SREBPs

the crossroads of physiological and pathological lipid homeostasis

Rajendra Raghow, Chandrahasa Yellaturu, Xiong Deng, Edwards Park, Marshall Elam

Research output: Contribution to journalReview article

217 Citations (Scopus)

Abstract

The uptake, biosynthesis and metabolism of cholesterol and other lipids are exquisitely regulated by feedback and feed-forward pathways in organisms ranging from Caenorhabditis elegans to humans. As endoplasmic reticulum (ER) membrane-embedded transcription factors that are activated in the Golgi apparatus, sterol regulatory element-binding proteins (SREBPs) are central to the intracellular surveillance of lipid catabolism and de novo biogenesis. The biosynthesis of SREBP proteins, their migration from the ER to the Golgi compartment, intra-membrane proteolysis, nuclear translocation and trans-activation potential are tightly controlled in vivo. Here we summarize recent studies elucidating the transcriptional and post-transcriptional regulation of SREBP-1c through nutrition and the action of hormones, particularly insulin, and the resulting implications for dyslipidemia of obesity, metabolic syndrome and type 2 diabetes.

Original languageEnglish (US)
Pages (from-to)65-73
Number of pages9
JournalTrends in Endocrinology and Metabolism
Volume19
Issue number2
DOIs
StatePublished - Mar 1 2008

Fingerprint

Sterol Regulatory Element Binding Proteins
Endoplasmic Reticulum
Homeostasis
Sterol Regulatory Element Binding Protein 1
Lipids
Nuclear Envelope
Caenorhabditis elegans
Golgi Apparatus
Dyslipidemias
Type 2 Diabetes Mellitus
Proteolysis
Transcription Factors
Obesity
Cholesterol
Hormones
Insulin
Membranes
Proteins

All Science Journal Classification (ASJC) codes

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

SREBPs : the crossroads of physiological and pathological lipid homeostasis. / Raghow, Rajendra; Yellaturu, Chandrahasa; Deng, Xiong; Park, Edwards; Elam, Marshall.

In: Trends in Endocrinology and Metabolism, Vol. 19, No. 2, 01.03.2008, p. 65-73.

Research output: Contribution to journalReview article

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