scholarly journals Epigenomic maintenance through dietary intervention can facilitate DNA repair process to slow down the progress of premature aging

IUBMB Life ◽  
2016 ◽  
Vol 68 (9) ◽  
pp. 717-721 ◽  
Author(s):  
Shampa Ghosh ◽  
Jitendra Kumar Sinha ◽  
Manchala Raghunath
Keyword(s):  
Dna Repair ◽  
Dietary Intervention ◽  
Repair Process ◽  
Premature Aging

DNA Repair and Transcription in Human Premature Aging Disorders

1998 ◽  
Vol 3 (1) ◽  
pp. 11-13 ◽  
Author(s):  
Vilhelm A Bohr ◽  
Grigoiy Dianov ◽  
Adayabalam Balajee ◽  
Alfred May ◽  
David K Orren
Keyword(s):  
Dna Repair ◽  
Premature Aging

scholarly journals a/alpha-control of DNA repair in the yeast Saccharomyces cerevisiae: genetic and physiological aspects.

Genetics ◽  
1993 ◽  
Vol 133 (3) ◽  
pp. 489-498 ◽  
Author(s):  
M Heude ◽  
F Fabre
Keyword(s):  
Dna Repair ◽  
Gamma Rays ◽  
Repair Process ◽  
Yeast Saccharomyces Cerevisiae ◽  
Dna Structures ◽  
Induced Mutagenesis ◽  
Error Prone Repair ◽  
G2 Phase ◽  
Mat Locus ◽  
Mat Genes

Abstract It has long been known that diploid strains of yeast are more resistant to gamma-rays than haploid cells, and that this is in part due to heterozygosity at the mating type (MAT) locus. It is shown here that the genetic control exerted by the MAT genes on DNA repair involves the a1 and alpha 2 genes, in a RME1-independent way. In rad18 diploids, affected in the error-prone repair, the a/alpha effects are of a very large amplitude, after both UV and gamma-rays, and also depends on a1 and alpha 2. The coexpression of a and alpha in rad18 haploids suppresses the sensitivity of a subpopulation corresponding to the G2 phase cells. Related to this, the coexpression of a and alpha in RAD+ haploids depresses UV-induced mutagenesis in G2 cells. For srs2 null diploids, also affected in the error-prone repair pathway, we show that their G1 UV sensitivity, likely due to lethal recombination events, is partly suppressed by MAT homozygosity. Taken together, these results led to the proposal that a1-alpha 2 promotes a channeling of some DNA structures from the mutagenic into the recombinational repair process.

scholarly journals Molecular cloning and chromosomal localization of DNA sequences associated with a human DNA repair gene.

1985 ◽  
Vol 5 (2) ◽  
pp. 398-405 ◽  
Author(s):  
J S Rubin ◽  
V R Prideaux ◽  
H F Willard ◽  
A M Dulhanty ◽  
G F Whitmore ◽  
...  
Keyword(s):  
Dna Repair ◽  
Dna Sequences ◽  
Chromosomal Localization ◽  
Excision Repair ◽  
Repair Process ◽  
Human Cells ◽  
Gene Products ◽  
Repair Gene ◽  
Human Dna ◽  
Dna Repair Gene

The genes and gene products involved in the mammalian DNA repair processes have yet to be identified. Toward this end we made use of a number of DNA repair-proficient transformants that were generated after transfection of DNA from repair-proficient human cells into a mutant hamster line that is defective in the initial incision step of the excision repair process. In this report, biochemical evidence is presented that demonstrates that these transformants are repair proficient. In addition, we describe the molecular identification and cloning of unique DNA sequences closely associated with the transfected human DNA repair gene and demonstrate the presence of homologous DNA sequences in human cells and in the repair-proficient DNA transformants. The chromosomal location of these sequences was determined by using a panel of rodent-human somatic cell hybrids. Both unique DNA sequences were found to be on human chromosome 19.

Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction

2021 ◽  
Author(s):  
Mansoor Hussain ◽  
Sudarshan Krishnamurthy ◽  
Jaimin Patel ◽  
Edward Kim ◽  
Beverly A. Baptiste ◽  
...  
Keyword(s):  
Dna Repair ◽  
Mitochondrial Dysfunction ◽  
Premature Aging ◽  
Skin Abnormalities

scholarly journals The emerging role of RNAs in DNA damage repair

2017 ◽  
Vol 24 (4) ◽  
pp. 580-587 ◽  
Author(s):  
Ben R Hawley ◽  
Wei-Ting Lu ◽  
Ania Wilczynska ◽  
Martin Bushell
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Critical Role ◽  
Repair Process ◽  
Rna Molecules ◽  
Processing Enzymes ◽  
Damage Repair ◽  
New Findings ◽  
Integral Role ◽  
Repair Mechanisms

