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398 results on '"Dianov, Grigory L."'

2. DNA polymerase δ-dependent repair of DNA single strand breaks containing 3′-end proximal lesions

Author

Parsons, Jason L, Preston, Bradley D, O'Connor, Timothy R, and Dianov, Grigory L

Subjects
Biological Sciences, Environmental Sciences, Chemical Sciences, Genetics, Aetiology, 2.1 Biological and endogenous factors, Generic health relevance, Animals, Cells, Cultured, DNA Breaks, Single-Stranded, DNA Ligases, DNA Polymerase III, DNA Polymerase beta, DNA Repair, Exodeoxyribonucleases, HeLa Cells, Humans, Hypoxanthine, Mice, Mutation, Uracil, Hela Cells, Information and Computing Sciences, Developmental Biology, Biological sciences, Chemical sciences, Environmental sciences
Abstract

Base excision repair (BER) is the major pathway for the repair of simple, non-bulky lesions in DNA that is initiated by a damage-specific DNA glycosylase. Several human DNA glycosylases exist that efficiently excise numerous types of lesions, although the close proximity of a single strand break (SSB) to a DNA adduct can have a profound effect on both BER and SSB repair. We recently reported that DNA lesions located as a second nucleotide 5'-upstream to a DNA SSB are resistant to DNA glycosylase activity and this study further examines the processing of these 'complex' lesions. We first demonstrated that the damaged base should be excised before SSB repair can occur, since it impaired processing of the SSB by the BER enzymes, DNA ligase IIIalpha and DNA polymerase beta. Using human whole cell extracts, we next isolated the major activity against DNA lesions located as a second nucleotide 5'-upstream to a DNA SSB and identified it as DNA polymerase delta (Pol delta). Using recombinant protein we confirmed that the 3'-5'-exonuclease activity of Pol delta can efficiently remove these DNA lesions. Furthermore, we demonstrated that mouse embryonic fibroblasts, deficient in the exonuclease activity of Pol delta are partially deficient in the repair of these 'complex' lesions, demonstrating the importance of Pol delta during the repair of DNA lesions in close proximity to a DNA SSB, typical of those induced by ionizing radiation.

Published
2007

25. NEIL1 is the major DNA glycosylase that processes 5-hydroxyuracil in the proximity of a DNA single-strand break

Author

Parsosn, Jason L., Kavli, Bodil, Slupphaug, Geir, and Dianov, Grigory L.

Subjects
Polymerase chain reaction -- Research, Ligases -- Research, Biological sciences, Chemistry
Abstract

The repair of DNA substrates containing 5-OHU lesions in the proximity of the 3'-end of a single strand break (SSB) was examined. It was found that SSB repair by DNA ligase III[alpha] and DNA polymerase [beta] is impaired by the presence of the nearby 5-OHU lesion.

Published
2007

33. Exchangeability of mammalian DNA ligases between base excision repair pathways

Author

Sleeth, Kate M., Robson, Robert L., and Dianov, Grigory L.

Subjects
Mammals -- Genetic aspects, DNA -- Research, Ligases -- Research, Biological sciences, Chemistry
Abstract

DNA ligase IIIalpha and DNA ligase I participate in the short- and long- patch base excision repair pathways in a mammalian cell respectively. Immunodepletion of DNA ligase I did not affect the short-patch repair pathways but blocked long-patch repair, suggesting that DNA ligase IIIalpha is not able to substitute DNA ligase I during long-patch repair are indicated by the findings.

Published
2004

40. Biochemical characterization of the WRN-FEN-1 functional interaction

Author

Brosh, Robert M., Jr., Driscoll, Henry C., Dianov, Grigory L., and Sommers, Joshua A.

Subjects
Biochemistry -- Research, Nucleases -- Genetic aspects, Exonucleases -- Genetic aspects, DNA repair -- Genetic aspects, Biological sciences, Chemistry
Abstract

Research has been conducted on the WRN-5' flap endonuclease/5'-3' exonuclease functional interaction. The mechanistic aspects of this interaction have been investigated and the ability of WRN to stimulate 5' flap endonuclease/5'-3' exonuclease structure cleavage has been tested and is discussed.

