Ignet

Gene Information

Gene symbol: SREBF1

Gene name: sterol regulatory element binding transcription factor 1

HGNC ID: 11289

Synonyms: SREBP1, bHLHd1, SREBP-1c

Related Genes

#	Gene Symbol	Number of hits
1	AKT2	1 hits
2	CNBP	1 hits
3	FASN	1 hits
4	PIK3CA	1 hits

Related Sentences

#	PMID	Sentence
1	18420801	Activation of sterol regulatory element-binding protein 1c and fatty acid synthase transcription by hepatitis C virus non-structural protein 2.
2	18420801	Transcriptional factor sterol regulatory element-binding protein 1c (SREBP-1c) activates the transcription of lipogenic genes, including fatty acid synthase (FAS).
3	18420801	We also showed that FAS upregulation by HCV NS2 was SREBP-1-dependent since deleting the SRE sequence in a FAS promoter and expressing a dominant-negative SREBP-1 abrogated FAS promoter upregulation by HCV NS2.
4	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
5	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
6	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
7	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
8	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
9	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.
10	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
11	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
12	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
13	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
14	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
15	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.
16	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
17	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
18	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
19	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
20	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
21	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.
22	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
23	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
24	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
25	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
26	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
27	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.
28	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
29	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
30	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
31	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
32	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
33	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.
34	20130133	Hepatitis C virus genotype-3a core protein enhances sterol regulatory element-binding protein-1 activity through the phosphoinositide 3-kinase-Akt-2 pathway.
35	20130133	We previously showed that, through sterol regulatory element binding protein-1 (SREBP-1), HCV-3a core protein upregulates the promoter activity of fatty acid synthase, a major enzyme involved in de novo lipid synthesis.
36	20130133	In this study, we investigated whether HCV-3a core can activate SREBP-1 and studied the role of phosphoinositide 3-kinase (PI3K)-Akt-2 pathway in modulating SREBP-1 activity by HCV-3a core.
37	20130133	To investigate the role of the PI3K-Akt-2 pathway in SREBP-1 activation by HCV-3a core, PI3K and Akt-2 activity was inhibited by using the chemical inhibitor LY294002, a dominant-negative Akt-2 plasmid, or knockdown of Akt-2 by small hairpin RNA.
38	20130133	Our results showed that inhibition of PI3K and Akt-2 was associated with reduced SREBP-1 activation by HCV-3a core.
39	20130133	These results indicate a role for PI3K and Akt-2 in increasing SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV.