Inhibition of poly(ADP-ribose) polymerase (PARP) and ataxia telangiectasia mutated (ATM) on the chemosensitivity of mantle cell lymphoma to agents that induce DNA strand breaks

2011 ◽  
Vol 30 (4) ◽  
pp. 175-179 ◽  
Author(s):  
Radha M. Golla ◽  
Min Li ◽  
Yulei Shen ◽  
Ming Ji ◽  
Ying Yan ◽  
...  
Keyword(s):  
Mantle Cell Lymphoma ◽  
Ataxia Telangiectasia ◽  
Cell Lymphoma ◽  
Dna Strand Breaks ◽  
Ataxia Telangiectasia Mutated ◽  
Strand Breaks ◽  
Mantle Cell ◽  
Dna Strand

scholarly journals Ataxia telangiectasia mutated interacts with Parkin and induces mitophagy independent of kinase activity. Evidence from mantle cell lymphoma

Haematologica ◽  
2020 ◽  
pp. haematol.2019.234385 ◽  
Author(s):  
Aloke Sarkar ◽  
Christine M. Stellrecht ◽  
Hima V. Vangapandu ◽  
Mary Ayres ◽  
Benny A. Kaipparettu ◽  
...  
Keyword(s):  
Mantle Cell Lymphoma ◽  
Ataxia Telangiectasia ◽  
Kinase Activity ◽  
Cell Lymphoma ◽  
Ataxia Telangiectasia Mutated ◽  
Mantle Cell

scholarly journals Hyperthermia Activates a Subset of Ataxia-Telangiectasia Mutated Effectors Independent of DNA Strand Breaks and Heat Shock Protein 70 Status

2007 ◽  
Vol 67 (7) ◽  
pp. 3010-3017 ◽  
Author(s):  
Clayton R. Hunt ◽  
Raj K. Pandita ◽  
Andrei Laszlo ◽  
Ryuji Higashikubo ◽  
Manjula Agarwal ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Ataxia Telangiectasia ◽  
Heat Shock Protein 70 ◽  
Dna Strand Breaks ◽  
Ataxia Telangiectasia Mutated ◽  
Strand Breaks ◽  
Dna Strand

Abstract 313: Essential role of ataxia telangiectasia in mitochondrial autophagy in mantle cell lymphoma

2014 ◽  
Author(s):  
Aloke Kumar Sarkar ◽  
Kumudha Balakrishnan ◽  
Mary Ayres ◽  
Sattva S. Neelapu ◽  
Varsha Gandhi
Keyword(s):  
Mantle Cell Lymphoma ◽  
Ataxia Telangiectasia ◽  
Essential Role ◽  
Cell Lymphoma ◽  
Mantle Cell

scholarly journals Inhibition of replicon initiation in human cells following stabilization of topoisomerase-DNA cleavable complexes.

1991 ◽  
Vol 11 (7) ◽  
pp. 3711-3718 ◽  
Author(s):  
W K Kaufmann ◽  
J C Boyer ◽  
L L Estabrooks ◽  
S J Wilson
Keyword(s):  
Ataxia Telangiectasia ◽  
Topoisomerase I ◽  
Cellular Response ◽  
Human Fibroblasts ◽  
Dna Strand Breaks ◽  
Velocity Sedimentation ◽  
Type I ◽  
Dna Topoisomerase ◽  
Strand Breaks ◽  
Dna Strand

Diploid human fibroblast strains were treated for 10 min with inhibitors of type I and type II DNA topoisomerases, and after removal of the inhibitors, the rate of initiation of DNA synthesis at replicon origins was determined. By alkaline elution chromatography, 4'-(9-acridinylamino)methanesulfon-m-anisidide (amsacrine), an inhibitor of DNA topoisomerase II, was shown to produce DNA strand breaks. These strand breaks are thought to reflect drug-induced stabilization of topoisomerase-DNA cleavable complexes. Removal of the drug led to a rapid resealing of the strand breaks by dissociation of the complexes. Velocity sedimentation analysis was used to quantify the effects of amsacrine treatment on DNA replication. It was demonstrated that transient exposure to low concentrations of amsacrine inhibited replicon initiation but did not substantially affect DNA chainelongation within operating replicons. Maximal inhibition of replicon initiation occurred 20 to 30 min after drug treatment, and the initiation rate recovered 30 to 90 min later. Ataxia telangiectasia cells displayed normal levels of amsacrine-induced DNA strand breaks during stabilization of cleavable complexes but failed to downregulate replicon initiation after exposure to the topoisomerase inhibitor. Thus, inhibition of replicon initiation in response to DNA damage appears to be an active process which requires a gene product which is defective or missing in ataxia telangiectasia cells. In normal human fibroblasts, the inhibition of DNA topoisomerase I by camptothecin produced reversible DNA strand breaks. Transient exposure to this drug also inhibited replicon initiation. These results suggest that the cellular response pathway which downregulates replicon initiation following genotoxic damage may respond to perturbations of chromatin structure which accompany stabilization of topoisomerase-DNA cleavable complexes.

