R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
ARH3 (E8A6G) Rabbit mAb #32205
Filter:
- WB
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 39 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
ARH3 (E8A6G) Rabbit mAb recognizes endogenous levels of total ARH3 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro241 of human ARH3 protein.
Background
ADP-ribosylation is a reversible post-translational modification (PTM) where a single unit or polymers of ADP-ribose (ADPr) groups from β-nicotinamide adenine dinucleotide (NAD+) are transferred onto specific residues of target proteins (1). In addition to proteins, DNA and RNA molecules have also been identified as targets of ADP-ribosylation (2,3). This modification is catalyzed by a diverse group of ADP-ribosyltransferases (ARTs), with the majority of them functioning to add a single ADPr unit (MARylation) while the deposition of multiple ADPrs are done by poly (ADP-ribose) polymerases (PARPs). Reversal of ADP-ribosylation is accomplished by the evolutionarily distinct macrodomain and ADP-ribosylhydrolase (ARH) protein families (4). Specifically, poly (ADP-ribose) glycohydrolase (PARG) or ADP-ribosylhydrolase 3 (ARH3) degrade PARylation down to single ADPr units and MacroD1, MacroD2, TARG1, or ARH1 fully remove them from target residues (5). ADP-ribosylation and the enzymes that regulate it are involved in a wide range of cellular processes, such as DNA repair, chromatin regulation, transcription, and cellular stress response (1,4). Moreover, ADP-ribosylation has been shown to be a therapeutically critical PTM in various cancers, neurodegenerative diseases, and inflammation (6).
The ARH family of ADP-ribose hydrolases contains three proteins with similarities in amino acid sequence but differences in their enzymatic activities. ARH3, also known as ADPRHL2, is a ubiquitous protein that localizes to the nucleus, cytosol, and mitochondria in a cell-type specific manner (7-9). ARH3 exhibits partial redundancy with PARG in their preference for hydrolysis of DNA damage-induced serine ADP-ribosylation which underlies a key role for these enzymes in maintaining genomic stability. Arh3-KO mice have been shown to develop increased brain infarction in response to ischemia-reperfusion injury (10) and human ARH3-deficiency is a rare recessive autosomal disorder characterized by neurodegeneration and early death (11,12).
The ARH family of ADP-ribose hydrolases contains three proteins with similarities in amino acid sequence but differences in their enzymatic activities. ARH3, also known as ADPRHL2, is a ubiquitous protein that localizes to the nucleus, cytosol, and mitochondria in a cell-type specific manner (7-9). ARH3 exhibits partial redundancy with PARG in their preference for hydrolysis of DNA damage-induced serine ADP-ribosylation which underlies a key role for these enzymes in maintaining genomic stability. Arh3-KO mice have been shown to develop increased brain infarction in response to ischemia-reperfusion injury (10) and human ARH3-deficiency is a rare recessive autosomal disorder characterized by neurodegeneration and early death (11,12).
- Gibson, B.A. and Kraus, W.L. (2012) Nat Rev Mol Cell Biol 13, 411-24.
- Jankevicius, G. et al. (2016) Mol Cell 64, 1109-1116.
- Munnur, D. et al. (2019) Nucleic Acids Res 47, 5658-5669.
- Rack, J.G.M. et al. (2020) Genes Dev 34, 263-284.
- Vivelo, C.A. and Leung, A.K. (2015) Proteomics 15, 203-17.
- Curtin, N.J. and Szabo, C. (2013) Mol Aspects Med 34, 1217-56.
- Oka, S. et al. (2006) J Biol Chem 281, 705-13.
- Niere, M. et al. (2012) J Biol Chem 287, 16088-102.
- Mashimo, M. et al. (2013) Proc Natl Acad Sci USA 110, 18964-9.
- Mashimo, M. et al. (2019) JCI Insight 4, e124519. doi: 10.1172/jci.insight.124519.
- Danhauser, K. et al. (2018) Am J Hum Genet 103, 817-825.
- Ghosh, S.G. et al. (2018) Am J Hum Genet 103, 431-439.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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