Recombinant Mouse DNA damage-inducible transcript 3 protein (Ddit3)

1. 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 PMID: 28926118
2. Liver ischemia reperfusion injury induces CHOP expression, and CHOP deficiency attenuates liver IRI by inhibiting apoptosis. PMID: 29524333
3. 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. PMID: 28891115
4. these results suggest that CHOP plays a critical role in the progression of kidney fibrosis, likely through regulation of autophagy and apoptosis. PMID: 29425932
5. 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 PMID: 28969695
6. 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. PMID: 28600667
7. This study was undertaken to explore the mechanism whereby ERK5 inhibition instigates pancreatic beta-cell apoptosis via an endoplasmic reticulum stress-dependent signaling pathway. PMID: 28681594
8. 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. PMID: 28726788
9. Constitutive overexpression of the CHOP protein does not induce apoptosis in myelinating glia of the central and peripheral nervous systems PMID: 27335410
10. 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 PMID: 28292936
11. Chop was found to exacerbate allergic airway inflammation by enhancing M2 programming in macrophages PMID: 28238747
12. Our findings support that CHOP may be an important signaling molecule in the progression of chronic kidney disease PMID: 26942460
13. GPR4 blockade attenuated renal injury after IR and reduced the cell apoptosis through the suppression of CHOP expression. PMID: 29089376
14. CHOP deficiency prevents HFD-induced insulin resistance. PMID: 28228268
15. Endoplasmic reticulum stress-induced CHOP activation in the brain is a mechanistic link in the palmitate-induced negative regulation of leptin and IGF1. PMID: 27555288
16. a significant protein-protein interaction between GR and CHOP, (GR-CHOP heterocomplex formation) under endoplasmic reticulum stress conditions, is reported. PMID: 27496643
17. The study shows that FXR/RXR regulates Chop expression in a mouse model of steatohepatitis, providing novel insights into pathogenesis of this disorder. PMID: 28895119
18. Ddit3 suppresses the differentiation of ATDC5 cells PMID: 27845261
19. Free CNPY2 then engages protein kinase R-like endoplasmic reticulum kinase (PERK) to induce expression of the transcription factor C/EBP homologous protein (CHOP), thereby initiating the unfolded protein response. PMID: 28869608
20. SHP and REV-ERBalpha play a critical role in controlling rhythmic CHOP expression in alcoholic fatty liver PMID: 27664470
21. Upregulating HSF1 relieves the tau toxicity in N2a-TauRD DeltaK280 by reducing CHOP and increasing HSP70 a5 (BiP/GRP78). Our work reveals how the bidirectional crosstalk between the two stress response systems promotes early tau pathology and identifies HSF1 being one likely key player in both systems. PMID: 28678786
22. Study showed that Chop is involved in the pathogenesis of pulmonary fibrosis by regulating the generation of M2 macrophages and TGF-beta signaling. PMID: 26883801
23. AMPKalpha1 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. PMID: 27650555
24. The data presented indicate that the unfolded protein response is activated in fibrotic lung tissue and strongly localized to macrophages. GRP78- and CHOP-mediated macrophage apoptosis was found to protect against bleomycin-induced fibrosis. PMID: 27135434
25. Deletion of CHOP attenuates dysfunction of the autophagy/lysosomal pathway in beta-cells of transgenic mice. PMID: 26900721
26. this study demonstrates novel roles for the endoplasmic reticulum stress-response transducer PERK and a downstream effector of its activation, CHOP, in tubule cell production of fibronectin PMID: 26483256
27. CHOP regulates not only apoptosis-related signaling but also ROS formation and inflammation in renal tubular cells during ischemia/reperfusion (I/R). CHOP may play an important role in the pathophysiology of I/R-induced renal injury. PMID: 25178318