Normal Rejoining of DNA Strand Breaks in Ataxia Telangiectasia Fibroblast Lines after Low X-Ray Exposure

1981 ◽  
Vol 86 (3) ◽  
pp. 589 ◽  
Author(s):  
P. V. Hariharan ◽  
S. Eleczko ◽  
B. P. Smith ◽  
M. C. Paterson
Keyword(s):  
Ataxia Telangiectasia ◽  
Dna Strand Breaks ◽  
Strand Breaks ◽  
X Ray ◽  
Dna Strand ◽  
Low X

scholarly journals Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks

2006 ◽  
Vol 173 (2) ◽  
pp. 195-206 ◽  
Author(s):  
Simon Bekker-Jensen ◽  
Claudia Lukas ◽  
Risa Kitagawa ◽  
Fredrik Melander ◽  
Michael B. Kastan ◽  
...  
Keyword(s):  
Spatial Organization ◽  
Protein A ◽  
Dna Strand Breaks ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Ataxia Telangiectasia Mutated ◽  
Interacting Protein ◽  
Atm Kinase ◽  
Strand Breaks ◽  
Dna Strand

We show that DNA double-strand breaks (DSBs) induce complex subcompartmentalization of genome surveillance regulators. Chromatin marked by γ-H2AX is occupied by ataxia telangiectasia–mutated (ATM) kinase, Mdc1, and 53BP1. In contrast, repair factors (Rad51, Rad52, BRCA2, and FANCD2), ATM and Rad-3–related (ATR) cascade (ATR, ATR interacting protein, and replication protein A), and the DNA clamp (Rad17 and -9) accumulate in subchromatin microcompartments delineated by single-stranded DNA (ssDNA). BRCA1 and the Mre11–Rad50–Nbs1 complex interact with both of these compartments. Importantly, some core DSB regulators do not form cytologically discernible foci. These are further subclassified to proteins that connect DSBs with the rest of the nucleus (Chk1 and -2), that assemble at unprocessed DSBs (DNA-PK/Ku70), and that exist on chromatin as preassembled complexes but become locally modified after DNA damage (Smc1/Smc3). Finally, checkpoint effectors such as p53 and Cdc25A do not accumulate at DSBs at all. We propose that subclassification of DSB regulators according to their residence sites provides a useful framework for understanding their involvement in diverse processes of genome surveillance.

scholarly journals Inhibition of replicon initiation in human cells following stabilization of topoisomerase-DNA cleavable complexes

1991 ◽  
Vol 11 (7) ◽  
pp. 3711-3718
Author(s):  
W K Kaufmann ◽  
J C Boyer ◽  
L L Estabrooks ◽  
S J Wilson
Keyword(s):  
Ataxia Telangiectasia ◽  
Topoisomerase I ◽  
Cellular Response ◽  
Human Fibroblasts ◽  
Dna Strand Breaks ◽  
Velocity Sedimentation ◽  
Type I ◽  
Dna Topoisomerase ◽  
Strand Breaks ◽  
Dna Strand

Diploid human fibroblast strains were treated for 10 min with inhibitors of type I and type II DNA topoisomerases, and after removal of the inhibitors, the rate of initiation of DNA synthesis at replicon origins was determined. By alkaline elution chromatography, 4'-(9-acridinylamino)methanesulfon-m-anisidide (amsacrine), an inhibitor of DNA topoisomerase II, was shown to produce DNA strand breaks. These strand breaks are thought to reflect drug-induced stabilization of topoisomerase-DNA cleavable complexes. Removal of the drug led to a rapid resealing of the strand breaks by dissociation of the complexes. Velocity sedimentation analysis was used to quantify the effects of amsacrine treatment on DNA replication. It was demonstrated that transient exposure to low concentrations of amsacrine inhibited replicon initiation but did not substantially affect DNA chainelongation within operating replicons. Maximal inhibition of replicon initiation occurred 20 to 30 min after drug treatment, and the initiation rate recovered 30 to 90 min later. Ataxia telangiectasia cells displayed normal levels of amsacrine-induced DNA strand breaks during stabilization of cleavable complexes but failed to downregulate replicon initiation after exposure to the topoisomerase inhibitor. Thus, inhibition of replicon initiation in response to DNA damage appears to be an active process which requires a gene product which is defective or missing in ataxia telangiectasia cells. In normal human fibroblasts, the inhibition of DNA topoisomerase I by camptothecin produced reversible DNA strand breaks. Transient exposure to this drug also inhibited replicon initiation. These results suggest that the cellular response pathway which downregulates replicon initiation following genotoxic damage may respond to perturbations of chromatin structure which accompany stabilization of topoisomerase-DNA cleavable complexes.

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