scholarly journals The role of topoisomerase II beta on breakage and proximity of RUNX1 to partner alleles RUNX1T1 and EVI1

2013 ◽  
Vol 53 (2) ◽  
pp. 117-128 ◽  
Author(s):  
Kayleigh A. Smith ◽  
Ian G. Cowell ◽  
Yanming Zhang ◽  
Zbyslaw Sondka ◽  
Caroline A. Austin
Keyword(s):  
Topoisomerase Ii ◽  
Topoisomerase Ii Beta

scholarly journals Topoisomerase II is regulated by translationally controlled tumor protein for cell survival during organ growth in Drosophila

2021 ◽  
Vol 12 (9) ◽  
Author(s):  
Dae-Wook Yang ◽  
Jung-Wan Mok ◽  
Stephanie B. Telerman ◽  
Robert Amson ◽  
Adam Telerman ◽  
...  
Keyword(s):  
Cell Survival ◽  
Topoisomerase Ii ◽  
Wing Disc ◽  
Organ Development ◽  
Translationally Controlled Tumor Protein ◽  
Protein Levels ◽  
Eye Disc ◽  
Mutual Regulation

AbstractRegulation of cell survival is critical for organ development. Translationally controlled tumor protein (TCTP) is a conserved protein family implicated in the control of cell survival during normal development and tumorigenesis. Previously, we have identified a human Topoisomerase II (TOP2) as a TCTP partner, but its role in vivo has been unknown. To determine the significance of this interaction, we examined their roles in developing Drosophila organs. Top2 RNAi in the wing disc leads to tissue reduction and caspase activation, indicating the essential role of Top2 for cell survival. Top2 RNAi in the eye disc also causes loss of eye and head tissues. Tctp RNAi enhances the phenotypes of Top2 RNAi. The depletion of Tctp reduces Top2 levels in the wing disc and vice versa. Wing size is reduced by Top2 overexpression, implying that proper regulation of Top2 level is important for normal organ development. The wing phenotype of Tctp RNAi is partially suppressed by Top2 overexpression. This study suggests that mutual regulation of Tctp and Top2 protein levels is critical for cell survival during organ development.

Topoisomerase II beta levels are a determinant of melphalan-induced DNA crosslinks and sensitivity to cell death

2006 ◽  
Vol 72 (1) ◽  
pp. 11-18 ◽  
Author(s):  
M. Emmons ◽  
D. Boulware ◽  
D.M. Sullivan ◽  
L.A. Hazlehurst
Keyword(s):  
Cell Death ◽  
Topoisomerase Ii ◽  
Dna Crosslinks ◽  
Topoisomerase Ii Beta

Evidence for a Role of Vertebrate Rad52 in the Repair of Topoisomerase II–Mediated DNA Damage

2005 ◽  
Vol 24 (6) ◽  
pp. 388-393 ◽  
Author(s):  
Noritaka Adachi ◽  
Susumu Iiizumi ◽  
Hideki Koyama
Keyword(s):  
Dna Damage ◽  
Topoisomerase Ii

Clinically Translatable Prevention of Anthracycline Cardiotoxicity by Dexrazoxane Is Mediated by Topoisomerase II Beta and Not Metal Chelation

2021 ◽  
Author(s):  
Eduard Jirkovský ◽  
Anna Jirkovská ◽  
Hana Bavlovič-Piskáčková ◽  
Veronika Skalická ◽  
Zuzana Pokorná ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Topoisomerase Ii ◽  
Left Ventricular ◽  
Functional Markers ◽  
Metal Chelation ◽  
Anthracycline Cardiotoxicity ◽  
Ventricular Cardiomyocytes ◽  
Cardioprotective Effects ◽  
Topoisomerase Ii Beta

Background: Anthracycline-induced heart failure has been traditionally attributed to direct iron-catalyzed oxidative damage. Dexrazoxane (DEX)—the only drug approved for its prevention—has been believed to protect the heart via its iron-chelating metabolite ADR-925. However, direct evidence is lacking, and recently proposed TOP2B (topoisomerase II beta) hypothesis challenged the original concept. Methods: Pharmacokinetically guided study of the cardioprotective effects of clinically used DEX and its chelating metabolite ADR-925 (administered exogenously) was performed together with mechanistic experiments. The cardiotoxicity was induced by daunorubicin in neonatal ventricular cardiomyocytes in vitro and in a chronic rabbit model in vivo (n=50). Results: Intracellular concentrations of ADR-925 in neonatal ventricular cardiomyocytes and rabbit hearts after treatment with exogenous ADR-925 were similar or exceeded those observed after treatment with the parent DEX. However, ADR-925 did not protect neonatal ventricular cardiomyocytes against anthracycline toxicity, whereas DEX exhibited significant protective effects (10–100 µmol/L; P <0.001). Unlike DEX, ADR-925 also had no significant impact on daunorubicin-induced mortality, blood congestion, and biochemical and functional markers of cardiac dysfunction in vivo (eg, end point left ventricular fractional shortening was 32.3±14.7%, 33.5±4.8%, 42.7±1.0%, and 41.5±1.1% for the daunorubicin, ADR-925 [120 mg/kg]+daunorubicin, DEX [60 mg/kg]+daunorubicin, and control groups, respectively; P <0.05). DEX, but not ADR-925, inhibited and depleted TOP2B and prevented daunorubicin-induced genotoxic damage. TOP2B dependency of the cardioprotective effects was probed and supported by experiments with diastereomers of a new DEX derivative. Conclusions: This study strongly supports a new mechanistic paradigm that attributes clinically effective cardioprotection against anthracycline cardiotoxicity to interactions with TOP2B but not metal chelation and protection against direct oxidative damage.

scholarly journals Role of Aurora B and Haspin kinases in the metaphase Topoisomerase II checkpoint

Cell Cycle ◽  
2021 ◽  
Vol 20 (4) ◽  
pp. 345-352
Author(s):  
M. Johansson ◽  
Y. Azuma ◽  
D. J. Clarke
Keyword(s):  
Topoisomerase Ii ◽  
Aurora B
Sign in / Sign up

Export Citation Format

Share Document