Abstract Many surveillance and repair mechanisms exist to maintain the integrity of our genome. All of the pathways described to date are controlled exclusively by proteins, which through their enzymatic activities identify breaks, propagate the damage signal, recruit further protein factors and ultimately resolve the break with little to no loss of genetic information. RNA is known to have an integral role in many cellular pathways, but, until very recently, was not considered to take part in the DNA repair process. Several reports demonstrated a conserved critical role for RNA-processing enzymes and RNA molecules in DNA repair, but the biogenesis of these damage-related RNAs and their mechanisms of action remain unknown. We will explore how these new findings challenge the idea of proteins being the sole participants in the response to DNA damage and reveal a new and exciting aspect of both DNA repair and RNA biology.

scholarly journals A new role for a tumor-suppressing protein

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jeremy S Setton ◽  
Simon N Powell
Keyword(s):  
Dna Repair ◽  
Stress Response ◽  
Replication Stress ◽  
Repair Process ◽  
Protein P53

In addition to its role in preventing tumors, the protein p53 appears to participate in a DNA repair process known as the replication-stress response.

scholarly journals A Review on DNA Repair Inhibition by PARP Inhibitors in Cancer Therapy

Folia Medica ◽  
2018 ◽  
Vol 60 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Ashish P. Shah ◽  
Chhagan N. Patel ◽  
Dipen K. Sureja ◽  
Kirtan P. Sanghavi
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Cancer Therapy ◽  
Repair Process ◽  
Parp Inhibitors ◽  
Brca Mutations ◽  
Development Of Resistance ◽  
Damage Repair ◽  
Future Therapy

AbstractThe DNA repair process protects the cells from DNA damaging agent by multiple pathways. Majority of the cancer therapy cause DNA damage which leads to apoptosis. The cell has natural ability to repair this damage which ultimately leads to development of resistance of drugs. The key enzymes involved in DNA repair process are poly(ADP-ribose) (PAR) and poly(ADP-ribose) polymerases (PARP). Tumor cells repair their defective gene via defective homologues recombination (HR) in the presence of enzyme PARP. PARP inhibitors inhibit the enzyme poly(ADP-ribose) polymerases (PARPs) which lead to apoptosis of cancer cells. Current clinical data shows the role of PARP inhibitors is not restricted to BRCA mutations but also effective in HR dysfunctions related tumors. Therefore, investigation in this area could be very helpful for future therapy of cancer. This review gives detail information on the role of PARP in DNA damage repair, the role of PARP inhibitors and chemistry of currently available PARP inhibitors.

scholarly journals Clustered DNA Damage: Electronic Properties and Their Influence on Charge Transfer. 7,8-Dihydro-8-Oxo-2′-Deoxyguaosine Versus 5′,8-Cyclo-2′-Deoxyadenosines: A Theoretical Approach

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 424 ◽  
Author(s):  
Boleslaw T. Karwowski
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Charge Transfer ◽  
Human Cancer ◽  
Double Helix ◽  
Proximal Part ◽  
Repair Process ◽  
Dna Lesions ◽  
Human Cancer Cells ◽  
Order Of Magnitude

Approximately 3 × 1017 DNA damage events take place per hour in the human body. Within clustered DNA lesions, they pose a serious problem for repair proteins, especially for iron–sulfur glycosylases (MutyH), which can recognize them by the electron-transfer process. It has been found that the presence of both 5′,8-cyclo-2′-deoxyadenosine (cdA) diastereomers in the ds-DNA structure, as part of a clustered lesion, can influence vertical radical cation distribution within the proximal part of the double helix, i.e., d[~oxoGcAoxoG~] (7,8-dihydro-8-oxo-2′-deoxyguaosine - oxodG). Here, the influence of cdA, “the simplest tandem lesion”, on the charge transfer through ds-DNA was taken into theoretical consideration at the M062x/6-31+G** level of theory in the aqueous phase. It was shown that the presence of (5′S)- or (5′R)-cdA leads to a slowdown in the hole transfer by one order of magnitude between the neighboring dG→oxodG in comparison to “native” ds-DNA. Therefore, it can be concluded that such clustered lesions can lead to defective damage recognition with a subsequent slowing down of the DNA repair process, giving rise to an increase in mutations. As a result, the unrepaired, oxodG: dA base pair prior to genetic information replication can finally result in GC → TA or AT→CG transversion. This type of mutation is commonly observed in human cancer cells. Moreover, because local multiple damage sites (LMSD) are effectively produced as a result of ionization factors, the presented data in this article might be useful in developing a new scheme of radiotherapy treatment against the background of DNA repair efficiency.

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