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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 Antibodies (66) and Protein Phosphatase 1, Regulatory (Inhibitor) Subunit 15A Proteins (7) and many more products for this protein.
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Through aging or a high fat diet, insulin (show INS ELISA Kits) 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 ELISA Kits) combined with amino acid deprivation through regulation of mTOR (show FRAP1 ELISA Kits) 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 (show SLC38A7 ELISA Kits) SNAT2 (show SLC38A2 ELISA Kits).
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 ELISA Kits) expression, but also reduced hepatic damage.
Thus these results indicate that GADD34 appears to suppress myofibroblast differentiation through inhibiting Smad3 (show SMAD3 ELISA Kits)-dependent TGFbeta (show TGFB1 ELISA Kits) signal pathway and promote its apoptosis by activating caspase-3 (show CASP3 ELISA Kits) 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 indicate that GADD34 is the regulatory subunit of rotein phosphatase-1 (PP1 (show PPP1CC ELISA Kits)) to specify PP1 (show PPP1CC ELISA Kits) to dephosphorylate TGF-beta-activated kinase 1 (TAK1 (show MAP3K7 ELISA Kits)) Ser412.
The reactive oxygen species-generating NADPH oxidase-4 (Nox4 (show NOX4 ELISA Kits)) is induced downstream of ATF4 (show ATF4 ELISA Kits), binds to a PP1 (show PPA1 ELISA Kits)-targeting subunit GADD34 at the endoplasmic reticulum, and inhibits PP1 (show PPA1 ELISA Kits) activity to increase eIF2alpha (show EIF2A ELISA Kits) phosphorylation and ATF4 (show ATF4 ELISA Kits) 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 ELISA Kits) and eIF2alpha (show EIF2A ELISA Kits) 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 ELISA Kits) combined with amino acid deprivation through regulation of mTOR (show FRAP1 ELISA Kits) signaling pathway in macrophages.
Data indicate that protein phosphatase 1 (show PPP1CB ELISA Kits) subunit GADD34 directly interacts with eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha (show EIF2S1 ELISA Kits)).
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 ELISA Kits) SNAT2 (show SLC38A2 ELISA Kits).
Nuclear export of HTLV-1 basic leucine-zipper factor (HBZ (show HBZ ELISA Kits)) is essential for its interaction with GADD34 and increased phosphorylation of S6 kinase (show RPS6KB1 ELISA Kits), which is an established downstream target of the mTOR (show FRAP1 ELISA Kits) pathway.
GADD34 phosphorylation on tyrosine 262 modulates endoplasmic reticulum stress signaling and cell fate.
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