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Poly(ADP-ribose) glycohydrolase (PARG) is the major enzyme responsible for the catabolism of poly(ADP-ribose), a reversible covalent-modifier of chromosomal proteins. Additionally we are shipping PARG Proteins (5) and PARG Kits (4) and many more products for this protein.
Showing 10 out of 40 products:
Human Polyclonal PARG Primary Antibody for EIA, WB - ABIN953994
Whatcott, Meyer-Ficca, Meyer, Jacobson: A specific isoform of poly(ADP-ribose) glycohydrolase is targeted to the mitochondrial matrix by a N-terminal mitochondrial targeting sequence. in Experimental cell research 2009
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Human Polyclonal PARG Primary Antibody for IHC (p), WB - ABIN391439
Meyer, Meyer-Ficca, Whatcott, Jacobson, Jacobson: Two small enzyme isoforms mediate mammalian mitochondrial poly(ADP-ribose) glycohydrolase (PARG) activity. in Experimental cell research 2007
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Human Polyclonal PARG Primary Antibody for IF, WB - ABIN521952
Boudra, Bolin, Chiker, Fouquin, Zaremba, Vaslin, Biard, Cordelières, Mégnin-Chanet, Favaudon, Fernet, Pennaneach, Hall: PARP-2 depletion results in lower radiation cell survival but cell line-specific differences in poly(ADP-ribose) levels. in Cellular and molecular life sciences : CMLS 2015
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PARG inhibition leads to stalled replication forks and increased homologous recombination (HRR). The lack of HRR proteins at PARG inhibitor-induced replication stalling that induces cell death.
Data show that poly-(ADP-ribose) polymerase 1 (PARP1 (show PARP1 Antibodies)) opposes the function of poly-(ADP-ribose) glycohydrolase (PARG) during regulation of bone morphogenetic protein target gene expression.
Poly(ADP-ribosyl) glycohydrolase (PARG) is involved in cell proliferation and DNA synthesis, with depletion leading to replication-coupled H2AX (show H2AFX Antibodies) phosphorylation. In addition, PARG depletion or inhibition slows down individual replication forks similarly to mild chemotherapeutic treatment.
Studies indicate that poly (ADP-ribose) glycohydrolase (PARG) and terminal ADP-ribose glycohydrolase 1 (TARG1 (show NDRG1 Antibodies)) are key enzymes in poly(ADP-ribose) polymerases (PARPs)-mediated ADP-ribosylation.
Nuclear Smad (show SMAD1 Antibodies) function is negatively regulated by PARP-1 (show PARP1 Antibodies) that is assisted by PARP-2 (show PARP2 Antibodies) and positively regulated by PARG during the course of TGFB (show TGFB1 Antibodies) signaling.
Radiation-induced G2/M arrest was largely suppressed by PARG siRNA in PC-14 and A427 cells, which exhibited significantly enhanced radiosensitivity in response to PARG knockdown.
The amount of poly(ADP-ribose) in a cell is regulated under the control of PARP1 (show PARP1 Antibodies)/PARG gene expression balance.
PARG knockdown enhances sensitivity to MMS in MIAPaCa2 and RKO tumor cell lines.
poly(ADP-ribose) glycohydrolase is crucial for Trypanosoma cruzi infection cycle.
Therefore, strategies that target PAR (show JTB Antibodies) metabolism for the improved treatment of cancer may be required to target PARP-1 (show PARP1 Antibodies) and PARG individually in order to optimize cancer cell death.
This study contributes to the understanding of PARG catalytic and regulatory mechanisms as well as the rational design of PARG inhibitors.
PARG110 knockout retinal explants were highly resistant to cyclic GMP (show NT5C2 Antibodies) toxicity.
we investigated the role of PARG in photoreceptor degeneration using the PARG-110 knock out mouse and report for the first time on PARG expression in wild-type and knock-out retina.
PARG release of PAR (show AFG3L2 Antibodies) attached to nuclear proteins, followed by ARH3 (show ADPRHL2 Antibodies) cleavage of PAR (show AFG3L2 Antibodies), is essential in regulating PAR (show AFG3L2 Antibodies)-dependent apoptosis-inducing factor (show AIFM1 Antibodies) release from mitochondria and parthanatos.
Data indicate that poly(ADP-ribose) glycohydrolase Parg(-/-) cells were more sensitive to gamma-irradiation than poly(ADP-ribose) polymerase-1 Parp-1 (show PARP1 Antibodies)(-/-) cells.
Results define PARG as a coactivator regulating chromatin remodeling during retinoic acid receptor (show RARA Antibodies)-dependent gene expression.
Results demonstrate nuclear AIF (show AIFM1 Antibodies) translocation only in PARG-null TS cells, which demonstrates the presence of AIF (show AIFM1 Antibodies)-mediated cell death.
PARP-1 (show PARP1 Antibodies)/PARG control a cell death signal pathway that operates between five different cell compartments and communicates via three types of chemical messengers: a nucleotide, a cation, and proteins
PARG-deficient cells showed a compromised DNA repair and increased genomic instability.
Hydrolysis of PARP (show PARP1 Antibodies) requires PARG.
Poly(ADP-ribose) glycohydrolase (PARG) is the major enzyme responsible for the catabolism of poly(ADP-ribose), a reversible covalent-modifier of chromosomal proteins. The protein is found in many tissues and may be subject to proteolysis generating smaller, active products.
mitochondrial poly(ADP-ribose) glycohydrolase
, poly(ADP-ribose) glycohydrolase
, poly(ADP-ribose) glycohydrolase 60 kDa isoform
, cytosolic poly(ADP-ribose) glycohydrolase
, mitochondrial poly(ADP-ribose) glycohydrolase 63 kDa isoform