scholarly journals MSH2 and MSH6 in Mismatch Repair System Account for Soybean (Glycine max (L.) Merr.) Tolerance to Cadmium Toxicity by Determining DNA Damage Response

2020 ◽  
Vol 68 (7) ◽  
pp. 1974-1985 ◽  
Author(s):  
Qiang Zhao ◽  
Hetong Wang ◽  
Yanli Du ◽  
Hilary J. Rogers ◽  
Zhixin Wu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Glycine Max ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Cadmium Toxicity ◽  
Repair System ◽  
Damage Response ◽  
Mismatch Repair System ◽  
Glycine Max L ◽  
Tolerance To Cadmium

scholarly journals Mismatch Repair Processing of Carcinogen-DNA Adducts Triggers Apoptosis

1999 ◽  
Vol 19 (12) ◽  
pp. 8292-8301 ◽  
Author(s):  
Jianxin Wu ◽  
Liya Gu ◽  
Huixian Wang ◽  
Nicholas E. Geacintov ◽  
Guo-Min Li
Keyword(s):  
Dna Damage ◽  
Mismatch Repair ◽  
Repair System ◽  
Apoptotic Response ◽  
Chemical Carcinogens ◽  
P53 Expression ◽  
Dna Mismatch ◽  
Repair Deficiency ◽  
Mismatch Repair System

ABSTRACT The DNA mismatch repair pathway is well known for its role in correcting biosynthetic errors of DNA replication. We report here a novel role for mismatch repair in signaling programmed cell death in response to DNA damage induced by chemical carcinogens. Cells proficient in mismatch repair were highly sensitive to the cytotoxic effects of chemical carcinogens, while cells defective in either human MutS or MutL homologs were relatively insensitive. Since wild-type cells but not mutant cells underwent apoptosis upon treatment with chemical carcinogens, the apoptotic response is dependent on a functional mismatch repair system. By analyzing p53 expression in several pairs of cell lines, we found that the mismatch repair-dependent apoptotic response was mediated through both p53-dependent and p53-independent pathways. In vitro biochemical studies demonstrated that the human mismatch recognition proteins hMutSα and hMutSβ efficiently recognized DNA damage induced by chemical carcinogens, suggesting a direct participation of mismatch repair proteins in mediating the apoptotic response. Taken together, these studies further elucidate the mechanism by which mismatch repair deficiency predisposes to cancer, i.e., the deficiency not only causes a failure to repair mismatches generated during DNA metabolism but also fails to direct damaged and mutation-prone cells to commit suicide.

scholarly journals A novel DNA damage response mediated by DNA mismatch repair in Caenorhabditis elegans: induction of programmed autophagic cell death in non-dividing cells

2015 ◽  
Vol 6 (7-8) ◽  
pp. 341-355 ◽  
Author(s):  
Takahito Moriwaki ◽  
Yuichi Kato ◽  
Chihiro Nakamura ◽  
Satoru Ishikawa ◽  
Qiu-Mei Zhang-Akiyama
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Dna Mismatch Repair ◽  
Autophagic Cell Death ◽  
Dna Mismatch ◽  
Damage Response ◽  
Dividing Cells

The mismatch repair-dependent DNA damage response: Mechanisms and implications

DNA Repair ◽  
2019 ◽  
Vol 78 ◽  
pp. 60-69 ◽  
Author(s):  
Dipika Gupta ◽  
Christopher D. Heinen
Keyword(s):  
Dna Damage ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Damage Response

scholarly journals DNA mismatch repair and the DNA damage response

DNA Repair ◽  
2016 ◽  
Vol 38 ◽  
pp. 94-101 ◽  
Author(s):  
Zhongdao Li ◽  
Alexander H. Pearlman ◽  
Peggy Hsieh
Keyword(s):  
Dna Damage ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Dna Mismatch Repair ◽  
Dna Mismatch ◽  
Damage Response

DNA mismatch repair and the DNA damage response to ionizing radiation: Making sense of apparently conflicting data

2010 ◽  
Vol 36 (7) ◽  
pp. 518-527 ◽  
Author(s):  
Lynn M. Martin ◽  
Brian Marples ◽  
Mary Coffey ◽  
Mark Lawler ◽  
Thomas H. Lynch ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Dna Mismatch Repair ◽  
Dna Mismatch ◽  
Making Sense ◽  
Damage Response

scholarly journals DNMT1 deficiency triggers mismatch repair defects in human cells through depletion of repair protein levels in a process involving the DNA damage response

2011 ◽  
Vol 20 (16) ◽  
pp. 3241-3255 ◽  
Author(s):  
Jayne E.P. Loughery ◽  
Philip D. Dunne ◽  
Karla M. O'Neill ◽  
Richard R. Meehan ◽  
Jennifer R. McDaid ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mismatch Repair ◽  
Dna Damage Response ◽  
Human Cells ◽  
Protein Levels ◽  
Repair Protein ◽  
Damage Response

scholarly journals Exploring the Involvement of FoxM1 in CML Cells from DNA Damage Response-Regulatory Prospective

2021 ◽  
Author(s):  
Lin Du ◽  
Manli Wang ◽  
Hui Li ◽  
Fang Wang
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Dna Damage Response ◽  
Repair System ◽  
Downstream Target ◽  
Damage Repair ◽  
Healthy Donors ◽  
Damage Response ◽  
M Phase ◽  
The Status

Abstract Background FoxM1 is widely accepted as an oncogenesis factor, for it is one of the most frequently upregulated genes in a broad spectrum of human malignancies. Herein, we presented the status of FoxM1 in CML samples and cell lines. Methods We compared FoxM1 abundance and phosphorylation using PB-MNC samples from CML patients and healthy donors. DNA damage response (DDR) was investigated in the presence of oncogene or chemical. Through enforced expression of FoxM1 or lentivirus mediated silencing, we explored the participation of FoxM1 in DDR regulation. Results Overexpression of FoxM1 was only observed in 3 samples from patients of advanced stage. However, hyper-phosphorylation of FoxM1 was evidently detected in the CML cohort. Furtherly, the DNA damage response that in accompany with the formation of Bcr/Abl was responsible for the rise in FoxM1 phosphorylation. Bcr/Abl provoked a modest extent of DNA damage, which, in turn, roused the repair system, mirrored by phosphorylation of the ATM/ATR-CHK1/2 axis. FoxM1 was a downstream target of CHK1 which directly associated with FoxM1 in the presence of DNA damage. Activation of FoxM1 served as a DDR regulator by inducing the expression of Rad51 and Brca1, genes that participated in DNA repair. Depletion of FoxM1 impaired DNA repair, leading to cell cycle arrest in G2/M phase and the onset of apoptosis in a P53-dependent fashion. Finally, our data demonstrated that phosphorylation of FoxM1 did not rely on Bcr/Abl kinase activity. Suppression of FoxM1 showed lethal potential to primary CML cells, and most importantly, the lethality was not affected by the TKIs insensitiveness. Conclusions Abnormality in FoxM1 activity in CML cells enlightened us that constantly present DNA damage rendered leukemia cells more reliant upon the DNA damage repair system. Targeting FoxM1 could be exploit as an alternative strategy to overcome TKIs resistance.

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