ArticlePloS one2012
Structures of the human poly (ADP-ribose) glycohydrolase catalytic domain confirm catalytic mechanism and explain inhibition by ADP-HPD derivatives.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Poly(ADP-ribose) (PAR) exhibits ion-dependent structural properties distinct from RNA.Nucleic acids research · 2026Article
- Article
- Insights into mechanisms of ubiquitin ADP-ribosylation reversal.Biochemical Society transactions · 2024Review
- An NADTetrahedron · 2024Article
- Article
- ADP-ribose hydrolases: biological functions and potential therapeutic targets.Expert reviews in molecular medicine · 2024Review
- The function and regulation of ADP-ribosylation in the DNA damage response.Biochemical Society transactions · 2023Article
- Serine ADP-ribosylation in Drosophila provides insights into the evolution of reversible ADP-ribosylation signalling.Nature communications · 2023Article
- Switch-like compaction of poly(ADP-ribose) upon cation binding.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Reversible modification of mitochondrial ADP/ATP translocases by pairedProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Targeting SARS-CoV-2 Nsp3 macrodomain structure with insights from human poly(ADP-ribose) glycohydrolase (PARG) structures with inhibitors.Progress in biophysics and molecular biology · 2021Article
- Mechanistic insights into the three steps of poly(ADP-ribosylation) reversal.Nature communications · 2021Article
- A Bifunctional NADACS chemical biology · 2021Article
- ADP-ribosylhydrolases: from DNA damage repair to COVID-19.Journal of Zhejiang University. Science. B · 2021Review
- The Making and Breaking of Serine-ADP-Ribosylation in the DNA Damage Response.Frontiers in cell and developmental biology · 2021Review
- Reduced Tumorigenicity of Mouse ES Cells and the Augmented Anti-Tumor Therapeutic Effects underCancers · 2020Article
- (ADP-ribosyl)hydrolases: structure, function, and biology.Genes & development · 2020Review
- Selective small molecule PARG inhibitor causes replication fork stalling and cancer cell death.Nature communications · 2019Article
- ADP-ribosylation signalling and human disease.Open biology · 2019Review
- Structural and biochemical evidence supporting poly ADP-ribosylation in the bacterium Deinococcus radiodurans.Nature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) glycohydrolase (PARG) is the only enzyme known to catalyse hydrolysis of the O-glycosidic linkages of ADP-ribose polymers, thereby reversing the effects of poly(ADP-ribose) polymerases. PARG deficiency leads to cell death whilst PARG depletion causes sensitisation to certain DNA damaging agents, implicating PARG as a potential therapeutic target in several disease areas. Efforts to develop small molecule inhibitors of PARG activity have until recently been hampered by a lack of structural information on PARG. We have used a combination of bio-informatic and experimental approaches to engineer a crystallisable, catalytically active fragment of human PARG (hPARG). Here, we present high-resolution structures of the catalytic domain of hPARG in unliganded form and in complex with three inhibitors: ADP-ribose (ADPR), adenosine 5'-diphosphate (hydroxymethyl)pyrrolidinediol (ADP-HPD) and 8-n-octyl-amino-ADP-HPD. Our structures confirm conservation of overall fold amongst mammalian PARG glycohydrolase domains, whilst revealing additional flexible regions in the catalytic site. These new structures rationalise a body of published mutational data and the reported structure-activity relationship for ADP-HPD based PARG inhibitors. In addition, we have developed and used biochemical, isothermal titration calorimetry and surface plasmon resonance assays to characterise the binding of inhibitors to our PARG protein, thus providing a starting point for the design of new inhibitors.
Indexed as
Identifiers
What OpenQuestion holds
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.