Ignet

Gene Information

Gene symbol: DR1

Gene name: down-regulator of transcription 1, TBP-binding (negative cofactor 2)

HGNC ID: 3017

Synonyms: NC2, NC2-BETA

Related Genes

#	Gene Symbol	Number of hits
1	AR	1 hits
2	HAGH	1 hits
3	HNF4A	1 hits
4	IDDM2	1 hits
5	INS	1 hits
6	MRAP	1 hits
7	NR2F2	1 hits
8	PPARA	1 hits
9	PPARG	1 hits
10	RXRA	1 hits
11	TNFRSF10A	1 hits
12	TNFRSF25	1 hits
13	TOR1B	1 hits

Related Sentences

#	PMID	Sentence
1	1357169	Accordingly, no overrepresentation of homozygosity for HLA-DR4 was found among the total number of 25 patients with RA as well as insulin dependent diabetes mellitus, though the opposite might be expected as these diseases have a common DR4 association--RA with DR4 and DR1 and insulin dependent diabetes mellitus with DR4 and DR3.
2	1633634	The association of insulin-dependent diabetes mellitus and HLA began with weak associations of Class I antigens (B8 and B15) and progressed to Class II antigens (DR3 and DR4), then to subtypes of DR4 (Dw4, 10, and 14), and now to DQ molecules including the absence of aspartic acid at position 57 of the DQ beta chain and the presence of arginine at position 52 of the DQ alpha chain.
3	1633634	In rheumatoid arthritis (RA) the HLA antigen association remains with certain Class II molecules of the DR series (DR4 and DR1) that share amino acid sequences with a restricted number of other DR antigens seen in RA, as well as a segment of the gp 110 protein of the Epstein-Barr virus.
4	1698309	Interleukin 1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF-alpha) may be pathogenetically important in insulin-dependent diabetes mellitus (IDDM), which is associated with genes of the HLA region.
5	1698309	Since a regulatory role of HLA region genes on monokine production may exist, we looked for an association between the monokine and prostaglandin E2 (PGE2) responses of monocytes (Mo) from 20 healthy males (18-50 years) with HLA-DR types relevant for IDDM susceptibility and resistance (DR1,2, DR1,3, DR1,4, DR3,4).
6	1698309	Monokine assays were established and evaluated and the secretions of IL-1 beta, TNF-alpha, and PGE2 measured in Mo cultures (2h, 6h, 20h) prepared by endotoxin-free techniques and stimulated by low-dose E. coli lipopolysaccharides (LPS).
7	1698309	In the HLA class III region a diallelic TNF-beta gene NcoI polymorphism consisting of alleles of 5.5 kb and 10.5 kb was recently described and associated with susceptibility to autoimmune diseases including IDDM.
8	1698309	We report that IL-1 beta and TNF-alpha responses of Mo from TNF-beta 10.5 kb homozygous healthy individuals were significantly higher than for TNF-beta 5.5/10.5 kb heterozygotes.
9	1698309	IL-1 beta and TNF-alpha responses of Mo from males (18-35 years) with newly diagnosed (n = 10) and long-standing IDDM (n = 10) and from age- and HLA-DR-matched healthy males (n = 10) were studied.
10	1698309	LPS, gamma interferon (IFN), and TNF-alpha-stimulated Mo cultures were investigated.
11	1698309	IFN (1000 U/ml) in the presence of LPS significantly potentiated LPS-stimulated Mo TNF-alpha secretion and reduced the levels of IL-1 beta immunoreactivity in Mo lysates.
12	1698309	IFN and TNF-alpha did not have any effects on LPS-stimulated Mo secretion of IL-1 beta immunoreactivity.
13	1698309	We conclude that Mo IL-1 beta and TNF-alpha production is normal in patients with recent-onset and long-standing IDDM.
14	2210066	The analysis of HLA-DQ beta nucleotide sequence polymorphism in insulin-dependent diabetes mellitus (IDDM) patients and control subjects suggests a role for the DQ beta-chain in genetic susceptibility.
15	2210066	However, important exceptions to this pattern have been identified in the analysis of heterozygous DR1/4 IDDM patients.
