Ignet

Gene Information

Gene symbol: DDIT3

Gene name: DNA-damage-inducible transcript 3

HGNC ID: 2726

Synonyms: CHOP10, GADD153, CHOP

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	ALB	1 hits
3	APLN	1 hits
4	ATF6	1 hits
5	CASP12	1 hits
6	CCL2	1 hits
7	CDK5	1 hits
8	CEBPA	1 hits
9	CXCL1	1 hits
10	CXCL2	1 hits
11	DDN	1 hits
12	EBP	1 hits
13	EIF2S1	1 hits
14	FUS	1 hits
15	GADD45A	1 hits
16	GAS5	1 hits
17	GTF2A1	1 hits
18	HSPA5	1 hits
19	IL6	1 hits
20	INS	1 hits
21	NPHS1	1 hits
22	NPHS2	1 hits
23	PAWR	1 hits
24	SH3D19	1 hits
25	TAS2R13	1 hits
26	TLR4	1 hits
27	WT1	1 hits
28	WTIP	1 hits
29	XBP1	1 hits

Related Sentences

#	PMID	Sentence
1	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
2	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
3	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
4	34993544	ER stress biomarkers (GRP78, p-eIF2α or CHOP), intracellular ROS generation, integrin-β3 and cell adhesion and migration were studied in a treatment of experiment using TGF-β1 with and without the ER stress inhibitors: 4-phenylbutyric acid (4-PBA, a chemical chaperone), salubrinal (an eIF2α dephosphorylation inhibitor) and N-acetylcysteine (NAC, an antioxidant).
5	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
6	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
7	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
8	34993544	ER stress biomarkers (p-eIF2α/eIF2α and GRP78), ROS generation and intergrin-β3 expression increased after TGF-β1 treatment.
9	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
10	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
11	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
12	34993544	NAC down-regulated the expression of GRP78 after TGF-β1 treatment. 4-PBA attenuated TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation and intergrin-β3 expression.
13	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
14	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
15	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
16	34993544	However, salubrinal did not inhibit TGF-β1-induced p-eIF2α/eIF2α, CHOP, ROS generation or integrin-β3 expression.
17	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
18	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
19	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
20	34993544	This study demonstrated that TGF-β1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2α/CHOP pathway.
21	33776779	Reduction in CHOP expression and IL-6 release was observed in jj primary aortic endothelial cells exposed to PA compared to Nj cells.
22	33776779	Upon Ang II treatment, primary podocytes from jj Gunn rats showed lower DNA fragmentation, cleaved caspase-3, and cleaved PARP induction than primary podocytes from Nj Gunn rats.
23	33776779	In HK2 cells, the induction by Ang II of HIF-1α and LOXl2 was significantly reduced by UCB pretreatment.
24	33323915	RESULTS Paclitaxel restored downregulated expression of nephrin and synaptopodin and upregulated VEGF expression after injury induced by palmitate.
25	33323915	Four endoplasmic reticulum stress markers, ATF-6alpha, Bip, CHOP, and spliced xBP1, were significantly increased in palmitate-treated podocytes compared with control podocytes.
26	33323915	Paclitaxel alleviated the expression levels of the antioxidant molecules, Nrf-2, HO-1, SOD-1, and SOD-2.
27	33323915	The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3.
28	32691413	Thus, in this study, the role of miR-27a-3p-prohibitin/TMBIM6 signaling axis in the progression of DN was elucidated.
29	32691413	Our results showed that miR-27a-3p was upregulated and prohibitin or transmembrane BAX inhibitor motif containing 6 (TMBIM6) was downregulated in the kidney tissues of db/db mice and HG-treated HK-2 cells.
30	32691413	Silencing miR-27a-3p enhanced the expression of prohibitin and TMBIM6 in the kidney tissues and HK-2 cells.
31	32691413	MiR-27a-3p silencing ameliorated renal fibrosis, reflected by reduced profibrogenic genes (e.g., transforming growth factor β1, fibronectin, collagen I and III, and α-smooth muscle actin).
32	32691413	In addition, miR-27a-3p silencing attenuated endoplasmic reticulum (ER) stress, reflected by reduced expression of p-IRE1α, p-eIF2α, XBP1s, and CHOP.
33	32691413	Mechanically, we identified prohibitin and TMBIM6 as direct targets of miR-27a-3p.
34	32691413	Inhibition of miR-27a-3p protected HG-treated HK-2 cells from apoptosis, extracellular matrix accumulation, mitochondrial dysfunction, and ER stress by regulating prohibitin or TMBIM6.
