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Sterol Resistance in CHO Cells Traced to Point Mutation in SREBP Cleavage–Activating Protein

Hua, Xianxin, Nohturfft, Axel, Goldstein, Joseph L, Brown, Michael S·1996·Cell
DOI 10.1016/s0092-8674(00)81362-8
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  • Under sufficient cellular sterols, SREBPs are retained in the ER through formation of a tripartite complex with SCAP and INSIG1/2.

    “Under conditions of sufficient cellular sterols, SREBPs are retained in the ER through formation of a tripartite complex with the sterol-sensing SREBP cleavage-activating protein (SCAP)7,8, and the ER anchor proteins insulin-induced genes 1 and 2 (INSIG1 and 2)9,10.”

    From Haploid genetic screens identify SPRING/C12ORF49 as a determinant of SREBP signaling and cholesterol metabolism (2020) · cites this paper as [7]

    The Discussion describes SCAP as a component of sterol-regulated SREBP cleavage, and the paper describes a possible sterol-sensing region in SCAP. It does not establish that sterols retain SREBPs in the ER through a SCAP–INSIG tripartite complex. The citing sentence assigns the INSIG proteins to separate citations. (LLM, conf=0.86)

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  • SCAP acts as a cholesterol sensor to regulate the release of inactive SREBP-2 from the ER membrane to the nucleus.

    “SCAP acts as a cholesterol sensor, to regulate the release of inactive SREBP-2 from the ER membrane to the nucleus69.”

    From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [69]

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Citations

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Research works printed but not linked: 40

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  12. Goldstein, J.L., Hobbs, H.H., and Brown, M.S. (1995). Familial hypercholesterolemia. In The Metabolic and Molecular Bases of Inherited Disease, C.R. Scriver, A.L. Beaudet, W.S. Sly, and D. Valle, eds. (New York: McGraw-Hill, Inc.), pp. 1981–2030.
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Metadata

Authors
Hua, X., Nohturfft, A., Goldstein, J. L., & Brown, M. S.
Venue
Cell
Publisher
Elsevier BV
Published
1996-11
Volume
87
Issue
3
Pages
415-426
ISSN
0092-8674
DOI
10.1016/s0092-8674(00)81362-8
Cited by
426
References
2
Language
en
Licence

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