16	3471665	DR4 and DR3 are in strongest linkage disequilibrium with IDDM susceptibility genes, and DR1 demonstrates a lesser degree of positive disequilibrium.
17	3471665	DR3/DR4 heterozygotes have the highest risk.
18	3471665	The DR1 increase occurs almost exclusively in DR4/DR1 heterozygotes, suggesting that DR1 may be in disequilibrium with the same susceptibility gene as DR3.
19	3471665	GLO-2 is increased in diabetic haplotypes carrying DR4, DR3 or DR1.
20	3471665	DR4 and DR3 are in strongest linkage disequilibrium with IDDM susceptibility genes, and DR1 demonstrates a lesser degree of positive disequilibrium.
21	3471665	DR3/DR4 heterozygotes have the highest risk.
22	3471665	The DR1 increase occurs almost exclusively in DR4/DR1 heterozygotes, suggesting that DR1 may be in disequilibrium with the same susceptibility gene as DR3.
23	3471665	GLO-2 is increased in diabetic haplotypes carrying DR4, DR3 or DR1.
24	3471665	DR4 and DR3 are in strongest linkage disequilibrium with IDDM susceptibility genes, and DR1 demonstrates a lesser degree of positive disequilibrium.
25	3471665	DR3/DR4 heterozygotes have the highest risk.
26	3471665	The DR1 increase occurs almost exclusively in DR4/DR1 heterozygotes, suggesting that DR1 may be in disequilibrium with the same susceptibility gene as DR3.
27	3471665	GLO-2 is increased in diabetic haplotypes carrying DR4, DR3 or DR1.
28	3497624	HLA typing, carried out for 27 family members, showed an increased incidence of HLA-B22, B27, B39, and DR1 when compared to Yuendumu Aborigines (B27 and DR1), or Australian Caucasians (B22), or both (B39).
29	8816975	Insulin-dependent diabetes (IDDM) is probably mediated by T lymphocytes recognizing critical beta cell autoantigens.
30	8816975	Glutamic acid decarboxylase (GAD) 65 is a major antigen in IDDM.
31	8816975	T cells in both IDDM patients and controls respond to GAD 65 and certain epitopes of this molecule.
32	8816975	We obtained T cells clones to GAD 65 peptides 161-175 (from a healthy individual), and 505-519 and 521-535 (from two IDDM patients).
33	8816975	Reactivity of clones to peptide 505-519 was either HLA DR1 or DQ1 restricted.
34	8816975	In conclusion, T cell clones to specific epitopes of GAD 65 provide a model to clarify those differences in the immune response to this autoantigen between controls and IDDM patients.
35	8900244	We report here our analysis of HLA class II alleles in 180 Caucasian nuclear families with at least two children with insulin-dependent diabetes mellitus (IDDM).
36	8900244	DRB1, DQA1, DQB1, and DPB1 genotypes were determined with PCR/sequence-specific oligonucleotide probe typing methods.
37	8900244	Consistent with other studies, our data indicate an increase in DR3/DR4, DR3/DR3, and DR4/DR4 genotypes in patients compared to controls.
38	8900244	In addition, we found an increase in DR1/DR4, DR1/DR3, and DR4/DR8 genotypes.
39	10197051	Blockade of this presentation event via synthetic ligands that bind to disease-associated MHCs (such as DR1 and DR4) may be useful for the treatment of autoimmune diseases such as rheumatoid arthritis, Type 1 diabetes, multiple sclerosis, lupus erthymatosis and Graves disease.
40	10197051	Recently reported synthetic ligands for DR1 and DR4 are short modified peptides (2-7 mers) capable of competing at nanomolar concentrations with antigenic peptides for the DR (MHC) binding groove.
41	10197051	Blockade of this presentation event via synthetic ligands that bind to disease-associated MHCs (such as DR1 and DR4) may be useful for the treatment of autoimmune diseases such as rheumatoid arthritis, Type 1 diabetes, multiple sclerosis, lupus erthymatosis and Graves disease.
