Ignet

Gene Information

Gene symbol: BACH1

Gene name: BTB and CNC homology 1, basic leucine zipper transcription factor 1

HGNC ID: 935

Synonyms: BACH-1, BTBD24

Related Genes

#	Gene Symbol	Number of hits
1	CAT	1 hits
2	GCLC	1 hits
3	HMOX1	1 hits
4	INS	1 hits
5	NFE2L2	1 hits
6	NQO1	1 hits
7	SLC7A11	1 hits
8	SOD1	1 hits

Related Sentences

#	PMID	Sentence
1	23880309	BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1).
2	23880309	Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance.
3	23880309	In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation.
4	23880309	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.
5	23880309	Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.
6	23880309	BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1).
7	23880309	Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance.
8	23880309	In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation.
9	23880309	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.
10	23880309	Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.
11	23880309	BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1).
12	23880309	Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance.
13	23880309	In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation.
14	23880309	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.
15	23880309	Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.
16	23880309	BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1).
17	23880309	Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance.
18	23880309	In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation.
19	23880309	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.
20	23880309	Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.
21	23880309	BTB and CNC homology 1 (Bach1) is a transcriptional repressor of antioxidative enzymes, such as heme oxygenase-1 (HO-1).
22	23880309	Unexpectedly, glucose and insulin tolerance tests showed no differences in obese wild-type (WT) and obese Bach1-deficient mice after high-fat diet loading for 6 wk, suggesting minimal roles of Bach1 in the development of insulin resistance.
23	23880309	In contrast, Bach1 deficiency significantly suppressed alloxan-induced pancreatic insulin content reduction and the resultant glucose elevation.
24	23880309	HO-1 expression in islets was significantly upregulated in alloxan-injected Bach1-deficient mice, whereas expression of other antioxidative enzymes, e.g., catalase, superoxide dismutase, and glutathione peroxidase, was not changed by either alloxan administration or Bach1 deficiency.
25	23880309	Our results suggest that Bach1 deficiency protects pancreatic β-cells from oxidative stress-induced apoptosis and that the enhancement of HO-1 expression plays an important role in this protection.
26	23974919	We examined the effects of GDM on the proteome, redox status, and nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant gene expression in human fetal endothelial cells.
27	23974919	In GDM cells, the lipid peroxidation product 4-hydroxynonenal (HNE) failed to induce nuclear Nrf2 accumulation and mRNA and/or protein expression of Nrf2 and its target genes NAD(P)H:quinone oxidoreductase 1 (NQO1), Bach1, cystine/glutamate transporter, and glutamate cysteine ligase.
28	23974919	Although methylation of CpG islands in Nrf2 or NQO1 promoters was unaltered by GDM, decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3β levels may account for impaired Nrf2 signaling.
29	23974919	HNE-induced increases in GSH and NQO1 levels were abrogated by Nrf2 small interfering RNA in normal cells, and overexpression of Nrf2 in GDM cells partially restored NQO1 induction.