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Human Monoclonal DDIT3 Primary Antibody for GS, ICC - ABIN269517
Hull, Zraika, Udayasankar, Aston-Mourney, Subramanian, Kahn: Amyloid formation in human IAPP transgenic mouse islets and pancreas, and human pancreas, is not associated with endoplasmic reticulum stress. in Diabetologia 2009
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Human Polyclonal DDIT3 Primary Antibody for IHC, IHC (p) - ABIN4313145
Nashine, Liu, Kim, Clark, Pang: Role of C/EBP homologous protein in retinal ganglion cell death after ischemia/reperfusion injury. in Investigative ophthalmology & visual science 2015
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Human Polyclonal DDIT3 Primary Antibody for IF (p), IHC (p) - ABIN685447
Du, Zhou, Jia, Huang: SelK is a novel ER stress-regulated protein and protects HepG2 cells from ER stress agent-induced apoptosis. in Archives of biochemistry and biophysics 2010
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Mouse (Murine) Monoclonal DDIT3 Primary Antibody for IP, WB - ABIN2668558
Wang, Kuroda, Sok, Batchvarova, Kimmel, Chung, Zinszner, Ron: Identification of novel stress-induced genes downstream of chop. in The EMBO journal 1998
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Human Polyclonal DDIT3 Primary Antibody for ELISA, WB - ABIN560585
Hong, Kim, Kim, Lee, Shin, Son, Han, Sung, Kwon: Apoptosis induction of 2'-hydroxycinnamaldehyde as a proteasome inhibitor is associated with ER stress and mitochondrial perturbation in cancer cells. in Biochemical pharmacology 2007
Human Monoclonal DDIT3 Primary Antibody for ELISA, WB - ABIN560586
Kemmner, Kessel, Sanchez-Ruderisch, Möller, Hinderlich, Schlag, Detjen: Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2012
Human Polyclonal DDIT3 Primary Antibody for IP, IHC - ABIN223141
Zenkel, Kruse, Naumann, Schlötzer-Schrehardt: Impaired cytoprotective mechanisms in eyes with pseudoexfoliation syndrome/glaucoma. in Investigative ophthalmology & visual science 2007
Atg7 (显示 ATG7 抗体) ablation mainly induced the PERK (显示 EIF2AK3 抗体)-ATF4 (显示 ATF4 抗体)-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
These results suggest JUN (显示 JUN 抗体) and DDIT3 are independently regulated pro-death signaling molecules in retinal ganglion cells and together account for the vast majority of apoptotic signaling in retinal ganglion cells after axonal injury
We demonstrated that PPARalpha (显示 PPARA 抗体) activation contributes to liver protection and decreases liver inflammation in acute liver failue (ALF (显示 GTF2A1L 抗体)), particularly through regulating CHOP. Our findings may provide a rationale for targeting PPARalpha (显示 PPARA 抗体) as a potential therapeutic strategy to ameliorate ALF (显示 GTF2A1L 抗体).
This study was undertaken to explore the mechanism whereby ERK5 (显示 MAPK7 抗体) inhibition instigates pancreatic beta-cell apoptosis via an endoplasmic reticulum stress-dependent signaling pathway.
ER stress is induced early in EAE and that modulation of ER stress by inhibition of eIF2alpha (显示 EIF2A 抗体)-CHOP and activation of XBP-1 (显示 XBP1 抗体) in RGC specifically, protects RGC somata and axons and preserves visual function.
Constitutive overexpression of the CHOP protein does not induce apoptosis in myelinating glia of the central and peripheral nervous systems
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 (显示 D4S234E 抗体).
Activation of the ER stress execution proteins, PERK (显示 EIF2AK3 抗体) and CHOP10, was evaluated to determine whether this process was involved in 15d-PMJ2 cell death. 15d-PMJ2 increased the phosphorylation of PERK (显示 EIF2AK3 抗体) 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
activation of the IGF-IR/PI3K (显示 PIK3CA 抗体)/Akt (显示 AKT1 抗体) signaling system is a common pattern in MLS which appears to be transcriptionally controlled, at least in part by induction of IGF2 gene transcription in a FUS (显示 FUS 抗体)-DDIT3-dependent manner.
GRP78 (显示 HSPA5 抗体) silencing promoted lung epithelial cell apoptosis during hyperoxia, via regulation of the CHOP pathway.
siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 (显示 TNFRSF10B 抗体) 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
GPR4 (显示 GPR4 抗体) blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression.
Endoplasmic reticulum stress-induced CHOP activation in the brain is a mechanistic link in the palmitate-induced negative regulation of leptin (显示 LEP 抗体) and IGF1 (显示 IGF1 抗体).
CHOP negatively regulates Polo-like kinase 2 (显示 PLK2 抗体) expression via recruiting C/EBPalpha (显示 CEBPA 抗体) 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 (显示 HSPA5 抗体) inhibition enhances ATF4 (显示 ATF4 抗体)-induced cell death by the deubiquitination and stabilization of CHOP in human osteosarcoma cells.
a significant protein-protein interaction between GR and CHOP, (GR-CHOP heterocomplex formation) under endoplasmic reticulum stress conditions, is reported.
CHOP (GADD153) is an inhibitor of Wnt (显示 WNT2 抗体)/TCF (显示 HNF4A 抗体) 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