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The study shows that FXR (show NR1H4 ELISA Kits)/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
Free CNPY2 (show CNPY2 ELISA Kits) then engages protein kinase (show CDK7 ELISA Kits) R-like endoplasmic reticulum kinase (PERK (show EIF2AK3 ELISA Kits)) to induce expression of the transcription factor C/EBP homologous protein (CHOP), thereby initiating the unfolded protein response.
SHP (show LAMC1 ELISA Kits) and REV-ERBalpha (show NR1D1 ELISA Kits) play a critical role in controlling rhythmic CHOP expression in alcoholic fatty liver
ER stress-induced increase in ATF4 (show ATF4 ELISA Kits) and CHOP expression is initiated by an increase in Atf4 (show ATF4 ELISA Kits) and Chop mRNA, which is also dependent upon eIF2alpha (show EIF2A ELISA Kits) phosphorylation.
Upregulating HSF1 (show HSF1 ELISA Kits) relieves the tau toxicity in N2a-TauRD DeltaK280 by reducing CHOP and increasing HSP70 (show HSP70 ELISA Kits) a5 (BiP/GRP78 (show HSPA5 ELISA Kits)). Our work reveals how the bidirectional crosstalk between the two stress response systems promotes early tau pathology and identifies HSF1 (show HSF1 ELISA Kits) being one likely key player in both systems.
Study showed that Chop is involved in the pathogenesis of pulmonary fibrosis by regulating the generation of M2 macrophages and TGF-beta (show TGFB1 ELISA Kits) signaling.
AMPKalpha1 (show PRKAA1 ELISA Kits) mediates CHOP ubiquitination and proteasomal degradation in macrophages by promoting the phosphorylation of CHOP at serine 30. Transfection of Chop-specific siRNA but not control siRNA reduced both CHOP level and injury-induced neointimal disruption in vivo.
The data presented indicate that the unfolded protein response is activated in fibrotic lung tissue and strongly localized to macrophages. GRP78 (show HSPA5 ELISA Kits)- and CHOP-mediated macrophage apoptosis was found to protect against bleomycin-induced fibrosis.
Deletion of CHOP attenuates dysfunction of the autophagy/lysosomal pathway in beta-cells of transgenic mice.
These results suggest that Bacteroides fragilis enterotoxin induced accumulation of autophagosomes in endothelial cells, but activation of a signaling pathway involving JNK (show MAPK8 ELISA Kits), AP-1 (show FOSB ELISA Kits), and CHOP may interfere with complete autophagy.
The role of neutrophil elastase (show ELANE ELISA Kits) in the activation of unfolded protein response effector molecules via PERK (show EIF2AK3 ELISA Kits) and CHOP is reported.
The PERK (show EIF2AK3 ELISA Kits)-eIF2alpha (show EIF2A ELISA Kits)-ATF4 (show ATF4 ELISA Kits)-CHOP signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review)
HDL (show HSD11B1 ELISA Kits) isolated from patients with metabolic syndrome induced macrophage apoptosis, oxidative stress, and CHOP upregulation, which were blocked by PBA and DPI (show DSP ELISA Kits). These data indicate that ox-HDL (show HSD11B1 ELISA Kits) may activate ER stress-CHOP-induced apoptotic pathway in macrophages via enhanced oxidative stress and that this pathway may be mediated by TLR4 (show TLR4 ELISA Kits).
We found that 25-epi (show TFPI ELISA Kits) Ritterostatin GN1N induced cell death in melanoma cells at nanomolar concentrations, and this cell death was characterized by inhibition of GRP78 (show HSPA5 ELISA Kits) expression, increased expression of the ER stress marker CHOP, loss of mitochondrial membrane potential, and lipidation of the autophagy marker protein LC3B (show MAP1LC3B ELISA Kits).
Western blot analysis of subcutaneously implanted AsPC-1 and BxPC-3 tumors as well as orthotopically implanted Panc-1 tumors demonstrated upregulation of BIP (show GDF10 ELISA Kits), CHOP, and IRE1alpha (show ERN1 ELISA Kits) expression in the tumor lysates from penfluridol-treated mice as compared to tumors from control mice
CHOP protects hepatocytes from a diet high in fat, fructose, and cholesterol (HFCD) and its induced ER stress, and has a significant role in the mechanism of liraglutide-mediated protection against non-alcoholic steatohepatitis (NASH (show SAMSN1 ELISA Kits)) pathogenesis.
Downregulation of CHOP by small interfering RNA somewhat restored expression of AR suggesting that AR degradation is dependent on ER stress pathway. Future studies will need to evaluate other aspects of the unfolded protein response pathway to characterize the regulation of AR degradation
Herein, the authors extend their previous research and provide evidence that ORF57 of human herpesvirus-8 interacts with CHTOP (show CHTOP ELISA Kits) and CIP29 (show SARNP ELISA Kits), in contrast to POLDIP3 (show POLDIP3 ELISA Kits).
CHOP (GADD153) is an inhibitor of Wnt (show WNT2 ELISA Kits)/TCF (show HNF4A ELISA Kits) 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