35	32691413	Taken together, we reveal that miR-27a-3p-prohibitin/TMBIM6 signaling axis regulates the progression of DN, which can be a potential therapeutic target.
36	31115515	Enhanced TUG1 expression by exogenous recombinant vector regulated the expression of podocyte associated proteins [Nephrin, Podocin and CCAAT/enhancer‑binding protein (CHOP)].
37	31115515	Enhanced TUG1 expression by exogenous recombinant vector regulated the expression of podocyte associated proteins [Nephrin, Podocin and CCAAT/enhancer‑binding protein (CHOP)].
38	31115515	The decreased Nephrin and Podocin expression, upregulated CHOP expression and the increased albumin influx were slightly enhanced by miR‑197 mimic transfection, while markedly suppressed by miR‑197 inhibitor transfection in LPS‑induced podocytes.
39	31115515	The decreased Nephrin and Podocin expression, upregulated CHOP expression and the increased albumin influx were slightly enhanced by miR‑197 mimic transfection, while markedly suppressed by miR‑197 inhibitor transfection in LPS‑induced podocytes.
40	31115515	However, the p38 MAPK inhibitor SB203580 reversed the changes that TUG1 induced in the levels of Beclin1, LC3 II/LC3 I and p62.
41	31115515	However, the p38 MAPK inhibitor SB203580 reversed the changes that TUG1 induced in the levels of Beclin1, LC3 II/LC3 I and p62.
42	29500363	Enhanced insulin receptor, but not PI3K, signalling protects podocytes from ER stress.
43	29500363	Here we use established activating transcription factor 6 (ATF6)- and ER stress element (ERSE)-luciferase assays alongside a novel high throughput imaging-based C/EBP homologous protein (CHOP) assay to examine three models of improved insulin sensitivity.
44	29500363	We find that by improving insulin sensitivity at the level of the insulin receptor (IR), either by IR over-expression or by knocking down the negative regulator of IR activity, protein tyrosine-phosphatase 1B (PTP1B), podocytes are protected from ER stress caused by fatty acids or diabetic media containing high glucose, high insulin and inflammatory cytokines TNFα and IL-6.
45	29500363	However, contrary to this, knockdown of the negative regulator of PI3K-Akt signalling, phosphatase and tensin homolog deleted from chromosome 10 (PTEN), sensitizes podocytes to ER stress and apoptosis, despite increasing Akt phosphorylation.
46	28024901	Cyclin-dependent kinase 5 contributes to endoplasmic reticulum stress induced podocyte apoptosis via promoting MEKK1 phosphorylation at Ser280 in diabetic nephropathy.
47	28024901	The results showed that along with induction of Cdk5 and apoptosis, GRP78 and its two sensors as well as CHOP and cleaved caspase-12 were induced in high glucose treated podocytes.
48	28024901	The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78.
49	28024901	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.
50	28024901	Therefore, our study proved that Cdk5 may play an important role in ER stress induced podocyte apoptosis through MEKK1/JNK pathway in diabetic nephropathy.
51	27236787	Furthermore, animals with genetic ablation of UPR-activated transcription factor C/EBP homologous protein CHOP allocated in high-AGEs diet, exhibited relative resistance to UPR induction (BiP levels) and XBP1 activation in major metabolic organs.
52	27221629	The expression levels of light chain 3‑II (LC3 II), beclin‑1, P62, CCAAT‑enhancer‑binding protein homologous protein (CHOP) and podocin were determined by western blot analysis.
53	27221629	The expression levels of light chain 3‑II (LC3 II), beclin‑1, P62, CCAAT‑enhancer‑binding protein homologous protein (CHOP) and podocin were determined by western blot analysis.
54	27221629	Furthermore, the autophagy enhancer rapamycin reversed the downregulation of LC3 II and podocin, and the upregulation of CHOP induced by LPS, while the autophagy inhibitor 3‑MA aggravated the effects of LPS.
55	27221629	Furthermore, the autophagy enhancer rapamycin reversed the downregulation of LC3 II and podocin, and the upregulation of CHOP induced by LPS, while the autophagy inhibitor 3‑MA aggravated the effects of LPS.
56	26197866	AOPP treatment induced overexpression of glucose-regulated protein 78 and CCAAT/enhancer-binding protein-homologous protein (CHOP) in podocytes, indicating that AOPPs induced ER stress.
57	26197866	Moreover, silencing of the three ER stress sensors, protein kinase-like ER kinase (PERK), activating transcription factor 6 (ATF6), and inositol requiring 1 (IRE1), respectively, significantly lowered the apoptotic rate of the cells compared with that of the scramble siRNA-transfected cells.