42	10197051	Recently reported synthetic ligands for DR1 and DR4 are short modified peptides (2-7 mers) capable of competing at nanomolar concentrations with antigenic peptides for the DR (MHC) binding groove.
43	18469482	One half (0.5) mg/ml of Hachimi-jio-gan activated peroxisome proliferator-activated receptor (PPARalpha), mediating the activation by 3.1-fold on DR1 response elements; however, it did not affect PPARgamma, thyroid hormone receptor, androgen receptor, estrogen receptor or RXR.
44	18474611	The MODY1 gene for hepatocyte nuclear factor 4alpha and a feedback loop control COUP-TFII expression in pancreatic beta cells.
45	18474611	Knockout mice with the heterozygous deletion of the gene for chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) or the complete disruption of the gene for hepatocyte nuclear factor 4alpha (HNF4alpha) in pancreatic beta cells have similar insulin secretion defects, leading us to hypothesize that there is transcriptional cross talk between these two nuclear receptors.
46	18474611	Here, we demonstrate specific HNF4alpha activation of a reporter plasmid containing the COUP-TFII gene promoter region in transfected pancreatic beta cells.
47	18474611	The stable association of the endogenous HNF4alpha with a region of the COUP-TFII gene promoter that contains a direct repeat 1 (DR-1) binding site was revealed by chromatin immunoprecipitation.
48	18474611	Mutation experiments showed that this DR-1 site is essential for HNF4alpha transactivation of COUP-TFII.
49	18474611	The dominant negative suppression of HNF4alpha function decreased endogenous COUP-TFII expression, and the specific inactivation of COUP-TFII by small interfering RNA caused HNF4alpha mRNA levels in 832/13 INS-1 cells to decrease.
50	18474611	This positive regulation of HNF4alpha by COUP-TFII was confirmed by the adenovirus-mediated overexpression of human COUP-TFII (hCOUP-TFII), which increased HNF4alpha mRNA levels in 832/13 INS-1 cells and in mouse pancreatic islets.
51	18474611	Finally, hCOUP-TFII overexpression showed that there is direct COUP-TFII autorepression, as COUP-TFII occupies the proximal DR-1 binding site of its own gene in vivo.
52	18474611	Therefore, COUP-TFII may contribute to the control of insulin secretion through the complex HNF4alpha/maturity-onset diabetes of the young 1 (MODY1) transcription factor network operating in beta cells.
53	18474611	The MODY1 gene for hepatocyte nuclear factor 4alpha and a feedback loop control COUP-TFII expression in pancreatic beta cells.
54	18474611	Knockout mice with the heterozygous deletion of the gene for chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) or the complete disruption of the gene for hepatocyte nuclear factor 4alpha (HNF4alpha) in pancreatic beta cells have similar insulin secretion defects, leading us to hypothesize that there is transcriptional cross talk between these two nuclear receptors.
55	18474611	Here, we demonstrate specific HNF4alpha activation of a reporter plasmid containing the COUP-TFII gene promoter region in transfected pancreatic beta cells.
56	18474611	The stable association of the endogenous HNF4alpha with a region of the COUP-TFII gene promoter that contains a direct repeat 1 (DR-1) binding site was revealed by chromatin immunoprecipitation.
57	18474611	Mutation experiments showed that this DR-1 site is essential for HNF4alpha transactivation of COUP-TFII.
58	18474611	The dominant negative suppression of HNF4alpha function decreased endogenous COUP-TFII expression, and the specific inactivation of COUP-TFII by small interfering RNA caused HNF4alpha mRNA levels in 832/13 INS-1 cells to decrease.
