Results 81 to 90 of about 742,291 (286)

Poly(ADP-Ribose)Polymerase (PARP) Inhibitors and Radiation Therapy

open access: yesFrontiers in Pharmacology, 2020
Poly(ADP-ribose)polymerase-1 (PARP1) is a DNA repair enzyme highly expressed in the nuclei of mammalian cells, with a structure and function that have attracted interest since its discovery.
Stephen A. Jannetti   +10 more
doaj   +1 more source

Klotho‐Derived Peptide 1 Protects against Acute Kidney Injury by Directly Targeting Mitochondrial ATAD3A

open access: yesAdvanced Science, EarlyView.
This study uncovers that KP1, a Klotho‐derived peptide, protects the kidney against acute kidney injury, a clinical syndrome with high morbidity and mortality. KP1 enters tubular epithelial cells via endocytosis, directly interacts with the mitochondrial ATAD3A/HIGD2A complex, thereby preventing cytochrome c release, and caspases activation, and ...
Xiaoyao Zhang   +6 more
wiley   +1 more source

Novel dual inhibitors of PARP and HDAC induce intratumoral STING-mediated antitumor immunity in triple-negative breast cancer

open access: yesCell Death and Disease
PARP inhibitors and HDAC inhibitors have been approved for the clinical treatment of malignancies, but acquired resistance of or limited effects on solid tumors with a single agent remain as challenges.
Qingyun Zhu   +13 more
doaj   +1 more source

Inhibitors of poly ADP-ribose polymerase (PARP) induce apoptosis of myeloid leukemic cells: potential for therapy of myeloid leukemia and myelodysplastic syndromes

open access: yesHaematologica, 2009
Background Aberrant or impaired repair of double-strand DNA breaks is a common feature of de novo acute myeloid leukemia and myelodysplastic syndromes.
Terry J. Gaymes   +6 more
doaj   +1 more source

RSF1‐Dependent PAR Turnover Promotes 53BP1 Liquid Condensate Formation at DNA Damage Sites

open access: yesAdvanced Science, EarlyView.
At sites of DNA damage, RSF1 recruits PARG to accelerate PAR turnover, triggering a switch from PAR‐driven condensates to 53BP1 condensates. This condensate transition enables p53‐dependent gene transcription and coordinates the DNA damage response.
Yungyeong Heo   +10 more
wiley   +1 more source

Update on Combination Strategies of PARP Inhibitors

open access: yesCancer Control
The application of PARP inhibitors has revolutionized cancer treatment and has achieved significant advancements, particularly with regard to tumors with defects in genes involved in homologous recombination repair (HRR) processes, such as BRCA1 and ...
Zhuoqun Lin   +4 more
doaj   +1 more source

Colon-Targeted Poly(ADP-ribose) Polymerase Inhibitors Synergize Therapeutic Effects of Mesalazine Against Rat Colitis Induced by 2,4-Dinitrobenzenesulfonic Acid

open access: yesPharmaceutics
Background/Objectives: In addition to oncological applications, poly(ADP-ribose) polymerase (PARP) inhibitors have potential as anti-inflammatory agents.
Changyu Kang   +4 more
doaj   +1 more source

Combined Strategies with Poly (ADP-Ribose) Polymerase (PARP) Inhibitors for the Treatment of Ovarian Cancer: A Literature Review

open access: yesDiagnostics, 2019
Poly (ADP-ribose) polymerase (PARP) inhibitors are the first clinically approved drugs designed to exploit synthetic lethality, and were first introduced as a cancer-targeting strategy in 2005. They have led to a major change in the treatment of advanced
Stergios Boussios   +6 more
doaj   +1 more source

Gut Microbiota‐Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1‐Mediated Parthanatos

open access: yesAdvanced Science, EarlyView.
ABSTRACT Bile acids have been implicated in calcium oxalate (CaOx) nephrolithiasis. Here, we employ multi‐omics approaches to identify isoallolithocholic acid (isoalloLCA) as the key bile acid elevated in the feces, serum, kidney, and urine of CaOx rats, confirmed by spatial metabolomics.
Zijian Zhou   +9 more
wiley   +1 more source

Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation

open access: yesAdvanced Science, EarlyView.
Chromosome 16q loss drives genomic instability through disruption of the CYLD–TIRR–53BP1 axis. CYLD preserves homologous recombination by stabilizing TIRR and limiting 53BP1 accumulation at DNA double‐strand breaks. CYLD deficiency redirects repair toward error‐prone non‐homologous end joining, promotes mutational burden and homologous recombination ...
Mingming Lu   +14 more
wiley   +1 more source

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