Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Mouse (Murine) Antibodies:
anti-Rat (Rattus) Antibodies:
Go to our pre-filtered search.
Human Polyclonal PPP1R15A Primary Antibody for WB - ABIN2473740
Luo, Gong, Dong: [Gastric elimination research on patients with gastric disease]. in Zhonghua nei ke za zhi 1991
Show all 4 Pubmed References
Human Polyclonal PPP1R15A Primary Antibody for ELISA, IHC - ABIN262735
Kojima, Takeuchi, Haneda, Yagi, Hasegawa, Yamaki, Takeda, Akira, Shimokata, Isobe: The function of GADD34 is a recovery from a shutoff of protein synthesis induced by ER stress: elucidation by GADD34-deficient mice. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2003
Show all 2 Pubmed References
GADD34 suppresses lipopolysaccharide-induced sepsis and tissue injury through the regulation of macrophage activation.
Translation arrest is further demonstrated to be key for anti-viral response by acting synergistically with MAVS (show MAVS Antibodies) activation to amplify TBK1 (show TBK1 Antibodies) signaling and IFN-beta (show IFNB1 Antibodies) mRNA transcription, while GADD34-dependent protein synthesis recovery contributes to the heterogeneous expression of interferon (show IFNA Antibodies) observed in dsRNA-activated cells.
Results highlighted the essential roles played by GADD34 and CReP (show PPP1R15B Antibodies) in regulating mRNA translation during unstressed conditions and following endoplasmic reticulum stress.
Sustained protein synthesis sensitized cells to pharmacological induction of the Unfolded Protein Response (UPR), and the observed decrease in cell viability was restored upon inhibition of GADD34 activity. We conclude that NMP4 (show ZNF384 Antibodies) is a key regulator of ribosome biogenesis and the UPR, which together play a central role in determining cell viability during endoplasmic reticulum stress.
Through aging or a high fat diet, insulin (show INS Antibodies) signaling in GADD34-deficient liver converted to be down regulated compared with WT mice.
Results show that GADD34 plays a vital role in promoting cell death following proteasome inhibition via enhancing protein synthesis involved in endoplasmic reticulum stress, reactive oxygen species production and autophagy formation.
avidity for the substrate plays an important role in imparting specificity on the PPP1R15B-PP1G-actin ternary complex.
GADD34 enhances autophagy and suppresses apoptosis stimulated by LPS (show TLR4 Antibodies) combined with amino acid deprivation through regulation of mTOR (show FRAP1 Antibodies) signaling pathway in macrophages.
GADD34 upregulated pro-inflammatory mediator.
GADD34 promotes cell survival and adaptation to increased extracellular osmolarity by increasing the uptake of small neutral amino acids via the amino acid transporter SNAT2 (show SLC38A2 Antibodies).
GADD34 constitutes a mechanistic link between endoplasmic reticulum stress and mTOR (show FRAP1 Antibodies) inactivation, therefore promotes cell survival during endoplasmic reticulum stress.
reduction of GADD34 expression significantly suppressed tumor, and resulted in decreased accumulation of MDSCs and T-cells, and inhibition of GADD34 reduced secretion of vascular epithelial growth factor alpha and transforming growth factor beta by MDSCs
ANXA11 (show ANXA11 Antibodies) rs1049550 and PPP1R15A rs557806 may improve the identification of mCRC patients sensitive to bevacizumab regimens, and further validation is required in large cohorts
Data of this study strengthen the evidence of an unfolded protein response during the course of RA and provide an insight of the potential interest in GADD34 as a relevant marker for RA.
The results suggest that dephosphorylation of eIF2a (show EIF2S1 Antibodies) by GADD34 plays an important role in doxorubicin resistance of MCF-7/ADR (show AKR1B1 Antibodies) cells.
The reactive oxygen species-generating NADPH oxidase-4 (Nox4 (show NOX4 Antibodies)) is induced downstream of ATF4 (show ATF4 Antibodies), binds to a PP1 (show PPA1 Antibodies)-targeting subunit GADD34 at the endoplasmic reticulum, and inhibits PP1 (show PPA1 Antibodies) activity to increase eIF2alpha (show EIF2A Antibodies) phosphorylation and ATF4 (show ATF4 Antibodies) levels.
stress pathways lead to the induction of the protein GADD34, which appears to provide protection against the toxic effects of the secreted virulence factors in Pseudomonas aeruginosa infection
The data highlight independent interactions of PP1 (show PPA1 Antibodies) and eIF2alpha (show EIF2A Antibodies) with GADD34, demonstrating that GADD34 functions as a scaffold both in vitro and in cells
GADD34 may play a neuroprotective role against amyloid-beta toxicity.
GADD34 enhances autophagy and suppresses apoptosis stimulated by LPS (show IRF6 Antibodies) combined with amino acid deprivation through regulation of mTOR (show FRAP1 Antibodies) signaling pathway in macrophages.
This gene is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The induction of this gene by ionizing radiation occurs in certain cell lines regardless of p53 status, and its protein response is correlated with apoptosis following ionizing radiation.
protein phosphatase 1, regulatory (inhibitor) subunit 15A
, growth arrest and DNA damage-inducible protein GADD34
, growth arrest and DNA-damage-inducible 34
, myeloid differentiation primary response gene 116
, myeloid differentiation primary response protein MyD116
, protein phosphatase 1 regulatory subunit 15A
, myeloid differentiation primary response protein MyD116 homolog
, progression elevated gene 3 protein