58	26197866	Lastly, our data suggested that CHOP- and caspase-12-dependent pathways were involved in ER stress-mediated podocyte apoptosis and that Bcl-2 suppression was involved in CHOP-mediated apoptosis.
59	26197866	Collectively, our results indicate for the first time that AOPPs trigger podocyte apoptosis through induction of ER stress, which might be regulated by NADPH oxidase-dependent ROS through RAGE, and that this apoptosis is mediated by three unfolded protein response pathways, the PERK, ATF6, and IRE1 pathways, and the mediators, CHOP and caspase-12.
60	26103809	Apelin increased albuminuria and decreased podocyte foot process proteins expression in kk-Ay mice, which is consistent with the results that apelin receptor (APLNR) levels increased in glomeruli of patients or mice with DN.
61	26103809	These effects seemed to be related to endoplasmic reticulum (ER) stress, as apelin increased C/EBP homologous protein (CHOP) and peiFα levels while cAMP or oleuropein reduced it in high glucose and apelin treated podocytes.
62	25754093	Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy.
63	25754093	Here we show that nuclear translocation of the transcription factor spliced X-box binding protein-1 (sXBP1) is selectively impaired in DN, inducing activating transcription factor-6 (ATF6) and C/EBP homology protein (CHOP).
64	25754093	Podocyte-specific genetic ablation of XBP1 or inducible expression of ATF6 in mice aggravates DN. sXBP1 lies downstream of insulin signalling and attenuating podocyte insulin signalling by genetic ablation of the insulin receptor or the regulatory subunits phosphatidylinositol 3-kinase (PI3K) p85α or p85β impairs sXBP1 nuclear translocation and exacerbates DN.
65	25754093	Thus, signalling via the insulin receptor, p85, and XBP1 maintains podocyte homeostasis, while disruption of this pathway impairs podocyte function in DN.
66	25322957	Thapsigargin/tunicamycin treatment induced a significant increase in endoplasmic reticulum stress and of cell death, represented by higher GADD153 and GRP78 expression and propidium iodide flow cytometry, respectively.
67	25173645	Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
68	25173645	Renal remodeling, function, ER stress (CHOP and GRP78) and inflammation (infiltration of inflammatory cells, NF-κB p65) were evaluated 12 weeks after MI.
69	25173645	However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
70	25173645	However, MI significantly increased the glomerular expression of GRP78 and CHOP in UNX and DB rats.
71	25173645	In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
72	25173645	In addition, it also promoted the infiltration of CD4+ T cells, particularly inflammatory cytokine (IFN-γ, IL-17, IL-4)-producing CD4+ T cells, and the expression of NF-κB p65 in the glomeruli.
73	24503896	Glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/GADD153) and caspase-12 expression was analyzed by RT-PCR, western blot analysis and immunocytochemistry.
74	24503896	Glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/GADD153) and caspase-12 expression was analyzed by RT-PCR, western blot analysis and immunocytochemistry.
75	24503896	Glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/GADD153) and caspase-12 expression was analyzed by RT-PCR, western blot analysis and immunocytochemistry.
76	24503896	CHOP/GADD153 expression reached its peak at 48 h, and caspase-12 expression gradually increased with time.
77	24503896	CHOP/GADD153 expression reached its peak at 48 h, and caspase-12 expression gradually increased with time.
78	24503896	CHOP/GADD153 expression reached its peak at 48 h, and caspase-12 expression gradually increased with time.
79	24503896	Spearman's correlation analysis revealed that caspase-12 and CHOP/GADD153 positively correlated with the apoptotic rate (r=0.915, P<0.01 and r=0.639, P<0.01).
80	24503896	Spearman's correlation analysis revealed that caspase-12 and CHOP/GADD153 positively correlated with the apoptotic rate (r=0.915, P<0.01 and r=0.639, P<0.01).
81	24503896	Spearman's correlation analysis revealed that caspase-12 and CHOP/GADD153 positively correlated with the apoptotic rate (r=0.915, P<0.01 and r=0.639, P<0.01).
82	24376653	Wtip- and gadd45a-interacting protein dendrin is not crucial for the development or maintenance of the glomerular filtration barrier.
