Inputs and outputs of poly(ADP-ribosyl)ation: Relevance to oxidative stress
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
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Chronic PARP-1 inhibition reduces carotid vessel remodeling and oxidative damage of the dorsal hippocampus in spontaneously hypertensive rats. [PDF]
Vascular remodeling during chronic hypertension may impair the supply of tissues with oxygen, glucose and other compounds, potentially unleashing deleterious effects.
Krisztian Eros +10 more
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This work reports the development of a fluorescence method for the detection of poly(ADP-ribose) polymerase-1 (PARP1), in which a phenylboronic acid-modified fluorescein isothiocyanate dye (FITC-PBA) was used to recognize the formed poly(ADP-ribose) (PAR)
Fengli Gao +4 more
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Poly(ADP-ribose) synthetase, a main acceptor of poly(ADP-ribose) in isolated nuclei.
Poly(ADP-ribose) synthetase was identified as the main acceptor of this polymer produced in isolated nuclei of rat liver. When the nuclei were incubated with [32P]NAD at a limited concentration (2.4 microM) and for a brief period (10 s), a protein with Mr = 110,000 was predominantly poly(ADP-ribosyl)ated, as judged by sodium dodecyl sulfate ...
N, Ogata +3 more
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CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh +12 more
wiley +1 more source
Inhibition of Poly(ADP-ribose)polymerase impairs Epstein Barr Virus lytic cycle progression-7
Copyright information:Taken from "Inhibition of Poly(ADP-ribose)polymerase impairs Epstein Barr Virus lytic cycle progression"http://www.infectagentscancer.com/content/2/1/18Infectious Agents and Cancer 2007;2():18-18.Published online 11 Oct 2007PMCID ...
Giulia Matusali (83277) +8 more
core +1 more source
Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +1 more source
ADP-ribose hydrolases: biological functions and potential therapeutic targets
ADP-ribosylation (ADPRylation), which encompasses poly(ADP-ribosyl)ation and mono(ADP-ribosyl)ation, is an important post-translational modification catalysed by the poly(ADP-ribose) polymerase (PARP) enzyme superfamily.
Jingpeng Wang, Zhao-Qi Wang, Wen Zong
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Mcl-1 suppresses abasic site repair following bile acid–induced hepatic cellular DNA damage
In cholestasis, increases in bile acid levels result in the generation of reactive oxygen species and the induction of DNA damage and mutation. It is believed that bile acid accumulation is associated with liver tumorigenesis. However, the mechanism that
Haiyang Yu +11 more
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