ArticleThe Journal of biological chemistry2012
ADP-ribosylhydrolase 3 (ARH3), not poly(ADP-ribose) glycohydrolase (PARG) isoforms, is responsible for degradation of mitochondrial matrix-associated poly(ADP-ribose).
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
64 citing papers in PubMed, 107 citations in OpenAlex.
- The Expanding Landscape of ADP-Ribosylation: Protein, DNA, RNA, and Mitochondrial Regulation.Chemical research in toxicology · 2026Review
- Article
- Hepatocyte mitochondrial NADNature metabolism · 2025Article
- Prospects for PARG inhibitors in cancer therapy.Journal of molecular cell biology · 2025Review
- Family-wide analysis of human macrodomains reveals novel activities and identifies PARG as most efficient ADPr-RNA hydrolase.Communications biology · 2025Article
- ADP-ribose hydrolases: biological functions and potential therapeutic targets.Expert reviews in molecular medicine · 2024Review
- Crosstalk between protein post-translational modifications and phase separation.Cell communication and signaling : CCS · 2024Review
- Activated NAD+ biosynthesis pathway induces olaparib resistance in BRCA1 knockout pancreatic cancer cells.PloS one · 2024Article
- PARP12 is required for mitochondrial function maintenance in thermogenic adipocytes.Adipocyte · 2022Article
- ARH Family of ADP-Ribose-Acceptor Hydrolases.Cells · 2022Review
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- Development and characterization of new tools for detecting poly(ADP-ribose) in vitro and in vivo.eLife · 2022Article
- Research Progress on Mono-ADP-Ribosyltransferases in Human Cell Biology.Frontiers in cell and developmental biology · 2022Review
- Review
- Mitochondrial NADMolecular cell · 2021Article
- NADFrontiers in molecular biosciences · 2021Review
- Pathogenic ARH3 mutations result in ADP-ribose chromatin scars during DNA strand break repair.Nature communications · 2020Article
- Therapeutic Strategies and Biomarkers to Modulate PARP Activity for Targeted Cancer Therapy.Cancers · 2020Review
- (ADP-ribosyl)hydrolases: structure, function, and biology.Genes & development · 2020Review
- Poly(ADP-Ribose) Glycohydrolase (PARG) vs. Poly(ADP-Ribose) Polymerase (PARP) - Function in Genome Maintenance and Relevance of Inhibitors for Anti-cancer Therapy.Frontiers in molecular biosciences · 2020Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Important cellular processes are regulated by poly(ADP-ribosyl)ation. This protein modification is catalyzed mainly by nuclear poly(ADP-ribose) polymerase (PARP) 1 in response to DNA damage. Cytosolic PARP isoforms have been described, whereas the presence of poly(ADP-ribose) (PAR) metabolism in mitochondria is controversial. PAR is degraded by poly(ADP-ribose) glycohydrolase (PARG). Recently, ADP-ribosylhydrolase 3 (ARH3) was also shown to catalyze PAR-degradation in vitro. PARG is encoded by a single, essential gene. One nuclear and three cytosolic isoforms result from alternative splicing. The presence and origin of a mitochondrial PARG is still unresolved. We establish here the genetic background of a human mitochondrial PARG isoform and investigate the molecular basis for mitochondrial poly(ADP-ribose) degradation. In common with a cytosolic 60-kDa human PARG isoform, the mitochondrial protein did not catalyze PAR degradation because of the absence of exon 5-encoded residues. In mice, we identified a transcript encoding an inactive cytosolic 52-kDa PARG lacking the mitochondrial targeting sequence and a substantial portion of exon 5. Thus, mammalian PARG genes encode isoforms that do not catalyze PAR degradation. On the other hand, embryonic fibroblasts from ARH3(-/-) mice lack most of the mitochondrial PAR degrading activity detected in wild-type cells, demonstrating a potential involvement of ARH3 in PAR metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.