83	24376653	This is highlighted by the fact that mutations in molecular components of the slit diaphragm, including nephrin and Cd2-associated protein (Cd2ap), result in proteinuric diseases in man.
84	24376653	Dendrin is a poorly characterized cytosolic component of the slit diaphragm in where it interacts with nephrin and Cd2ap.
85	24376653	Yeast two-hybrid screen and co-immunoprecipitation experiments showed that dendrin binds to Wt1-interacting protein (Wtip) and growth arrest and DNA-damage-inducible 45 alpha (Gadd45a).
86	24376653	Wtip and Gadd45a mediate gene transcription in the nucleus, suggesting that dendrin may have similar functions in podocytes.
87	24376653	Our results indicate that dendrin is dispensable for the function of the normal glomerular filtration barrier and that dendrin interacts with Wtip and Gadd45a.
88	23235477	Unexpectedly, while Toll-like receptor 4 (TLR4) expression levels were comparable in kidneys of CHOP(-/-) and wild-type (WT) mice, CHOP(-/-) mice developed more severe AKI after LPS injection.
89	23235477	Unexpectedly, while Toll-like receptor 4 (TLR4) expression levels were comparable in kidneys of CHOP(-/-) and wild-type (WT) mice, CHOP(-/-) mice developed more severe AKI after LPS injection.
90	23235477	Additionally, the kidneys of LPS-treated CHOP(-/-) mice had a more prominent increase in NF-κB activation and further upregulation of proinflammatory genes, i.e., c-x-c motif ligand 1 (CXCL-1), macrophage inflammatory protein-2 (MIP-2), and IL-6.
91	23235477	Additionally, the kidneys of LPS-treated CHOP(-/-) mice had a more prominent increase in NF-κB activation and further upregulation of proinflammatory genes, i.e., c-x-c motif ligand 1 (CXCL-1), macrophage inflammatory protein-2 (MIP-2), and IL-6.
92	20660016	TRB3 is stimulated in diabetic kidneys, regulated by the ER stress marker CHOP, and is a suppressor of podocyte MCP-1.
93	20660016	TRB3 is stimulated in diabetic kidneys, regulated by the ER stress marker CHOP, and is a suppressor of podocyte MCP-1.
94	20660016	In summary, enhanced ROS and/or FFA associated with the diabetic milieu induce podocyte CHOP and TRB3 expression.
95	20660016	In summary, enhanced ROS and/or FFA associated with the diabetic milieu induce podocyte CHOP and TRB3 expression.
96	20660016	Because TRB3 inhibits MCP-1, manipulation of TRB3 expression could provide a novel therapeutic approach in diabetic kidney disease.
97	20660016	Because TRB3 inhibits MCP-1, manipulation of TRB3 expression could provide a novel therapeutic approach in diabetic kidney disease.
98	19640905	This study addresses how FSGS-associated mutant alpha-actinin-4 may induce GEC injury, focusing on endoplasmic reticulum (ER) stress and metabolism of mutant alpha-actinin-4 via the ubiquitin-proteasome system.
99	19640905	This study addresses how FSGS-associated mutant alpha-actinin-4 may induce GEC injury, focusing on endoplasmic reticulum (ER) stress and metabolism of mutant alpha-actinin-4 via the ubiquitin-proteasome system.
100	19640905	In a model of experimental FSGS induced by expression of an alpha-actinin-4 K256E transgene in podocytes, we show induction of ER stress, including upregulation of ER chaperones (bip, grp94), phosphorylation of the eukaryotic translation initiation factor-2alpha subunit, and induction of the proapoptotic gene C/EBP homologous protein-10 (CHOP).
101	19640905	In a model of experimental FSGS induced by expression of an alpha-actinin-4 K256E transgene in podocytes, we show induction of ER stress, including upregulation of ER chaperones (bip, grp94), phosphorylation of the eukaryotic translation initiation factor-2alpha subunit, and induction of the proapoptotic gene C/EBP homologous protein-10 (CHOP).
102	19640905	In the present study, we show that alpha-actinin-4 K256E upregulates grp94 and CHOP expression in COS cells and significantly exacerbates induction of bip and CHOP in GEC in the presence of tunicamycin.
103	19640905	In the present study, we show that alpha-actinin-4 K256E upregulates grp94 and CHOP expression in COS cells and significantly exacerbates induction of bip and CHOP in GEC in the presence of tunicamycin.
104	19640905	ER stress was associated with aggregation and ubiquitination of alpha-actinin-4 K256E and impairment of the ubiquitin-proteasome system.
105	19640905	ER stress was associated with aggregation and ubiquitination of alpha-actinin-4 K256E and impairment of the ubiquitin-proteasome system.
106	16400006	Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein).