Cited by 56

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Blunted feedback suppression of SREBP processing by dietary cholesterol in transgenic mice expressing sterol-resistant SCAP(D443N)

Korn, B S, Shimomura, I, Bashmakov, Y, Hammer, R E, Horton, J D, Goldstein, J L, Brown, M S·1998·Journal of Clinical Investigation

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Crossref · 10.1172/jci5341

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  • Over-accumulation of dietary cholesterol in the liver inhibits SREBP-mediated LDLR gene transcription, leading to reduced hepatic LDLR mRNA levels in hypercholesterolemic animals.

    “It is well-established that over-accumulation of dietary cholesterol in the liver inhibits sterol-regulatory element binding protein (SREBP)-mediated LDL receptor (LDLR) gene transcription leading to a reduced hepatic LDLR mRNA level in hypercholesterolemic animals.”

    From A novel posttranscriptional mechanism for dietary cholesterol-mediated suppression of liver LDL receptor expression (2014) · cites this paper as [15]

    The Results report that a cholesterol/cholic acid diet increased liver cholesterol in wild-type mice and reduced hepatic LDL receptor mRNA by 20%. The Discussion links cholesterol feeding to reduced nuclear SREBP-2, but describes the connection to LDL receptor transcription as a suggestion rather than establishing the claimed causal chain across hypercholesterolemic animals generally. Page numbers are unavailable in our copy. (LLM, conf=0.84)

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  • Over-accumulation of dietary cholesterol in the liver prevents proteolytic activation of SREBPs and leads to a decline in expression of SREBP target genes, including LDLR and SREBP2 itself.

    “Over-accumulation of dietary cholesterol in the liver prevents the proteolytic activation of SREBPs and leads to a decline in the expression of SREBP target genes, including LDLR and SREBP2 itself.”

    From A novel posttranscriptional mechanism for dietary cholesterol-mediated suppression of liver LDL receptor expression (2014) · cites this paper as [15]

    The Results (page not specified) show that a cholesterol/cholic acid diet sharply reduced nuclear SREBP-2 in wild-type mouse liver and reduced LDL receptor mRNA by 20%. The paper does not report that dietary cholesterol reduced SREBP-2 gene expression itself; the Discussion describes SREBP-2 self-regulation as a possibility. Suppression was also blunted, rather than complete, in the SCAP(D443N) transgenic mice. (LLM, conf=0.87)

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Citations

Cites

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Research works printed but not linked: 6

  1. Hua, X., C. Yokoyama, J. Wu, M.R. Briggs, M.S. Brown, J.L. Goldstein, and X. Wang. 1993. SREBP-2, a second basic-helix-loop-helix-leucine zipper protein that stimulates transcription by binding to a sterol regulatory element. Proc. Natl. Acad. Sci. USA. 90:11603-11607.
  2. Lopez, J.M., M.K. Bennett, H.B. Sanchez, J.M. Rosenfeld, and T.F. Os- borne. 1996. Sterol regulation of acetyl CoA carboxylase: a mechanism for co- ordinate control of cellular lipid. Proc. Natl. Acad. Sci. USA. 93:1049-1053.
  3. Nohturfft, A., M.S. Brown, and J.L. Goldstein. 1998. Sterols regulate processing of carbohydrate chains of wild-type SREBP cleavage-activating pro- tein (SCAP), but not sterol-resistant mutants Y298C or D443N. Proc. Natl. Acad. Sci. USA. 95:12848-12853.
  4. Palmiter, R.D., E.P. Sandgren, M.R. Avarbock, D.D. Allen, and R.L. Brinster. 1991. Heterologous introns can enhance expression of transgenes in mice. Proc. Natl. Acad. Sci. USA. 88:478-482.
  5. Sheng, Z., H. Otani, M.S. Brown, and J.L. Goldstein. 1995. Independent regulation of sterol regulatory element binding proteins 1 and 2 in hamster liver. Proc. Natl. Acad. Sci. USA. 92:935-938.
  6. Shimomura, I., H. Shimano, B.S. Korn, Y. Bashmakov, and J.D. Hor- ton. 1999. Nuclear sterol regulatory element-binding proteins activate genes re- sponsible for the entire program of unsaturated fatty acid biosynthesis in trans- genic mouse liver. J. Biol. Chem. In press.

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Metadata

Authors
Korn, B. S., Shimomura, I., Bashmakov, Y., Hammer, R. E., Horton, J. D., Goldstein, J. L., & Brown, M. S.
Venue
Journal of Clinical Investigation
Published
1998-12-15
Volume
102
Issue
12
Pages
2050-2060
ISSN
0021-9738
Cited by
56
References
3
Language
en

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