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SREBPs: metabolic integrators in physiology and metabolism

Jeon, Tae-Il, Osborne, Timothy F.·2012·Trends in Endocrinology & Metabolism
DOI 10.1016/j.tem.2011.10.004PMC PMC3273665
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Crossref · 10.1016/j.tem.2011.10.004

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  • SREBP2 is the master transcription factor that activates the expression of most cholesterol biosynthesis genes.

    “Cholesterol biosynthesis is regulated by sterol regulatory element binding protein 2 (SREBP2), the master transcription factor that activates the expression of most cholesterol biosynthesis genes.”

    From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [11]

    The Introduction (page unavailable) calls SREBP-2 the main regulator of cholesterol metabolism, and the section on mammalian SREBP gene expression says it has a strong transcriptional activation domain. These passages support its central regulatory role, but our copy does not establish the more specific claim that it activates most cholesterol biosynthesis genes. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • SREBPs are central transcriptional regulators of lipid metabolism.

    “The sterol-regulatory element binding proteins (SREBP) are central transcriptional regulators of lipid metabolism.”

    From Haploid genetic screens identify SPRING/C12ORF49 as a determinant of SREBP signaling and cholesterol metabolism (2020) · cites this paper as [3]

  • Association of SREBPs with SCAP and INSIG couples their ER retention and proteolytic activation to sensing of ER membrane cholesterol by SCAP.

    “Their association in a complex with SCAP and INSIG couples their retention in the ER and subsequent proteolytic activation to the sensing of cholesterol content in the ER membrane by SCAP1–3.”

    From Hepatic SREBP signaling requires SPRING to govern systemic lipid metabolism in mice and humans (2023) · cites this paper as [2]

  • When cholesterol level is low, SREBP2 is cleaved by SCAP, leading to its activation and translocation from the ER to the Golgi apparatus.

    “When the cholesterol level is low, SREBP2 is cleaved by SREBP cleavage activation protein (SCAP), leading to SREBP2 activation and translocation from the endoplasmic reticulum (ER) to the Golgi apparatus.”

    From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [11]

  • The active N-terminal fragment of SREBP2 moves to the nucleus, binds the sterol response element, and activates transcription of target genes.

    “Within the Golgi apparatus, SREBP2 is cleaved by two proteases called the site 1 (S1P) and site 2 (S2P) proteases, resulting in an active 68-kDa N-terminal fragment that moves to the nucleus, binds the sterol response element (SRE) in the promoters of target genes, and activates their transcription 11 .”

    From SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington’s disease phenotypes (2021) · cites this paper as [11]

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Research works printed but not linked: 62

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Metadata

Authors
Jeon, T.-I., & Osborne, T. F.
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2012-02
Volume
23
Issue
2
Pages
65-72
ISSN
1043-2760
DOI
10.1016/j.tem.2011.10.004
PMC
PMC3273665
Cited by
464
References
14
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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