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RNF168 (Montrer RNF168 Protéines) interacts with TOP2alpha to mediate its polyubiquitylation and RNF168 (Montrer RNF168 Protéines) deficiency confers resistance to ICRF (Montrer REG1A Protéines)-193, a TOP2 catalytic inhibitor, and cytotoxic anti-cancer drug etoposide in cultured mouse cells.
our data support further assessment of TOP2A and EZH2 (Montrer EZH2 Protéines) as biomarkers for early identification of patients with increased metastatic potential that may benefit from adjuvant or neoadjuvant targeted therapy approaches
High mRNA levels of TOP2A is independent predictor of poor outcome in Renal Cell Carcinoma (Montrer MOK Protéines) patients.
findings implicate TOP2A cleavage as a broad DNA damage mechanism in oncogenic translocations as well as a functional role of TOP2A cleavage in regulating transcription elongation and gene activation.
TOP2A acts as a co-activator of beta-catenin (Montrer CTNNB1 Protéines) and activates Epithelial-mesenchymal transition process.
ProEx C is an immunohistochemical cocktail containing antibodies direct against topoisomerase IIalpha (TOP2A) and minichromosome maintenance 2 (MCM2 (Montrer MCM2 Protéines)) proteins. This brief review covers the effective utility of ProEx C as adjunct tool in assessing the urothelial lesions in urine cytology, also providing prognostic and therapeutic information to help in clinical decisions.
High TOP2A expression was significantly associated with longer time to progression after EDP-M. TOP2A and TS proteins assessed by immunohistochemistry significantly correlated with mRNA expression. Immunohistochemical TOP2A expression was associated with a non-significant better response and longer TTP (Montrer ADAMTS13 Protéines) after EDP-M.
Data show that comparing with Ki-67 (Montrer MKI67 Protéines) and TOP2A, RacGAP1 (Montrer RACGAP1 Protéines) allowed for a clearer prognostic statement.
These findings reveal a novel, p53 (Montrer TP53 Protéines)-independent activity of Mdm2 (Montrer MDM2 Protéines) and have important implications for the choice of chemotherapeutic agents in the treatment of Mdm2 (Montrer MDM2 Protéines)-overexpressing tumors. Herein is shown that tumor cells with MDM2 (Montrer MDM2 Protéines) amplification are selectively resistant to treatment with topoisomerase II (Montrer TOP2 Protéines) poisons but not other DNA damaging agents
The methodology is useful for a high-throughput analysis of drugs that poison Top2, allowing not just the discrimination of the Top2 isoform that is targeted but also to track its removal
RNF168 (Montrer RNF168 Protéines) interacts with TOP2alpha to mediate its polyubiquitylation and RNF168 (Montrer RNF168 Protéines) deficiency confers resistance to ICRF (Montrer REG1A Protéines)-193, a TOP2 (Montrer TOP2 Protéines) catalytic inhibitor, and cytotoxic anti-cancer drug etoposide in cultured mouse cells.
Polyamide functionalisation at the N1-position offers a design strategy to improve drug-like properties. Dicationic HxIP* 3 increased topo IIalpha expression and chemosensitivity to topo II (Montrer TOP2 Protéines)-targeting agents.
TOP2 (Montrer TOP2 Protéines) and BAF (Montrer BANF1 Protéines) cooperate to recruit pluripotency factors, which explains some of the instructive roles of BAF (Montrer BANF1 Protéines) complexes.
Deletion or deficiency of PTEN leads to down regulation of TOP2A, dysfunction of the decatenation checkpoint and incomplete DNA decatenation in G2 and M phases.
Inhibition of DNA topoisomerase II (Montrer TOP2 Protéines) selectively reduces the threat of tumorigenicity
Cohesin removal is a prerequisite for the posterior topoisomerase IIalpha-mediated resolution of persisting catenations between segregating chromatids during anaphase II.
Data show that unfolded protein response (UPR)-induced changes in topoisomerase IIalpha (Topo IIalpha) protein levels are not responsible for resistance to etoposide, and that the PERK plays a Topo IIalpha-independent role in altered sensitivity to the drug.
Topoisomerase IIa not only contributes to stem-cell transcriptome regulation but also primes developmental genes for subsequent activation upon differentiation.
studies indicate that the ability of TOP2A to prevent DNA entanglement at mitosis requires BAF (Montrer BANF1 Protéines) complexes and suggest that this activity contributes to the role of BAF (Montrer BANF1 Protéines) subunits as tumour suppressors
our data reveal TDP2 (Montrer TDP2 Protéines)-mediated error-free NHEJ as an efficient and accurate mechanism to repair TOP2 (Montrer TOP2 Protéines)-induced DSBs
This gene encodes a DNA topoisomerase, an enzyme that controls and alters the topologic states of DNA during transcription. This nuclear enzyme is involved in processes such as chromosome condensation, chromatid separation, and the relief of torsional stress that occurs during DNA transcription and replication. It catalyzes the transient breaking and rejoining of two strands of duplex DNA which allows the strands to pass through one another, thus altering the topology of DNA. Two forms of this enzyme exist as likely products of a gene duplication event. The gene encoding this form, alpha, is localized to chromosome 17 and the beta gene is localized to chromosome 3. The gene encoding this enzyme functions as the target for several anticancer agents and a variety of mutations in this gene have been associated with the development of drug resistance. Reduced activity of this enzyme may also play a role in ataxia-telangiectasia.
, DNA topoisomerase (ATP-hydrolyzing)
, DNA topoisomerase 2-alpha
, DNA topoisomerase II, 170 kD
, DNA topoisomerase II, alpha isozyme
, DNA Topoisomerase II alpha
, topoisomerase (DNA) 2 alpha
, DNA topoisomeraseII_alpha
, topoisomerase (DNA) II alpha
, Thimet metalloendopeptidase 2
, Zincin-like metalloproteases family protein 2