acids research, 46(9), 4392-4404 (2018-03-01)
Reactive oxygen species (ROS) are a byproduct of cell metabolism, and can also arise from environmental sources, such as toxins or radiation. Depending on dose and context, ROS have both beneficial and deleterious roles in mammalian development and disease, therefore
Antonio Galarreta et al.
The EMBO journal, 40(11), e99692-e99692 (2021-04-16)
Chemical inhibitors of the deubiquitinase USP7 are currently being developed as anticancer agents based on their capacity to stabilize P53. Regardless of this activity, USP7 inhibitors also generate DNA damage in a p53-independent manner. However, the mechanism of this genotoxicity
Christian R Loehberg et al.
Cancer research, 67(24), 12026-12033 (2007-12-20)
The use of agents to prevent the onset of and/or the progression to breast cancer has the potential to lower breast cancer risk. We have previously shown that the tumor-suppressor gene p53 is a potential mediator of hormone (estrogen/progesterone)-induced protection
Daniel Wells et al.
eLife, 9 (2020-08-04)
During meiosis, homologous chromosomes pair and recombine, enabling balanced segregation and generating genetic diversity. In many vertebrates, double-strand breaks (DSBs) initiate recombination within hotspots where PRDM9 binds, and deposits H3K4me3 and H3K36me3. However, no protein(s) recognising this unique combination of
Lei Zhang et al.
Methods in molecular biology (Clifton, N.J.), 1896, 231-250 (2018-11-27)
Nuclear factor κB (NF-κB) is a family of transcription factors important for regulating innate and adaptive immunity, cellular proliferation, apoptosis and senescence. The NF-κB family is comprised of five subunits, RelA/p65, RelB, C-Rel, p50 (p105/NF-κB1), and p52 (p100/NF-κB2). NF-κB activity
Sonja J Gill et al.
PloS one, 10(10), e0140988-e0140988 (2015-10-28)
Ewing's sarcoma is a malignant pediatric bone tumor with a poor prognosis for patients with metastatic or recurrent disease. Ewing's sarcoma cells are acutely hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibition and this is being evaluated in clinical trials, although
Zachary Mirman et al.
Nature, 560(7716), 112-116 (2018-07-20)
In DNA repair, the resection of double-strand breaks dictates the choice between homology-directed repair-which requires a 3' overhang-and classical non-homologous end joining, which can join unresected ends1,2. BRCA1-mutant cancers show minimal resection of double-strand breaks, which renders them deficient in
Lucy H Swift et al.
Biology of the cell, 108(5), 127-148 (2016-02-13)
Checkpoint adaptation (entry into mitosis with damaged DNA) is a process that links arrest at the G2/M cell cycle checkpoint and cell death in cancer cells. It is not known, however, whether cells treated with the genotoxic agent, cisplatin, undergo
Selvakumar Anbalagan et al.
Scientific reports, 11(1), 7119-7119 (2021-03-31)
Recent clinical trials in breast and prostate cancer have established that fewer, larger daily doses (fractions) of radiotherapy are safe and effective, but these do not represent personalised dosing on a patient-by-patient basis. Understanding cell and molecular mechanisms determining fraction
Ning Wang et al.
Scientific reports, 7(1), 10011-10011 (2017-09-01)
Multiple labs have reported that mammalian ovaries contain oogonial stem cells (OSCs), which can differentiate into oocytes that fertilize to produce offspring. However, the physiological relevance of these observations to adult ovarian function is unknown. Here we performed targeted and
Jay Oza et al.
The Journal of biological chemistry, 291(44), 22881-22893 (2016-10-30)
Induction of DNA damage induces a dynamic repair process involving DNA repair factors and epigenetic regulators. Chromatin alterations must occur for DNA repair factors to gain access to DNA lesions and restore original chromatin configuration to preserve the gene expression
Seong-Ok Lee et al.
The Journal of biological chemistry, 299(8), 105043-105043 (2023-07-15)
The ubiquitin signaling pathway is crucial for the DNA damage response pathway. More specifically, RNF168 is integral in regulating DNA repair proteins at damaged chromatin. However, the detailed mechanism by which RNF168 is regulated in cells is not fully understood.
Paola Scaffidi et al.
Nature cell biology, 10(4), 452-459 (2008-03-04)
The premature-ageing disease Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A. Progerin is also expressed sporadically in wild-type cells and has been linked to physiological ageing. Cells
Birgit Lohberger et al.
Oncology letters, 21(6), 428-428 (2021-04-20)
Chondrosarcomas represent a heterogeneous group of primary bone cancers that are characterized by hyaline cartilaginous neoplastic tissue and are predominantly resistant to radiation and chemotherapy. However, adjuvant radiotherapy is often recommended in inoperable cases or after incomplete resections. To improve
Sophie Gay et al.
Molecular cell, 70(4), 628-638 (2018-05-19)
Cell survival to replication stress depends on the activation of the Mec1ATR-Rad53 checkpoint response that protects the integrity of stalled forks and controls the origin firing program. Here we found that Mad2, a member of the spindle assembly checkpoint (SAC), contributes
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