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anti-Mouse (Murine) DDIT3 Antikörper:
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Human Monoclonal DDIT3 Primary Antibody für 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
Show all 20 Pubmed References
Human Polyclonal DDIT3 Primary Antibody für 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 für ELISA, ICC - ABIN6260817
Zhao, Liu, Wang, Dai, Cheng, Cheng, Chen, Zhang, Chen: In vitro additive antitumor effects of dimethoxycurcumin and 5-fluorouracil in colon cancer cells. in Cancer medicine 2018
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Human Polyclonal DDIT3 Primary Antibody für ELISA, ICC - ABIN6260816
Yang, Teng, Li, Xue, Guo, Xiao, Wu: Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress. in Oxidative medicine and cellular longevity 2016
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Mouse (Murine) Monoclonal DDIT3 Primary Antibody für 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 für IHC (fro), IP - ABIN549269
Lu, Struijs, Mei, Witte-Bouma, Korteland-van Male, de Bruijn, van Goudoever, Renes: Endoplasmic reticulum stress, unfolded protein response and altered T cell differentiation in necrotizing enterocolitis. in PLoS ONE 2013
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Human Polyclonal DDIT3 Primary Antibody für 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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Human Polyclonal DDIT3 Primary Antibody für 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 Polyclonal DDIT3 Primary Antibody für IP, IHC - ABIN223141
Zenkel, Kruse, Naumann, Schlötzer-Schrehardt: Impaired cytoprotective mechanisms in eyes with pseudoexfoliation syndrome/glaucoma. in Investigative ophthalmology & visual science 2007
Human Monoclonal DDIT3 Primary Antibody für 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
Data suggest that endoplasmic reticulum stress-induced CHOP/Ddit3 inhibits expression of Bip/Grp78 and Atf4; ATF4, in turn, plays critical role in CHOP-mediated regulation of B-cell receptor-controlled murine gammaherpesvirus-68 lytic replication. (CHOP/Ddit3 = DNA-damage inducible transcript-3; Bip/Grp78 = chaperone BiP 78 kDa; Atf4 = activating transcription factor-4)
Endoplasmic reticulum stress-induced activation of CHOP suppresses intestinal stem cell proliferation and intestinal epithelial cell renewal, which leads to disruption of intestinal barrier function, massive bacterial translocation, activation of kupffer cells, and periportal inflammation and, eventually, results in fibrosis in the liver
Liver ischemia reperfusion injury induces CHOP expression, and CHOP deficiency attenuates liver IRI by inhibiting apoptosis.
Study indicates that CHOP deficiency protects against Western diet-induced AoV calcification in Apoe(-/-) mice. CHOP deficiency prevents oxLDL-induced VIC osteoblastic differentiation via preventing VIC-derived ABs releasing.
these results suggest that CHOP plays a critical role in the progression of kidney fibrosis, likely through regulation of autophagy and apoptosis.
Atg7 ablation mainly induced the PERK-ATF4-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
These results suggest JUN 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 activation contributes to liver protection and decreases liver inflammation in acute liver failue (ALF), particularly through regulating CHOP. Our findings may provide a rationale for targeting PPARalpha as a potential therapeutic strategy to ameliorate ALF.
This study was undertaken to explore the mechanism whereby ERK5 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-CHOP and activation of XBP-1 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.
Activation of the ER stress execution proteins, PERK and CHOP10, was evaluated to determine whether this process was involved in 15d-PMJ2 cell death. 15d-PMJ2 increased the phosphorylation of PERK 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 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression.
CHOP deficiency prevents HFD-induced insulin resistance.
Endoplasmic reticulum stress-induced CHOP activation in the brain is a mechanistic link in the palmitate-induced negative regulation of leptin and IGF1.
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/RXR regulates Chop expression in a mouse model of steatohepatitis, providing novel insights into pathogenesis of this disorder.
The herein presented data uncover a novel mechanism by which the fusion oncogene FUS-CHOP actively promotes invasion in myxoid and round cell liposarcoma through the activation of a SRC/FAK/RHO/ROCK signaling axis.
Low expression of CHOP predicts the poor prognosis of advanced gastric cancer patients, and CHOP may be a prognostic biomarker for patients with advanced gastric cancer.
This study demonstrates increased placental expression of HIF-1alpha and CHOP in preeclampsia compared to normotensive pregnancies which correlate to their increased syncytiotrophoblast microvesicles concentration in maternal circulation.
CHOP/GADD153-dependent apoptosis reflects expression of micro-RNA, miR-216b.
These results indicated activation of Unfolded Protein Response (UPR) in different cell types derived from Gaucher disease patients, highlighting the generality of this process in this disease. They also showed that the UPR-regulated CHOP transcription factor induces transcription of the GBA1 gene.
activation of the IGF-IR/PI3K/Akt 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-DDIT3-dependent manner.
GRP78 silencing promoted lung epithelial cell apoptosis during hyperoxia, via regulation of the CHOP pathway.
siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 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 expression via recruiting C/EBPalpha 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 inhibition enhances ATF4-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, AP-1, and CHOP may interfere with complete autophagy.
The role of neutrophil elastase in the activation of unfolded protein response effector molecules via PERK and CHOP is reported.
The PERK-eIF2alpha-ATF4-CHOP signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review)
HDL isolated from patients with metabolic syndrome induced macrophage apoptosis, oxidative stress, and CHOP upregulation, which were blocked by PBA and DPI. These data indicate that ox-HDL may activate ER stress-CHOP-induced apoptotic pathway in macrophages via enhanced oxidative stress and that this pathway may be mediated by TLR4.
CHOP (GADD153) is an inhibitor of Wnt/TCF 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