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Results identify endoplasmic reticulum stress as an age-dependent modifier of islet survival and function by mechanisms implicating enhancement of CHOP activity and inhibition of the protective activity of p21.
Activation of the ER stress execution proteins, PERK (show EIF2AK3 Proteins) and CHOP10, was evaluated to determine whether this process was involved in 15d-PMJ2 cell death. 15d-PMJ2 increased the phosphorylation of PERK (show EIF2AK3 Proteins) and expression of CHOP10 in tumorigenic but not nontumorigenic cells
Chop was found to exacerbate allergic airway inflammation by enhancing M2 programming in macrophages
Our findings support that CHOP may be an important signaling molecule in the progression of chronic kidney disease
GPR4 (show GPR4 Proteins) blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression.
CHOP deficiency prevents HFD-induced insulin (show INS Proteins) resistance.
Endoplasmic reticulum stress-induced CHOP activation in the brain is a mechanistic link in the palmitate-induced negative regulation of leptin (show LEP Proteins) and IGF1 (show IGF1 Proteins).
a significant protein-protein interaction between GR and CHOP, (GR-CHOP heterocomplex formation) under endoplasmic reticulum stress conditions, is reported.
The study shows that FXR (show NR1H4 Proteins)/RXR regulates Chop expression in a mouse model of steatohepatitis, providing novel insights into pathogenesis of this disorder.
Ddit3 suppresses the differentiation of ATDC5 cells
siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 (show TNFRSF10B Proteins) up-regulation and TRAIL sensitivity in prostate cancer cells. Our study shows a novel effect of cyproterone acetate on apoptosis pathways in prostate cancer cells and raises the possibility that a combination of TRAIL with cyproterone acetate could be a promising strategy for treating castration-resistant prostate cancer
asthmatic patients exhibited aberrant Chop expression along with endoplasmic reticulum stress
CHOP negatively regulates Polo-like kinase 2 (show PLK2 Proteins) expression via recruiting C/EBPalpha (show CEBPA Proteins) to the upstream-promoter in human osteosarcoma cell line during ER stress
VEGF is an important angiogenic signal required for tissue expansion. We show that VEGFA variation giving allele-specific response to transcription factors with overlapping binding sites associate closely with circulating TSH levels. Because CHOP is induced by several types of intracellular stress, this indicates that cellular stress could be involved in the normal or pathophysiological response of the thyroid to TSH
GRP78 (show HSPA5 Proteins) inhibition enhances ATF4 (show ATF4 Proteins)-induced cell death by the deubiquitination and stabilization of CHOP in human osteosarcoma cells.
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK (show MAPK8 Proteins), AP-1 (show FOSB Proteins), and CHOP may interfere with complete autophagy.
The role of neutrophil elastase (show ELANE Proteins) in the activation of unfolded protein response effector molecules via PERK (show EIF2AK3 Proteins) and CHOP is reported.
CHOP (GADD153) is an inhibitor of Wnt (show WNT2 Proteins)/TCF (show HNF4A Proteins) signals
This gene encodes a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors. The protein functions as a dominant-negative inhibitor by forming heterodimers with other C/EBP members, such as C/EBP and LAP (liver activator protein), and preventing their DNA binding activity. The protein is implicated in adipogenesis and erythropoiesis, is activated by endoplasmic reticulum stress, and promotes apoptosis. Fusion of this gene and FUS on chromosome 16 or EWSR1 on chromosome 22 induced by translocation generates chimeric proteins in myxoid liposarcomas or Ewing sarcoma. Multiple alternatively spliced transcript variants encoding two isoforms with different length have been identified.
C/EBP homoologous protein 10
, C/EBP zeta
, CCAAT/enhancer-binding protein homologous protein
, DNA damage-inducible transcript 3 protein
, c/EBP-homologous protein 10
, growth arrest and DNA-damage-inducible protein GADD153
, C/EBP homologous protein
, growth arrest and DNA damage-inducible protein GADD153
, growth arrest and DNA damage-inducible
, transcription factor GADD153
, C/EBP-homologous protein 10
, DNA-damage inducible transcript 3