SREBP: a novel therapeutic target

被引：111

作者：

Xiao, Xu ^{[1
]}

Song, Bao-Liang ^{[1
]}

机构：

[1] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Biochem & Cell Biol, Shanghai 200031, Peoples R China

来源：

ACTA BIOCHIMICA ET BIOPHYSICA SINICA | 2013年 / 45卷 / 01期

关键词：

SREBP; insulin; cAMP; vitamin A; miRNA; therapeutic target; ELEMENT-BINDING PROTEIN-1C; HMG-COA REDUCTASE; LIVER-X-RECEPTOR; FATTY-ACID SYNTHESIS; NECROSIS-FACTOR-ALPHA; CHOLESTEROL HOMEOSTASIS; ENDOPLASMIC-RETICULUM; INSULIN-RESISTANCE; LIPID-METABOLISM; COPII PROTEINS;

D O I：

10.1093/abbs/gms112

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Sterol regulatory element-binding proteins (SREBPs) are major transcription factors regulating the biosynthesis of cholesterol, fatty acid, and triglyceride. They control the expression of crucial genes involved in lipogenesis and uptake. In this review, we summarize the processing of SREBPs and their regulation by insulin, cAMP, and vitamin A, and the relationship between miRNA and lipid metabolism. We also discuss the recent functional studies on SREBPs. These discoveries suggest that inhibition of SREBP can be a novel strategy to treat metabolic diseases, such as type II diabetes, insulin resistance, fatty liver, and atherosclerosis.

引用

页码：2 / 10

页数：9

共 84 条

[61]

SATO R, 1994, J BIOL CHEM, V269, P17267

[62] Sterol metabolism and SREBP activation [J].

Sato, Ryuichiro .

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2010, 501 (02) :177-181

[63] Insig-dependent ubiquitination and degradation of mammalian 3-hydroxy-3-methylglutaryl-CoA reductase stimulated by sterols and geranylgeraniol [J].

Sever, N ;

Song, BL ;

Yabe, D ;

Goldstein, JL ;

Brown, MS ;

DeBose-Boyd, RA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (52) :52479-52490

[64] Accelerated degradation of HMG CoA reductase mediated by binding of Insig-1 to its sterol-sensing domain [J].

Sever, N ;

Yang, T ;

Brown, MS ;

Goldstein, JL ;

DeBose-Boyd, RA .

MOLECULAR CELL, 2003, 11 (01) :25-33

[65] Human obesity and type 2 diabetes are associated with alterations in SREBP1 isoform expression that are reproduced ex vivo by tumor necrosis factor-α [J].

Sewter, C ;

Berger, D ;

Considine, RV ;

Medina, G ;

Rochford, J ;

Ciaraldi, T ;

Henry, R ;

Dohm, L ;

Flier, JS ;

O'Rahilly, S ;

Vidal-Puig, AJ .

DIABETES, 2002, 51 (04) :1035-1041

[66] Insulin selectively increases SREBP-1c mRNA in the livers of rats with streptozotocin-induced diabetes [J].

Shimomura, L ;

Bashmakov, Y ;

Ikemoto, S ;

Horton, JD ;

Brown, MS ;

Goldstein, JL .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (24) :13656-13661

[67] Gp78, a membrane-anchored ubiquitin ligase, associates with Insig-1 and couples sterol-regulated ubiquitination to degradation of HMG CoA reductase [J].

Song, BL ;

Sever, N ;

DeBose-Boyd, RA .

MOLECULAR CELL, 2005, 19 (06) :829-840

[68] Atherogenesis in perspective: Hypercholesterolemia and inflammation as partners in crime [J].

Steinberg, D .

NATURE MEDICINE, 2002, 8 (11) :1211-1217

[69] Sterol-regulated transport of SREBPs from endoplasmic reticulum to Golgi: Insig renders sorting signal in Scap inaccessible to COPII proteins [J].

Sun, Li-Ping ;

Seemann, Joachim ;

Goldstein, Joseph L. ;

Brown, Michael S. .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (16) :6519-6526

[70] Insig required for sterol-mediated inhibition of Scap/SREBP binding to COPII proteins in vitro [J].

Sun, LP ;

Li, L ;

Goldstein, JL ;

Brown, MS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (28) :26483-26490

← 1 2 3 4 5 6 7 8 9 →