Ignet

Gene Information

Gene symbol: ACACB

Gene name: acetyl-CoA carboxylase beta

HGNC ID: 85

Synonyms: HACC275, ACC2, ACCB

Related Genes

#	Gene Symbol	Number of hits
1	ACACA	1 hits
2	ALB	1 hits
3	ATIC	1 hits
4	BCL2A1	1 hits
5	INS	1 hits
6	NPHS2	1 hits
7	PPARGC1A	1 hits
8	PRKAA1	1 hits
9	SIRT1	1 hits
10	SYNPO	1 hits

Related Sentences

#	PMID	Sentence
1	29175208	A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) β gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes.
2	29175208	In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice.
3	29175208	In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions.
4	29175208	The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK).
5	29175208	A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) β gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes.
6	29175208	In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice.
7	29175208	In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions.
8	29175208	The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK).
9	29175208	A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) β gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes.
10	29175208	In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice.
11	29175208	In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions.
12	29175208	The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK).
13	29175208	A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) β gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes.
14	29175208	In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice.
15	29175208	In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions.
16	29175208	The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK).
17	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
18	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
19	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
20	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
21	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
22	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
23	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
24	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
25	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
26	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.
27	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
28	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
29	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
30	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
31	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
32	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
33	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
34	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
35	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
36	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.
37	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
38	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
39	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
40	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
41	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
42	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
43	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
44	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
45	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
46	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.
47	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
48	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
49	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
50	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
51	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
52	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
53	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
54	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
55	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
56	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.
57	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
58	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
59	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
60	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
61	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
62	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
63	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
64	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
65	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
66	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.
67	33957017	Faster lipid β-oxidation rate by acetyl-CoA carboxylase 2 inhibition alleviates high-glucose-induced insulin resistance via SIRT1/PGC-1α in human podocytes.
68	33957017	Increasing evidence shows that acetyl-CoA carboxylase 2 (ACC2) plays a crucial role in the metabolism of fatty acid, but its effect in podocyte injury of DN is still unclear.
69	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
70	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
71	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
72	33957017	Additionally, ACC2-shRNA restored the expression of glucose transporter 4 (GLUT4) on the cell surface, which was downregulated in HG and normalized in the insulin signaling pathway.
73	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
74	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
75	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
76	33957017	Taken together, our data suggest that podocyte injury mediated by HG-induced insulin resistance and lipotoxicity could be alleviated by ACC2 inhibition via SIRT1/PGC-1α.