Ignet

Gene Information

Gene symbol: BCL2A1

Gene name: BCL2-related protein A1

HGNC ID: 991

Synonyms: GRS, BFL1, BCL2L5, ACC-1, ACC-2

Related Genes

#	Gene Symbol	Number of hits
1	ACACA	1 hits
2	ACACB	1 hits
3	INS	1 hits
4	PPARGC1A	1 hits
5	SIRT1	1 hits
6	SLC2A4	1 hits

Related Sentences

#	PMID	Sentence
1	24338821	Genome-wide association studies indicate that expression of acetyl-CoA carboxylase (ACC) 2, a key enzyme of fatty acid oxidation (FAO), is associated with proteinuria in type 2 diabetes.
2	24338821	Here, we show that stimulation of FAO by aminoimidazole-4-carboxamide-1β-D-ribofuranoside (AICAR) or by adiponectin, activators of the low-energy sensor AMP-activated protein kinase (AMPK), protects from palmitic acid-induced podocyte death.
3	24338821	Conversely, inhibition of carnitine palmitoyltransferase (CPT-1), the rate-limiting enzyme of FAO and downstream target of AMPK, augments palmitic acid toxicity and impedes the protective AICAR effect.
4	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.
5	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.
6	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
7	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
8	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
9	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.
10	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
11	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
12	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
13	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.
14	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.
15	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.
16	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
17	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
18	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
19	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.
20	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
21	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
22	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
23	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.
24	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.
25	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.
26	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
27	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
28	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
29	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.
30	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
31	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
32	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
33	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.
34	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.
35	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.
36	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
37	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
38	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
39	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.
40	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
41	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
42	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
43	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.
44	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.
45	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.
46	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
47	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
48	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
49	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.
50	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
51	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
52	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
53	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.
54	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.
55	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.
56	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
57	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
58	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
59	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.
60	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
61	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
62	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
63	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.
64	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.
65	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.
66	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
67	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
68	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
69	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.
70	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
71	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
72	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
73	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.
74	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.
75	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.
76	33957017	In this study, we investigated whether ACC2 could be a therapeutic target of lipid deposition induced by hyperglycemia in the human podocytes.
77	33957017	It also contributed to the downregulation of phosphorylated ACC2 (p-ACC2), which is an inactive form of ACC2.
78	33957017	Knockdown of ACC2 by sh-RNA reduced lipid deposition induced by HG.
79	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.
80	33957017	Mechanistically, SIRT1/PGC-1α is close related to the insulin metabolism pathway.
81	33957017	ACC2-shRNA could restore the expression of SIRT1/PGC-1α, which was downregulated in HG.
82	33957017	Rescue experiment revealed that inhibition of SIRT1 by EX-527 counteracted the effect of ACC2-shRNA.
83	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.