Results 91 to 100 of about 70,337 (231)

PARP Inhibitors in Prostate and Urothelial Cancers

open access: yesFrontiers in Oncology, 2020
Poly(ADP-ribose) polymerase (PARP) inhibitors targeting DNA repair gene mutations have shown significant clinical benefit in patients with ovarian and breast cancers. In metastatic prostate cancers, the prevalence of DNA repair gene mutations is up to 20%
Rohan Garje   +2 more
doaj   +1 more source

Glycyrrhetinic acid and its derivatives as inhibitors of poly(ADP-ribose)polymerases 1 and 2, apurinic/apyrimidinic endonuclease 1 and DNA polymerase β [PDF]

open access: yes, 2012
Aim. For strengthening the efficiency of monofunctional alkylating antineoplastic drugs it is important to lower the capacity of base excision repair (BER) system which corrects the majority of DNA damages caused by these reagents.
Ilina E. S.   +8 more
core   +3 more sources

Mortality risk stratification for Takotsubo syndrome: Evaluating CRP measurement alongside the InterTAK prognostic score

open access: yesESC Heart Failure, Volume 12, Issue 2, Page 1427-1436, April 2025.
Abstract Background and objectives Initially described as a benign acute cardiomyopathy, Takotsubo syndrome has been linked to elevated mortality rates. Emerging evidence suggests that unresolved myocardial inflammation may contribute to this adverse prognosis.
Loïc Faucher   +12 more
wiley   +1 more source

The Elephant and the Blind Men: Making Sense of PARP Inhibitors in Homologous Recombination Deficient Tumor Cells

open access: yesFrontiers in Oncology, 2013
Poly(ADP-ribose) polymerase 1 (PARP1) is an important component of the base excision repair (BER) pathway as well as a regulator of homologous recombination (HR) and nonhomologous end-joining (NHEJ).
Silvana eDe Lorenzo   +3 more
doaj   +1 more source

Poly(ADP-ribose) polymerases regulate cell division and development in Arabidopsis roots [PDF]

open access: yes, 2017
Root organogenesis involves cell division, differentiation and expansion. The molecular mechanisms regulating root development are not fully understood. In this study, we identified poly (ADP-ribose) polymerases (PARPs) as new players in root development.
Ge, Xiaochun   +7 more
core   +1 more source

Poly(ADP-Ribose) Glycohydrolase (PARG) vs. Poly(ADP-Ribose) Polymerase (PARP) – Function in Genome Maintenance and Relevance of Inhibitors for Anti-cancer Therapy

open access: yesFrontiers in Molecular Biosciences, 2020
Poly(ADP-ribose) polymerases (PARPs) are a family of enzymes that catalyze the addition of poly(ADP-ribose) (PAR) subunits onto themselves and other acceptor proteins.
Daniel Harrision   +3 more
doaj   +1 more source

Assessment of Poly(ADP-ribose) Polymerase1 (PARP1) expression and activity in cells purified from blood and milk of dairy cattle [PDF]

open access: yes, 2018
Poly(ADP-ribosyl)ation (PAR) is a post-translational protein modification catalysed by enzyme member of the poly(ADP-ribose) polymerases (PARPs) family. The activation of several PARPs is triggered by DNA strand breakage and the main PARP enzyme involved
Buttazzoni, Luca   +7 more
core   +1 more source

ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition

open access: yesInternational Journal of Cancer, EarlyView.
What's New? Errors in DNA double‐strand break (DSB) repair can lead to mutations, chromosomal instability, and ultimately cancer. Inhibitor of DNA‐binding 3 (ID3), a transcriptional repressor, is crucial to promoting DSB repair and helping maintain genome stability. Here, the authors investigated ID3 regulation of DNA repair via chromatin accessibility
Giuditta Della Corte   +10 more
wiley   +1 more source

Hematologic complications in patients exposed to poly-ADP ribose polymerase inhibitors

open access: yesHaematologica
Not available.
Joseph M. Cannova   +16 more
doaj   +1 more source

Loss of amplified genes by poly(ADP-ribose) polymerase inhibitors.

open access: yesEnvironmental Health Perspectives, 1991
A poly(ADP-ribose) polymerase inhibitor, benzamide (BA), was found to induce flat revertants of NIH 3T3 cells that had been transformed by human Ha-ras, rat Ki-ras, rat c-raf, and human ret-II. These genes had been amplified in original transformants, but they were completely eliminated by BA.
M, Nagao   +4 more
openaire   +2 more sources

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