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PPP1R15A is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. Additionally we are shipping Protein Phosphatase 1, Regulatory (Inhibitor) Subunit 15A Proteins (7) and Protein Phosphatase 1, Regulatory (Inhibitor) Subunit 15A Kits (2) and many more products for this protein.
Showing 10 out of 68 products:
Human Polyclonal PPP1R15A Primary Antibody for IHC (p), WB - ABIN782866
Panaretakis, Kepp, Brockmeier, Tesniere, Bjorklund, Chapman, Durchschlag, Joza, Pierron, van Endert, Yuan, Zitvogel, Madeo, Williams, Kroemer: Mechanisms of pre-apoptotic calreticulin exposure in immunogenic cell death. in The EMBO journal 2009
Human Polyclonal PPP1R15A Primary Antibody for IHC, ELISA - ABIN184571
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
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 expression was upregulated in the liver of mice after exposure to a carcinogen, diethylnitrosamine (DEN). In both acute and chronic DEN treatment models, GADD34 deficiency not only decreased oncogene (show RAB1A Antibodies) expression, but also reduced hepatic damage.
Thus these results indicate that GADD34 appears to suppress myofibroblast differentiation through inhibiting Smad3 (show SMAD3 Antibodies)-dependent TGFbeta (show TGFB1 Antibodies) signal pathway and promote its apoptosis by activating caspase-3 (show CASP3 Antibodies) pathway
GADD34 works to inhibit the proliferation and differentiation of HSCs or myeloid precursor cells and maintains homeostatic differentiation of neutrophil-lineage cells to avoid early immunological senescence.
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.
Data indicate that protein phosphatase 1 (show PPP1CB Antibodies) subunit GADD34 directly interacts with eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha (show EIF2S1 Antibodies)).
GADD34 was increased in neurons of human Alzheimer's disease (AD) brains. Additionally, this finding was also observed in oligodendrocytes in human AD brains. GADD34 could be a therapeutic target for preventing ER stress in neuronal cells in AD.
GADD34 promotes cell survival and adaptation to increased extracellular osmolarity by increasing the uptake of small neutral amino acids via the amino acid transporter (show SLC43A2 Antibodies) SNAT2 (show SLC38A2 Antibodies).
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