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Cited by 209

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Expression of sterol regulatory element-binding protein 1c (SREBP-1c) mRNA in rat hepatoma cells requires endogenous LXR ligands

DeBose-Boyd, Russell A., Ou, Jiafu, Goldstein, Joseph L., Brown, Michael S.·2001·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.98.4.1477
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Abstract

The current paper describes a line of cultured rat hepatoma cells (McA-RH7777 cells) that mimics the behavior of rat liver by producing an excess of mRNA for sterol regulatory element-binding protein 1c (SREBP-1c) as opposed to SREBP-1a. These two transcripts are derived from a single gene by use of alternative promoters that are separated by many kilobases in the genome. The high level of SREBP-1c mRNA is abolished when cholesterol synthesis is blocked by compactin, an inhibitor of 3-hydroxy-3-methylglutaryl CoA (HMG CoA) reductase that inhibits cholesterol synthesis. Levels of SREBP-1c mRNA are restored by mevalonate, the product of the HMG CoA reductase reaction, and by ligands for the nuclear hormone receptor LXR, including 22( R )-hydroxycholesterol and T0901317. These data suggest that transcription of the SREBP-1c gene in hepatocytes requires tonic activation of LXR by an oxysterol intermediate in the cholesterol biosynthetic pathway. Reduction of this intermediate lowers SREBP-1c levels, and this in turn is predicted to lower the rates of fatty acid biosynthesis in liver.

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Crossref · 10.1073/pnas.98.4.1477

Cites

1 of 1 references verified0 citation errors · 0 not checkable

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Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • LXRs are critical for maximal transcription of SREBP-1c.

    “LXRs are critical for maximal transcription of SREBP-1c, and loss of hepatic LXR expression therefore compromises SREBP-1c-dependent lipogenesis (DeBose-Boyd et al., 2001; Repa et al., 2000a; Schultz et al., 2000).”

    From Inhibition of cholesterol biosynthesis through RNF145-dependent ubiquitination of SCAP (2017) · cites this paper as DeBose-Boyd et al., 2001

  • Loss of hepatic LXR expression compromises SREBP-1c-dependent lipogenesis.

    “LXRs are critical for maximal transcription of SREBP-1c, and loss of hepatic LXR expression therefore compromises SREBP-1c-dependent lipogenesis (DeBose-Boyd et al., 2001; Repa et al., 2000a; Schultz et al., 2000).”

    From Inhibition of cholesterol biosynthesis through RNF145-dependent ubiquitination of SCAP (2017) · cites this paper as DeBose-Boyd et al., 2001

Citations

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Research works printed but not linked: 31

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Metadata

Authors
DeBose-Boyd, R. A., Ou, J., Goldstein, J. L., & Brown, M. S.
Affiliations
Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9046
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2001-02-13
Volume
98
Issue
4
Pages
1477-1482
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.98.4.1477
Cited by
209
References
1
Language
en

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