scholarly journals Role of chromodomain helicase DNA-binding protein 2 in DNA damage response signaling and tumorigenesis

Oncogene ◽  
2009 ◽  
Vol 28 (8) ◽  
pp. 1053-1062 ◽  
Author(s):  
P Nagarajan ◽  
T M Onami ◽  
S Rajagopalan ◽  
S Kania ◽  
R Donnell ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Binding ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Damage Response

scholarly journals FBXL5-mediated degradation of single-stranded DNA-binding protein hSSB1 controls DNA damage response

2014 ◽  
Vol 42 (18) ◽  
pp. 11560-11569 ◽  
Author(s):  
Zhi-Wei Chen ◽  
Bin Liu ◽  
Nai-Wang Tang ◽  
Yun-Hua Xu ◽  
Xiang-Yun Ye ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Binding ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Single Stranded Dna ◽  
Damage Response

scholarly journals DDB2 (Damaged-DNA binding protein 2) in nucleotide excision repair and DNA damage response

Cell Cycle ◽  
2009 ◽  
Vol 8 (24) ◽  
pp. 4067-4071 ◽  
Author(s):  
Tanya Stoyanova ◽  
Nilotpal Roy ◽  
Dragana Kopanja ◽  
Pradip Raychaudhuri ◽  
Srilata Bagchi
Keyword(s):  
Dna Damage ◽  
Dna Binding ◽  
Nucleotide Excision Repair ◽  
Dna Damage Response ◽  
Excision Repair ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Nucleotide Excision ◽  
Damage Response ◽  
Damaged Dna

scholarly journals Human single-stranded DNA binding protein 1 (hSSB1, OBFC2B), a critical component of the DNA damage response

2019 ◽  
Vol 86 ◽  
pp. 121-128 ◽  
Author(s):  
Laura V. Croft ◽  
Emma Bolderson ◽  
Mark N. Adams ◽  
Serene El-Kamand ◽  
Ruvini Kariawasam ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Binding ◽  
Dna Damage Response ◽  
Binding Protein ◽  
Dna Binding Protein ◽  
Critical Component ◽  
Single Stranded Dna ◽  
Damage Response

scholarly journals FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein

Blood ◽  
2007 ◽  
Vol 110 (7) ◽  
pp. 2390-2398 ◽  
Author(s):  
Rigu Gupta ◽  
Sudha Sharma ◽  
Joshua A. Sommers ◽  
Mark K. Kenny ◽  
Sharon B. Cantor ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Binding ◽  
Binding Protein ◽  
Critical Role ◽  
Protein A ◽  
Replication Protein A ◽  
Dna Binding Protein ◽  
Replication Protein ◽  
Single Stranded Dna

The BRCA1 associated C-terminal helicase (BACH1, designated FANCJ) is implicated in the chromosomal instability genetic disorder Fanconi anemia (FA) and hereditary breast cancer. A critical role of FANCJ helicase may be to restart replication as a component of downstream events that occur during the repair of DNA cross-links or double-strand breaks. We investigated the potential interaction of FANCJ with replication protein A (RPA), a single-stranded DNA-binding protein implicated in both DNA replication and repair. FANCJ and RPA were shown to coimmunoprecipitate most likely through a direct interaction of FANCJ and the RPA70 subunit. Moreover, dependent on the presence of BRCA1, FANCJ colocalizes with RPA in nuclear foci after DNA damage. Our data are consistent with a model in which FANCJ associates with RPA in a DNA damage-inducible manner and through the protein interaction RPA stimulates FANCJ helicase to better unwind duplex DNA substrates. These findings identify RPA as the first regulatory partner of FANCJ. The FANCJ-RPA interaction is likely to be important for the role of the helicase to more efficiently unwind DNA repair intermediates to maintain genomic stability.

scholarly journals p53 Binding Protein 53BP1 Is Required for DNA Damage Responses and Tumor Suppression in Mice

2003 ◽  
Vol 23 (7) ◽  
pp. 2556-2563 ◽  
Author(s):  
Irene M. Ward ◽  
Kay Minn ◽  
Jan van Deursen ◽  
Junjie Chen
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Tumor Suppression ◽  
Binding Protein ◽  
Atm Kinase ◽  
Strand Breaks ◽  
Damage Response ◽  
Dna Strand ◽  
Dna Damage Response Pathway

ABSTRACT 53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53. It relocates to the sites of DNA strand breaks in response to DNA damage and is a putative substrate of the ataxia telangiectasia-mutated (ATM) kinase. To study the biological role of 53BP1, we disrupted the 53BP1 gene in the mouse. We show that, similar to ATM−/− mice, 53BP1-deficient mice were growth retarded, immune deficient, radiation sensitive, and cancer prone. 53BP1−/− cells show a slight S-phase checkpoint defect and prolonged G2/M arrest after treatment with ionizing radiation. Moreover, 53BP1−/− cells feature a defective DNA damage response with impaired Chk2 activation. These data indicate that 53BP1 acts downstream of ATM and upstream of Chk2 in the DNA damage response pathway and is involved in tumor suppression.

scholarly journals DNA Damage Response in Multiple Myeloma: The Role of the Tumor Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 504
Author(s):  
Takayuki Saitoh ◽  
Tsukasa Oda
Keyword(s):  
Multiple Myeloma ◽  
Dna Damage ◽  
Dna Repair ◽  
Tumor Microenvironment ◽  
Dna Damage Response ◽  
Genetic Instability ◽  
Dna Repair Mechanisms ◽  
Damage Response ◽  
Repair Mechanisms

Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by genomic instability. MM cells present various forms of genetic instability, including chromosomal instability, microsatellite instability, and base-pair alterations, as well as changes in chromosome number. The tumor microenvironment and an abnormal DNA repair function affect genetic instability in this disease. In addition, states of the tumor microenvironment itself, such as inflammation and hypoxia, influence the DNA damage response, which includes DNA repair mechanisms, cell cycle checkpoints, and apoptotic pathways. Unrepaired DNA damage in tumor cells has been shown to exacerbate genomic instability and aberrant features that enable MM progression and drug resistance. This review provides an overview of the DNA repair pathways, with a special focus on their function in MM, and discusses the role of the tumor microenvironment in governing DNA repair mechanisms.

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