Published
2002

43. DNA synthesis and dRPase activities of polymerase beta are both essential for single-nucleotide patch base excision repair in mammalian cell extracts

Author

Podlutsky, Andrej Ja., Dianova, Irina I., Wilson, Samuel H., Bohr, Vilhelm A., and Dianov, Grigory L.

Subjects
DNA repair -- Research, DNA polymerases -- Research, Biological sciences, Chemistry
Abstract

Mammalian DNA polymerase beta appears to be the only enzyme that can remove the 5' deoxyribose and simultaneously add a single nucleotide to the 3'-end of the nick during base excision repair. No other cellular enzymes can perform this function.

Published
2001

46. Src‐mediated phosphorylation of GAPDH regulates its nuclear localization and cellular response to DNA damage

Author

Ci, Shusheng, primary, Xia, Wen, additional, Liang, Weichu, additional, Qin, Lihong, additional, Zhang, Yilan, additional, Dianov, Grigory L., additional, Wang, Meina, additional, Zhao, Xingqi, additional, Wu, Congye, additional, Alagamuthu, Karthick Kumar, additional, Hu, Zhigang, additional, He, Lingfeng, additional, Pan, Feiyan, additional, and Guo, Zhigang, additional

Published
2020
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48. DNA base excision repair in human malaria parasites is predominantly by a long-patch pathway

Author

Haltiwanger, Brett M., Matsumoto, Yoshihiro, Nicolas, Emmanuelle, Dianov, Grigory L., Bohr, Vilhelm A., and Taraschi, Theodore F.

Subjects
Biochemistry -- Research, DNA -- Research, Malaria -- Physiological aspects, Cell research -- Analysis, Biological sciences, Chemistry
Abstract

Research has been conducted on the pathways of mammalian cells repair apurinic/apyrimidinic sites in DNA. Results demonstrate the ability of the a cell-free lysate to remove uracil and repair apurinic/apyrimidinic sites.

Published
2000

49. Replication protein A stimulates proliferating cell nuclear antigen-dependent repair of abasic sites in DNA by human cell extracts

Author

Dianov, Grigory L., Jensen, Bente R., Kenny, Mark K., and Bohr, Vilhelm A.

Subjects
Antigens -- Research, Cell proliferation -- Research, Chromosome replication -- Research, DNA repair -- Research, Human cell culture -- Research, Biological sciences, Chemistry
Abstract

Research was conducted to examine the role of replication protein A (RPA) in proliferating cell nuclear antigen (PCNA)-dependent, long-patch base excision repair pathways of apurinic/apyrimidinic (AP) sites in human cell extracts. An assay was developed for PCNA-dependent repair to directly address the role of RPA in a PCNA-dependent repair reaction. Results suggest that RPA stimulates the PCNA-dependent repair of AP sites in a crude protein fraction from human cells.

Published
1999

50. Sp1 phosphorylation by ATM downregulates BER and promotes cell elimination in response to persistent DNA damage

Author

Fletcher, Sally C, Grou, Claudia P, Legrand, Arnaud J, Chen, Xin, Soderstrom, Kalle, Poletto, Mattia, and Dianov, Grigory L

Subjects
Male, DNA Repair, Sp1 Transcription Factor, Down-Regulation, Apoptosis, Ataxia Telangiectasia Mutated Proteins, Genome Integrity, Repair and Replication, Killer Cells, Natural, X-ray Repair Cross Complementing Protein 1, Serine, Humans, Phosphorylation, Cells, Cultured, DNA Damage
Abstract

ATM (ataxia-telangiectasia mutated) is a central molecule for DNA quality control. Its activation by DNA damage promotes cell-cycle delay, which facilitates DNA repair prior to replication. On the other hand, persistent DNA damage has been implicated in ATM-dependent cell death via apoptosis; however, the mechanisms underlying this process remain elusive. Here we find that, in response to persistent DNA strand breaks, ATM phosphorylates transcription factor Sp1 and initiates its degradation. We show that Sp1 controls expression of the key base excision repair gene XRCC1, essential for DNA strand break repair. Therefore, degradation of Sp1 leads to a vicious cycle that involves suppression of DNA repair and further aggravation of the load of DNA damage. This activates transcription of pro-apoptotic genes and renders cells susceptible to elimination via both apoptosis and natural killer cells. These findings constitute a previously unrecognized ‘gatekeeper’ function of ATM as a detector of cells with persistent DNA damage.

Published
2017

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