Disease relevance of Ddb1

• DNA repair protein Ku80 suppresses chromosomal aberrations and malignant transformation [1].
• DNA repair defects in XP-D are associated with two additional, quite different diseases; XP, a sun-sensitive and cancer-prone repair disorder, and Cockayne syndrome (CS), a photosensitive condition characterized by physical and mental retardation and wizened facial appearance [2].
• DNA repair proteins affect the lifecycle of herpes simplex virus 1 [3].
• DNA repair in the c-myc proto-oncogene locus: possible involvement in susceptibility or resistance to plasmacytoma induction in BALB/c mice [4].
• DNA repair and repair fidelity in metastatic variants of the B16 murine melanoma [5].

High impact information on Ddb1

• DNA repair, genome stability, and aging [6].
• DNA repair was examined in the c-abl and c-mos proto-oncogenes in UV-irradiated mouse 3T3 fibroblasts using an optimized assay for measuring pyrimidine dimers in single-copy nucleotide sequences [7].
• DNA repair correlates with cell survival and is repressed by 25 microM LY294002, an inhibitor of DNA-activated protein kinases [8].
• Growth Retardation, DNA Repair Defects, and Lack of Spermatogenesis in BRCA1-Deficient Mice [9].
• DNA repair is almost completely blocked in PARP-deficient thymocytes regardless of p53 status [10].

Chemical compound and disease context of Ddb1

• The Effect of 3-Methyladenine DNA Glycosylase-Mediated DNA Repair on the Induction of Toxicity and Diabetes by the {beta}-Cell Toxicant Streptozotocin [11].
• DNA repair synthesis induced in permeable mouse ascites sarcoma cells by peplomycin, an antitumor antibiotic, was studied [12].

Biological context of Ddb1

• Reverse transcription-coupled polymerase chain reaction (RT-PCR) showed that mouse Ddb1 messenger is ubiquitously expressed in adult tissues as well as in embryo's. The gene was mapped to near the public locus D19Mit22 region of mouse chromosome 19 [13].
• A cDNA for the 127 kDa UV-damaged DNA-binding protein (p127-Ddb1) was isolated from a mouse fetal brain full length-enriched cDNA library, and an open reading frame of 1140 amino acids was identified [13].
• DNA repair defects associated with chromosomal translocation breaksite regions [14].
• DNA repair is activated in early stages of p53-induced apoptosis [15].
• DNA repair kinetics study suggests that NPM has a role in reducing the susceptibility of chromosomal DNA to damage rather than promoting DNA damage repair [16].

Anatomical context of Ddb1

• DNA repair gene Ercc1 is essential for normal spermatogenesis and oogenesis and for functional integrity of germ cell DNA in the mouse [17].
• DNA repair defect in poly(ADP-ribose) polymerase-deficient cell lines [18].
• DNA repair was assessed by: (i) the unscheduled DNA synthesis (UDS) assay, which measures [(3)H]thymidine incorporation into hepatocyte DNA undergoing excision repair; (ii) the Comet assay, which detects DNA strand breaks transiently produced between the incision and rejoining steps of the excision repair process [19].
• DNA repair capacity directly correlated with cell survival (p < 0.05) and with metastatic potential in the K-1735 clones and somatic cell hybrids (p < 0.05) [20].
• DNA repair and carcinogen binding are quantitatively similar in cultured cells of SENCAR and more resistant mouse strains [21].

Associations of Ddb1 with chemical compounds

• DNA repair synthesis was elicited by 15 alkaloids, including 11 of unknown carcinogenicity, i.e., senecionine, seneciphylline, jacobine, epoxyseneciphylline, senecicannabine, acetylfukinotoxin, syneilesine, dihydroclivorine, ligularidine, neoligularidine, and ligularizine [22].
• DNA repair synthesis was elicited by several compounds of unknown carcinogenicity, 5,6- dimethoxysterigmatocystin , versicolorins A and B, averufin , xanthomegnin , luteosporin , and chrysazin , as well as by the carcinogenic myocotoxins , aflatoxin B1, sterigmatocystin, luteoskyrin , ochratoxin A, azaserine, mitomycin C, and actinomycin D [23].
• Cyclin-Dependent Kinase 2 Functions in Normal DNA Repair and Is a Therapeutic Target in BRCA1-Deficient Cancers [24].
• DNA repair protein MGMT protects against N-methyl-N-nitrosourea-induced conversion of benign into malignant tumors [25].
• It also acted upon AP sites; however, no significant excision of 8-hydroxyguanine was observed [Rosenquist, T. A., Zaika, E., Fernandes, A. S., Zharkov, D. O., Miller, H., and Grollman, A. P. (2003) DNA Repair 2, 581-591] [26].

Other interactions of Ddb1

• Homology-directed dna repair, mitomycin-c resistance, and chromosome stability is restored with correction of a Brca1 mutation [27].
• DNA repair methyltransferase (Mgmt) knockout mice are sensitive to the lethal effects of chemotherapeutic alkylating agents [28].
• DNA repair deficient mice (SCID and PARP-1) with elevated levels of single and double-strand DNA breaks have spontaneously elevated ESTR mutation frequencies, and surprisingly do not show additional ESTR mutation induction following irradiation [29].
• Early decrease in dna repair proteins, Ku70 and Ku86, and subsequent DNA fragmentation after transient focal cerebral ischemia in mice [30].
• DNA repair proteins (protein involved in DNA double-strand break repair, Rad23 UV excision repair protein homologue and ubiquitin-conjugating enzyme); and (4). cell-surface antigens (lamimin receptor 1) [31].

Analytical, diagnostic and therapeutic context of Ddb1

• DNA repair synthesis was measured autoradiographically in organ cultures of the tumor, lung, and skin, exposed to chemical carcinogens or UV radiation [32].
• DNA repair status is recognized as an important determinant of the clinical efficacy of cancer chemotherapy [33].
• DNA repair was rapid during the first 5 h after treatment and slow thereafter [34].
• DNA repair in bleomycin-pretreated, permeable mouse sarcoma (SR-C3H/He) cells requires ATP for at least two steps, the repair DNA synthesis step and the repair patch ligation step [35].

References