Results 21 to 30 of about 43,499 (244)

Chromosomal instability syndromes are sensitive to poly ADP-ribose polymerase inhibitors

open access: yesHaematologica, 2008
Poly ADP-ribose polymerase inhibitors have been shown to target cells with homologous recombination DNA repair defects. We report that poly ADP-ribose polymerase inhibitors induces apoptosis in cells deficient in other key DNA repair components ...
Terry J. Gaymes   +3 more
doaj   +1 more source

Structural modeling of NAD+ binding modes to PARP-1

open access: yesВавиловский журнал генетики и селекции, 2017
The nuclear protein poly (ADP-ribose) polymerase-1 (PARP-1) plays an important role in the signaling and repair of DNA. PARP-1 catalyses covalent binding of poly (ADP-ribose) polymers with itself as well as with other acceptor proteins using NAD+ as a ...
N. V. Ivanisenko   +2 more
doaj   +1 more source

ARH Family of ADP-Ribose-Acceptor Hydrolases

open access: yesCells, 2022
The ARH family of ADP-ribose-acceptor hydrolases consists of three 39-kDa members (ARH1-3), with similarities in amino acid sequence. ARH1 was identified based on its ability to cleave ADP-ribosyl-arginine synthesized by cholera toxin.
Hiroko Ishiwata-Endo   +6 more
doaj   +1 more source

Human PARP1 substrates and regulators of its catalytic activity: An updated overview

open access: yesFrontiers in Pharmacology, 2023
Poly (ADP-ribose) polymerase 1 (PARP1) is a key DNA damage sensor that is recruited to damaged sites after DNA strand breaks to initiate DNA repair. This is achieved by catalyzing attachment of ADP-ribose moieties, which are donated from NAD+, on the ...
Tao Zhu   +5 more
doaj   +1 more source

Radiotherapy-Poly(ADP-ribose) Polymerase Inhibitor Combinations: Progress to Date [PDF]

open access: yesSeminars in Radiation Oncology, 2022
Radiation resistance remains a huge clinical problem for cancer patients and oncologists in the 21st century. In recent years, the mammalian DNA damage response (DDR) has been extensively characterized and shown to play a key role in determining cellular survival following ionizing radiation exposure.
Derby, Sarah J.   +2 more
openaire   +2 more sources

Poly(ADP-Ribose) Links the DNA Damage Response and Biomineralization

open access: yesCell Reports, 2019
Summary: Biomineralization of the extracellular matrix is an essential, regulated process. Inappropriate mineralization of bone and the vasculature has devastating effects on patient health, yet an integrated understanding of the chemical and cell ...
Karin H. Müller   +26 more
doaj   +1 more source

Poly (ADP-Ribose) Polymerase Inhibitors in Patients With Urothelial Cancer

open access: yesClinical Genitourinary Cancer, 2023
Poly ADP-ribose polymerase inhibitors (PARPis) have clinical activity in several cancers. The rationale of their therapeutic use in urothelial cancer (UC) resides in the high homologous-recombination repair (HRR) deficiency (HRD) prevalence and potential cross-sensitivity with platinum-based chemotherapy (PBCT).
Gamba, Teresa   +5 more
openaire   +2 more sources

Inputs and outputs of poly(ADP-ribosyl)ation: Relevance to oxidative stress

open access: yesRedox Biology, 2014
Oxidative stress can cause DNA breaks which induce activation of the DNA nick sensor enzyme poly(ADP-ribose) polymerase-1 (PARP-1), part of the 17 member PARP enzyme family.
Csaba Hegedűs, László Virág
doaj   +1 more source

Mechanisms of PARP inhibitor resistance in cancer and insights into the DNA damage response

open access: yesGenome Medicine, 2018
Editorial summary Inhibitors of poly(ADP-ribose) polymerase (PARPi) have entered the clinic for the treatment of patients with cancers that lack homology-directed DNA repair, but drug resistance remains a clinical hurdle.
Paola Francica, Sven Rottenberg
doaj   +1 more source

Poly(ADP-ribose) polymerase inhibitors as cancer therapy

open access: yesFrontiers in Bioscience, 2013
Poly(ADP-ribose) polymerase (PARP) inhibitors are pharmacologic agents which primarily inhibit the PARP-1 and PARP-2 enzymes within the cell. Inhibition of PARP results in failure of base-excision repair (BER) to correct single-stranded breaks in DNA.
John F, Hilton   +3 more
openaire   +2 more sources

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