Role of Chromatin Remodeling by RAD54 in DNA Damage Repair and Homologous Recombination

2003 ◽  
Author(s):  
Mariela Jaskelioff
Keyword(s):  
Dna Damage ◽  
Homologous Recombination ◽  
Chromatin Remodeling ◽  
Dna Damage Repair ◽  
Damage Repair

scholarly journals Metabolomics Reveals Aging-associated Attenuation of Noninvasive Radiation Biomarkers in Mice: Potential Role of Polyamine Catabolism and Incoherent DNA Damage-repair

2013 ◽  
Vol 12 (5) ◽  
pp. 2269-2281 ◽  
Author(s):  
Soumen K. Manna ◽  
Kristopher W. Krausz ◽  
Jessica A. Bonzo ◽  
Jeffrey R. Idle ◽  
Frank J. Gonzalez
Keyword(s):  
Dna Damage ◽  
Potential Role ◽  
Dna Damage Repair ◽  
Polyamine Catabolism ◽  
Damage Repair

Investigating the Role of SF3B1 Mutations in DNA Damage Repair in Myeloid Malignancies

2017 ◽  
Vol 55 ◽  
pp. S159-S160
Author(s):  
K. Lappin ◽  
F. Liberante ◽  
K. Savage ◽  
K. Mills
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Myeloid Malignancies ◽  
Damage Repair

The Rad17 homologue ofArabidopsisis involved in the regulation of DNA damage repair and homologous recombination

2004 ◽  
Vol 38 (6) ◽  
pp. 954-968 ◽  
Author(s):  
Fabian Heitzeberg ◽  
I-Peng Chen ◽  
Frank Hartung ◽  
Nadiya Orel ◽  
Karel J. Angelis ◽  
...  
Keyword(s):  
Dna Damage ◽  
Homologous Recombination ◽  
Dna Damage Repair ◽  
Damage Repair

Abstract 2039: The role of HORMAD1 in DNA damage repair in squamous cell carcinomas

2021 ◽  
Author(s):  
Jennifer Gantchev ◽  
Amelia Martinez Villarreal ◽  
Brandon Ramchatesingh ◽  
Ivan V. Litvinov
Keyword(s):  
Dna Damage ◽  
Squamous Cell ◽  
Dna Damage Repair ◽  
Squamous Cell Carcinomas ◽  
Damage Repair

scholarly journals Differentiation of Human Induced Pluripotent or Embryonic Stem Cells Decreases the DNA Damage Repair by Homologous Recombination

2017 ◽  
Vol 9 (5) ◽  
pp. 1660-1674 ◽  
Author(s):  
Kalpana Mujoo ◽  
Raj K. Pandita ◽  
Anjana Tiwari ◽  
Vijay Charaka ◽  
Sharmistha Chakraborty ◽  
...  
Keyword(s):  
Stem Cells ◽  
Dna Damage ◽  
Embryonic Stem Cells ◽  
Homologous Recombination ◽  
Dna Damage Repair ◽  
Embryonic Stem ◽  
Damage Repair ◽  
Induced Pluripotent

scholarly journals SIRT7-mediated ATM deacetylation is essential for its deactivation and DNA damage repair

2019 ◽  
Vol 5 (3) ◽  
pp. eaav1118 ◽  
Author(s):  
Ming Tang ◽  
Zhiming Li ◽  
Chaohua Zhang ◽  
Xiaopeng Lu ◽  
Bo Tu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Repair ◽  
Class Iii ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Repair ◽  
Damage Response ◽  
Late Stages

The activation of ataxia-telangiectasia mutated (ATM) upon DNA damage involves a cascade of reactions, including acetylation by TIP60 and autophosphorylation. However, how ATM is progressively deactivated after completing DNA damage repair remains obscure. Here, we report that sirtuin 7 (SIRT7)–mediated deacetylation is essential for dephosphorylation and deactivation of ATM. We show that SIRT7, a class III histone deacetylase, interacts with and deacetylates ATM in vitro and in vivo. In response to DNA damage, SIRT7 is mobilized onto chromatin and deacetylates ATM during the late stages of DNA damage response, when ATM is being gradually deactivated. Deacetylation of ATM by SIRT7 is prerequisite for its dephosphorylation by its phosphatase WIP1. Consequently, depletion of SIRT7 or acetylation-mimic mutation of ATM induces persistent ATM phosphorylation and activation, thus leading to impaired DNA damage repair. Together, our findings reveal a previously unidentified role of SIRT7 in regulating ATM activity and DNA damage repair.

scholarly journals Regulation and pharmacological targeting of RAD51 in cancer

NAR Cancer ◽  
2020 ◽  
Vol 2 (3) ◽  
Author(s):  
McKenzie K Grundy ◽  
Ronald J Buckanovich ◽  
Kara A Bernstein
Keyword(s):  
Ovarian Cancer ◽  
Dna Damage ◽  
Homologous Recombination ◽  
Patient Outcomes ◽  
Cancer Biology ◽  
Cancer Resistance ◽  
Breast And Ovarian Cancer ◽  
Resistance To Therapy ◽  
Damage Repair

Abstract Regulation of homologous recombination (HR) is central for cancer prevention. However, too little HR can increase cancer incidence, whereas too much HR can drive cancer resistance to therapy. Importantly, therapeutics targeting HR deficiency have demonstrated a profound efficacy in the clinic improving patient outcomes, particularly for breast and ovarian cancer. RAD51 is central to DNA damage repair in the HR pathway. As such, understanding the function and regulation of RAD51 is essential for cancer biology. This review will focus on the role of RAD51 in cancer and beyond and how modulation of its function can be exploited as a cancer therapeutic.

scholarly journals Long noncoding RNA HCP5 participates in premature ovarian insufficiency by transcriptionally regulating MSH5 and DNA damage repair via YB1

2020 ◽  
Vol 48 (8) ◽  
pp. 4480-4491 ◽  
Author(s):  
Xiaoyan Wang ◽  
Xinyue Zhang ◽  
Yujie Dang ◽  
Duan Li ◽  
Gang Lu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Noncoding Rna ◽  
Dna Damage Repair ◽  
Noncoding Rnas ◽  
Epigenetic Mechanism ◽  
Premature Ovarian Insufficiency ◽  
Genetic Etiology ◽  
Ovarian Insufficiency ◽  
Damage Repair

Abstract The genetic etiology of premature ovarian insufficiency (POI) has been well established to date, however, the role of long noncoding RNAs (lncRNAs) in POI is largely unknown. In this study, we identified a down-expressed lncRNA HCP5 in granulosa cells (GCs) from biochemical POI (bPOI) patients, which impaired DNA damage repair and promoted apoptosis of GCs. Mechanistically, we discovered that HCP5 stabilized the interaction between YB1 and its partner ILF2, which could mediate YB1 transferring into the nucleus of GCs. HCP5 silencing affected the localization of YB1 into nucleus and reduced the binding of YB1 to the promoter of MSH5 gene, thereby diminishing MSH5 expression. Taken together, we identified that the decreased expression of HCP5 in bPOI contributed to dysfunctional GCs by regulating MSH5 transcription and DNA damage repair via the interaction with YB1, providing a novel epigenetic mechanism for POI pathogenesis.

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