59	18474611	This positive regulation of HNF4alpha by COUP-TFII was confirmed by the adenovirus-mediated overexpression of human COUP-TFII (hCOUP-TFII), which increased HNF4alpha mRNA levels in 832/13 INS-1 cells and in mouse pancreatic islets.
60	18474611	Finally, hCOUP-TFII overexpression showed that there is direct COUP-TFII autorepression, as COUP-TFII occupies the proximal DR-1 binding site of its own gene in vivo.
61	18474611	Therefore, COUP-TFII may contribute to the control of insulin secretion through the complex HNF4alpha/maturity-onset diabetes of the young 1 (MODY1) transcription factor network operating in beta cells.
62	18474611	The MODY1 gene for hepatocyte nuclear factor 4alpha and a feedback loop control COUP-TFII expression in pancreatic beta cells.
63	18474611	Knockout mice with the heterozygous deletion of the gene for chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) or the complete disruption of the gene for hepatocyte nuclear factor 4alpha (HNF4alpha) in pancreatic beta cells have similar insulin secretion defects, leading us to hypothesize that there is transcriptional cross talk between these two nuclear receptors.
64	18474611	Here, we demonstrate specific HNF4alpha activation of a reporter plasmid containing the COUP-TFII gene promoter region in transfected pancreatic beta cells.
65	18474611	The stable association of the endogenous HNF4alpha with a region of the COUP-TFII gene promoter that contains a direct repeat 1 (DR-1) binding site was revealed by chromatin immunoprecipitation.
66	18474611	Mutation experiments showed that this DR-1 site is essential for HNF4alpha transactivation of COUP-TFII.
67	18474611	The dominant negative suppression of HNF4alpha function decreased endogenous COUP-TFII expression, and the specific inactivation of COUP-TFII by small interfering RNA caused HNF4alpha mRNA levels in 832/13 INS-1 cells to decrease.
68	18474611	This positive regulation of HNF4alpha by COUP-TFII was confirmed by the adenovirus-mediated overexpression of human COUP-TFII (hCOUP-TFII), which increased HNF4alpha mRNA levels in 832/13 INS-1 cells and in mouse pancreatic islets.
69	18474611	Finally, hCOUP-TFII overexpression showed that there is direct COUP-TFII autorepression, as COUP-TFII occupies the proximal DR-1 binding site of its own gene in vivo.
70	18474611	Therefore, COUP-TFII may contribute to the control of insulin secretion through the complex HNF4alpha/maturity-onset diabetes of the young 1 (MODY1) transcription factor network operating in beta cells.
71	18981473	PPARgamma and C/EBP factors orchestrate adipocyte biology via adjacent binding on a genome-wide scale.
72	18981473	Peroxisome proliferator-activated receptor gamma(PPARgamma), a nuclear receptor and the target of anti-diabetic thiazolinedione drugs, is known as the master regulator of adipocyte biology.
73	18981473	Although it regulates hundreds of adipocyte genes, PPARgamma binding to endogenous genes has rarely been demonstrated.
74	18981473	The consensus PPARgamma/RXRalpha "DR-1"-binding motif was found at most of the sites, and ChIP for RXRalpha showed colocalization at nearly all locations tested.
75	18981473	Bioinformatics analysis also revealed CCAAT/enhancer-binding protein (C/EBP)-binding motifs in the vicinity of most PPARgamma-binding sites, and genome-wide analysis of C/EBPalpha binding demonstrated that it localized to 3350 of the locations bound by PPARgamma.
76	18981473	C/EBPbeta also plays a role at many of these genes, such that both C/EBPalpha and beta are required along with PPARgamma for robust adipocyte-specific gene expression.
77	18981473	Thus, PPARgamma and C/EBP factors cooperatively orchestrate adipocyte biology by adjacent binding on an unanticipated scale.