Evidence map›Paper›PMID 15314177›Full record

ArticleMolecular and cellular biology2004

Role of an mSin3A-Swi/Snf chromatin remodeling complex in the feedback repression of bile acid biosynthesis by SHP.

Jongsook Kim Kemper, Hwajin Kim, Ji Miao, Sonali Bhalla, Yangjin Bae

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

55 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
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  13. Cholic Acid Feeding Leads to Increased CYP2D6 Expression in CYP2D6-Humanized Mice.Drug metabolism and disposition: the biological fate of chemicals · 2017
    Article
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  15. Article
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  17. Article
  18. Review
  19. Bile Acids as Hormones: The FXR-FGF15/19 Pathway.Digestive diseases (Basel, Switzerland) · 2015
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Jongsook Kim KemperDepartment of Molecular and Integrative Physiology, University of Illinois, Urbana, IL 61801, USA. jongsook@uiuc.edu
Hwajin Kim
Ji Miao
Sonali Bhalla
Yangjin Bae
University of Illinois Urbana-Champaign · US

Funding

Regulation of Cholesterol Catabolism by Bile AcidsR01DK062777 · NIDDK · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KEMPER, JONGSOOK KIM · 2003 to 2021
$5.8M
Regulation of cholesterol catabolism by bile acidsR56DK062777 · NIDDK · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI KEMPER, JONGSOOK KIM · 2008 to 2008
$192k
NIDDK NIH HHS DK062777NIDDK NIH HHS R01 DK062777NIDDK NIH HHS R56 DK062777
6 · The paper itself

Abstract

The orphan receptor SHP interacts with many nuclear receptors and inhibits their transcriptional activities. SHP is central to feedback repression of cholesterol 7alpha hydroxylase gene (CYP7A1) expression by bile acids, which is critical for maintaining cholesterol homeostasis. Using CYP7A1 as a model system, we studied the molecular mechanisms of SHP repression at the level of native chromatin. Chromatin immunoprecipitation studies showed that mSin3A and a Swi/Snf complex containing Brm as a central ATPase were recruited to the promoter. This recruitment was associated with chromatin remodeling after bile acid treatment that was blunted by inhibition of the endogenous Swi/Snf function by dominant-negative ATPase mutants. Biochemical studies indicated that SHP was associated with the mSin3A-Swi/Snf complex by direct interaction with Brm and mSin3A through its repression domain. Expression of Brm, but not an ATPase mutant, inhibited CYP7A1 promoter activity and further enhanced SHP-mediated repression. Bile acid-induced recruitment of mSin3A/Brm, chromatin remodeling, and concomitant repression of endogenous CYP7A1 expression were impaired when SHP expression was inhibited by SHP small interfering RNA. Our results suggest that SHP mediates recruitment of mSin3A-Swi/Snf to the CYP7A1 promoter, resulting in chromatin remodeling and gene repression, which may also be a mechanism for the repression by SHP of genes activated by many nuclear receptors. Our study establishes the first link between a Swi/Snf complex and regulation of cholesterol metabolism.

Indexed as

Feedback, PhysiologicalGene Expression RegulationAcetyltransferasesAdenosine TriphosphatasesBile Acids and SaltsCell Cycle ProteinsCell Line, TumorCholesterol 7-alpha-HydroxylaseChromatinChromosomal Proteins, Non-HistoneDrosophila ProteinsHistone AcetyltransferasesHistone Deacetylase 1Histone DeacetylasesHumansMacromolecular SubstancesAcetyltransferasesAdenosine TriphosphatasesBile Acids and Saltsbrm protein, DrosophilaCell Cycle ProteinsCholesterol 7-alpha-HydroxylaseChromatinChromosomal Proteins, Non-HistoneDrosophila ProteinsHDAC1 protein, humanHistone AcetyltransferasesHistone Deacetylase 1Histone DeacetylasesMacromolecular Substancesnuclear receptor subfamily 0, group B, member 2Receptors, Cytoplasmic and NuclearRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTrans-ActivatorsTranscription Factors

Identifiers

PMID15314177
PMCPMC506991
OpenAlexW2131566044

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.