28. As a dual function cytokine, IL-1alpha may contribute to the induction of CHOP intracellularly, while IL-1alpha released from necrotic cells accelerates steatohepatitis via induction of inflammatory cytokines by neighboring cells. PMID: 26022690
29. CHOP expression in myeloid cells plays an important role in determining the magnitude and duration of inflammatory response in vivo by modulating expression of proinflammatory cytokines such as IL-6 in infiltrating macrophages. PMID: 26134251
30. the ER stress-induced transcription factor, CHOP, at least in part, plays an important role in the development of bleomycin-induced pulmonary fibrosis PMID: 26005208
31. Data indicate that transcription factor Chop does not play a significant causal role during retinal degeneration. PMID: 26427410
32. Upregulation of PD-1 and PD-L1 was associated with marked increases in GADD153 during myocardial ischemic reperfusion injury. PMID: 25902191
33. Chop deficiency prevents unilateral ureteral obstruction-induced renal fibrosis by attenuating fibrotic signals originated from Hmgb1/TLR4/NFkappaB/IL-1beta signaling. PMID: 26247732
34. findings suggest that the balance between XBP1-mediated adaptive and CHOP-dependent apoptotic UPR is critically important for beta-cell survival during ER stress. PMID: 26135354
35. The enrichment of Gata2 target genes in Ddit3-dependent transcriptional responses suggests that Ddit3 functions in an erythroid transcriptional network nucleated by Gata2. PMID: 26051941
36. knockdown of a proton-sensing G protein-coupled receptor GPR4 markedly reduced CHOP expression and endothelial cell apoptosis after hypoxia exposure. PMID: 25343248
37. NR4A1 protects pancreatic beta-cells against endoplasmic reticulum stress-mediated apoptosis by up-regulating Survivin expression and down-regulating CHOP expression. PMID: 26157144
38. With the development of diabetes, the expression of GRP78 decreases while the expression of UPR-associated proapoptotic transcriptional regulator C/EBP homologous protein (CHOP) increases. PMID: 25529350
39. these data show that IEC-specific overexpression impairs epithelial cell proliferation and mucosal tissue regeneration, suggesting an important role for CHOP beyond mediating apoptosis. PMID: 24850428
40. Data imply the involvement of ER stress/CHOP signaling in CVB3-induced acute viral myocarditis via proapoptotic pathways. PMID: 25985795
41. Ablation of CHOP does not ameliorate cardiac remodeling induced by permanent myocardial infarction. PMID: 26111448
42. Data show that vascular smooth muscle cells (VSMCs)-C/EBP-homologous protein (CHOP) deficiency decreases the proliferation of aortic explant-dderived VSMCs. PMID: 25872946
43. Palmitate-induced apoptosis requires maximal expression of CHOP which is achieved via the downregulation of its repressive microRNA, miR-615-3p. PMID: 25314137
44. Data (including data from knockout mice) suggest that up-regulation of expression of CHOP (c/EBP-homologous protein) and ERO1alpha (oxidoreductin-1-L-alpha) is involved in liver apoptosis/necrosis exhibited in acute liver failure. PMID: 25387528
45. Fibroblasts from two long-lived mice mutants (Snell dwarf and PAPP-A knockout) expressed higher levels of Chop (a ATF4 target gene) during stress, suggesting a connection to longevity. PMID: 24691093
46. Endoplasmic reticulum stress-induced apoptosis contributes to articular cartilage degeneration via C/EBP homologous protein. PMID: 24795271
47. Absence of CHOP partially protects against RGC loss and reduction in retinal function after I/R injury, indicating that CHOP and, thus, ER stress play an important role in RGC apoptosis in retinal I/R injury. PMID: 25414185
48. a role for CHOP as a positive regulator of carcinogen-induced HCC progression PMID: 24339898
49. Suppression of CHOP impaired the transcriptional activation of FGF21. PMID: 24900988
50. following amino acid starvation there is a highly coordinated sequential program of molecular events involving CHOP and leading first to autophagy and then to apoptosis if stress is prolonged. PMID: 24657471

Show More

Hide All

KEGG: mmu:13198

STRING: 10090.ENSMUSP00000026475

UniGene: Mm.110220