Evidence map›Paper›PMID 16166625›Full record

ArticleMolecular and cellular biology2005

Tumor suppressor SMAR1 mediates cyclin D1 repression by recruitment of the SIN3/histone deacetylase 1 complex.

Shravanti Rampalli, L Pavithra, Altaf Bhatt, Tapas K Kundu, Samit Chattopadhyay

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

62 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. BEND3 safeguards pluripotency by repressing differentiation-associated genes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
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  11. Review
  12. Article
  13. Article
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Hypermethylation ofOncotarget · 2017
    Article
  20. Zebrafish sin3b mutants are viable but have size, skeletal, and locomotor defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Article

2 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Shravanti RampalliNational Center for Cell Science, Pune University Campus, Ganeshkhind, Pune 411007, India.
L Pavithra
Altaf Bhatt
Tapas K Kundu
Samit Chattopadhyay
National Centre for Cell Science · INJawaharlal Nehru Centre for Advanced Scientific Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Matrix attachment region binding proteins have been shown to play an important role in gene regulation by altering chromatin in a stage- and tissue-specific manner. Our previous studies report that SMAR1, a matrix-associated protein, regresses B16-F1-induced tumors in mice. Here we show SMAR1 targets the cyclin D1 promoter, a gene product whose dysregulation is attributed to breast malignancies. Our studies reveal that SMAR1 represses cyclin D1 gene expression, which can be reversed by small interfering RNA specific to SMAR1. We demonstrate that SMAR1 interacts with histone deacetylation complex 1, SIN3, and pocket retinoblastomas to form a multiprotein repressor complex. This interaction is mediated by the SMAR1(160-350) domain. Our data suggest SMAR1 recruits a repressor complex to the cyclin D1 promoter that results in deacetylation of chromatin at that locus, which spreads to a distance of at least the 5 kb studied upstream of the cyclin D1 promoter. Interestingly, we find that the high induction of cyclin D1 in breast cancer cell lines can be correlated to the decreased levels of SMAR1 in these lines. Our results establish the molecular mechanism exhibited by SMAR1 to regulate cyclin D1 by modification of chromatin.

Indexed as

Binding SitesCell CycleCell Cycle ProteinsCell LineCell Line, TumorCell ProliferationCell SizeChromatinChromatin ImmunoprecipitationCyclin D1DNA-Binding ProteinsDNA PrimersG1 PhaseGene Expression Regulation, NeoplasticGlutathione TransferaseHistone Deacetylase 1BANP protein, humanCell Cycle ProteinsChromatinCyclin D1DNA-Binding ProteinsDNA PrimersGlutathione TransferaseHDAC1 protein, humanHistone Deacetylase 1Histone DeacetylasesHistonesLuciferasesNuclear ProteinsRecombinant Fusion ProteinsRepressor ProteinsRetinoblastoma ProteinRNA, Small InterferingSaccharomyces cerevisiae ProteinsSIN3A transcription factorSIN3B protein, humanSin3 Histone Deacetylase and Corepressor ComplexSIN3 protein, S cerevisiaeTranscription Factors

Identifiers

PMID16166625
PMCPMC1265755
OpenAlexW2139655205

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.