Assessing AML susceptibility in rearrangement‐driven patients by DNA breakage at topoisomerase II and CTCF /cohesin binding sites

2021 ◽  
Author(s):  
Naomi D. Atkin ◽  
Heather M. Raimer ◽  
Zhenjia Wang ◽  
Chongzhi Zang ◽  
Yuh‐Hwa Wang
Keyword(s):  
Binding Sites ◽  
Topoisomerase Ii ◽  
Dna Breakage

Protein:DNA interactions at chromosomal loop attachment sites

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 503-509 ◽  
Author(s):  
Veronica C. Blasquez ◽  
Ann O. Sperry ◽  
Peter N. Cockerill ◽  
William T. Garrard
Keyword(s):  
Nuclear Matrix ◽  
Binding Sites ◽  
Topoisomerase Ii ◽  
Regulatory Sequences ◽  
Immunoglobulin Gene ◽  
Sequence Motifs ◽  
Cis Acting ◽  
Consensus Sequences ◽  
Dna And Rna ◽  
Multiple Binding Sites

We have recently identified an evolutionarily conserved class of sequences that organize chromosomal loops in the interphase nucleus, which we have termed "matrix association regions" (MARs). MARs are about 200 bp long, AT-rich, contain topoisomerase II consensus sequences and other AT-rich sequence motifs, often reside near cis-acting regulatory sequences, and their binding sites are abundant (> 10 000 per mammalian nucleus). Here we demonstrate that the interactions between the mouse κ immunoglobulin gene MAR and topoisomerase II or the "nuclear matrix" occur between multiple and sometimes overlapping binding sites. Interestingly, the sites most susceptible to topoisomerase II cleavage are localized near the breakpoints of a previously described illegitimate recombination event. The presence of multiple binding sites within single MARs may allow DNA and RNA polymerase passage without disrupting primary loop organization.Key words: MARs, chromatin loops, topoisomerase II, nuclear matrix.

Genomic sites of topoisomerase II activity determined by comparing DNA breakage enhanced by three distinct poisons 1 1Edited by J. Karn

1999 ◽  
Vol 285 (2) ◽  
pp. 545-554 ◽  
Author(s):  
M.Evelina Borgnetto ◽  
Stella Tinelli ◽  
Laura Carminati ◽  
Giovanni Capranico
Keyword(s):  
Topoisomerase Ii ◽  
Dna Breakage

Cell line selectivity and DNA breakage properties of the antitumour agent N-[2-(Dimethylamino)ethyl]acridine-4-carboxamide: role of DNA topoisomerase II

1988 ◽  
Vol 24 (11) ◽  
pp. 1783-1790 ◽  
Author(s):  
Erasmus Schneider ◽  
Sandra J. Darkin ◽  
Penelope A. Lawson ◽  
Lai-Ming Ching ◽  
Raymond K. Ralph ◽  
...  
Keyword(s):  
Cell Line ◽  
Topoisomerase Ii ◽  
Dna Topoisomerase Ii ◽  
Dna Topoisomerase ◽  
Dna Breakage ◽  
Antitumour Agent

scholarly journals Induction of calf thymus topoisomerase II-mediated DNA breakage by the antibacterial isothiazoloquinolones A-65281 and A-65282.

1992 ◽  
Vol 36 (1) ◽  
pp. 81-86 ◽  
Author(s):  
W E Kohlbrenner ◽  
N Wideburg ◽  
D Weigl ◽  
A Saldivar ◽  
D T Chu
Keyword(s):  
Topoisomerase Ii ◽  
Dna Breakage ◽  
Calf Thymus

Genistein induces apoptosis and topoisomerase II-mediated DNA breakage in colon cancer cells

2000 ◽  
Vol 36 (6) ◽  
pp. 796-802 ◽  
Author(s):  
G.I Salti ◽  
S Grewal ◽  
R.R Mehta ◽  
T.K Das Gupta ◽  
A.W Boddie Jr ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Topoisomerase Ii ◽  
Colon Cancer Cells ◽  
Dna Breakage

Differentiation of U-937 promonocytic cells by etoposide and ICRF-193, two antitumour DNA topoisomerase II inhibitors with different mechanisms of action

1997 ◽  
Vol 110 (3) ◽  
pp. 337-343 ◽  
Author(s):  
C. Perez ◽  
N.E. Vilaboa ◽  
L. Garcia-Bermejo ◽  
E. de Blas ◽  
A.M. Creighton ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Topoisomerase Ii ◽  
Binding Activity ◽  
Pulse Treatment ◽  
Dna Topoisomerase Ii ◽  
Dna Topoisomerase ◽  
Dna Breakage ◽  
Topoisomerase Ii Inhibitors ◽  
Kinase C ◽  
Membrane Bound

We have compared the action on U-937 human promonocytic leukemia cells of two DNA topoisomerase II inhibitors, namely the epipodophyllotoxin etoposide and the bisdioxopiperazine ICRF-193. One hour pulse-treatment with 3 microM etoposide caused topoisomerase associated, primary DNA breakage, which was rapidly followed by apoptosis. By contrast, these effects were not observed upon pulse-treatment with 6 microM ICRF-193. However, continuous treatments with subcytotoxic concentrations of etoposide (0.15 microM) and ICRF-193 (0.3 microM) produced several similar effects, namely decreased cell proliferation, accumulation of cells at G2, increase in cell mass, and induction of differentiation. Under these conditions, etoposide produced a biphasic activation of protein kinase C, which consisted in an early transient activation (from hours 1 to 6) of the membrane-bound enzyme followed by a later activation (hour 48) of the total, membrane-bound and cytosolic enzyme. By contrast, ICRF-193 only provoked a late activation (from hours 72 to 96) of the total enzyme. When used at differentiation-inducing concentrations, both topoisomerase inhibitors caused a great stimulation of AP-1 binding activity, with maximum value at hour 12 in etoposide-treated cells and at hour 48 in ICRF-193-treated cells. By contrast, the binding activity of the NF-kappa(B) and EGR-1 transcription factors was little affected. It is concluded that topoisomerase II inhibitors may induce the differentiation of promonocytic cells, independently of their capacity to cause DNA strand breaks. However, there are other effects, such as the early activation of protein kinase C, which are probably derived from the production of primary DNA breakage by some anti-topoisomerase drugs.

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