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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
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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
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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 (显示 MAVS 抗体) activation to amplify TBK1 (显示 TBK1 抗体) signaling and IFN-beta (显示 IFNB1 抗体) mRNA transcription, while GADD34-dependent protein synthesis recovery contributes to the heterogeneous expression of interferon (显示 IFNA 抗体) observed in dsRNA-activated cells.
Results highlighted the essential roles played by GADD34 and CReP (显示 PPP1R15B 抗体) 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 (显示 ZNF384 抗体) 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 (显示 INS 抗体) 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 (显示 TLR4 抗体) combined with amino acid deprivation through regulation of mTOR (显示 FRAP1 抗体) 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 (显示 SLC38A2 抗体).
GADD34 constitutes a mechanistic link between endoplasmic reticulum stress and mTOR (显示 FRAP1 抗体) 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 (显示 ANXA11 抗体) 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 (显示 EIF2S1 抗体) by GADD34 plays an important role in doxorubicin resistance of MCF-7/ADR (显示 AKR1B1 抗体) cells.
The reactive oxygen species-generating NADPH oxidase-4 (Nox4 (显示 NOX4 抗体)) is induced downstream of ATF4 (显示 ATF4 抗体), binds to a PP1 (显示 PPA1 抗体)-targeting subunit GADD34 at the endoplasmic reticulum, and inhibits PP1 (显示 PPA1 抗体) activity to increase eIF2alpha (显示 EIF2A 抗体) phosphorylation and ATF4 (显示 ATF4 抗体) 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 (显示 PPA1 抗体) and eIF2alpha (显示 EIF2A 抗体) 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 (显示 IRF6 抗体) combined with amino acid deprivation through regulation of mTOR (显示 FRAP1 抗体) 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