Evidence map›Paper›PMID 27622813›Full record

ArticleScientific reports2016

Pits, a protein interacting with Ttk69 and Sin3A, has links to histone deacetylation.

Gwo-Jen Liaw

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. IRF2BPL Is Associated with Neurological Phenotypes.American journal of human genetics · 2018
    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

1 author at 1 institution in 1 country.

Gwo-Jen LiawDepartment of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, 112-22, Taiwan, Republic of China.
National Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylation plays an important role in transcriptional repression. Previous results showed that the genetic interaction between ttk and rpd3, which encodes a class I histone deacetylase, is required for tll repression. This study investigated the molecular mechanism by which Ttk69 recruits Rpd3. Using yeast two-hybrid screening and datamining, one novel protein was found that weakly interacts with Ttk69 and Sin3A, designated as Protein interacting with Ttk69 and Sin3A (Pits). Pits protein expressed in the early stages of embryos and bound to the region of the tor response element in vivo. Expanded tll expression patterns were observed in embryos lacking maternal pits activity and the expansion was not widened by reducing either maternal ttk or sin3A activity. However, in embryos with simultaneously reduced maternal pits and sin3A activities or maternal pits, sin3A and ttk activities, the proportions of the embryos with expanded tll expression were significantly increased. These results indicate that all three gene activities are involved in tll repression. Level of histone H3 acetylation in the tll proximal region was found to be elevated in embryo with reduced these three gene activities. In conclusion, Ttk69 causes the histone deacetylation-mediated repression of tll via the interaction of Pits and Sin3A.

Indexed as

Transcription, GeneticAcetylationAnimalsDrosophila melanogasterDrosophila ProteinsHistone DeacetylasesHistonesNuclear ProteinsRepressor ProteinsResponse ElementsSin3 Histone Deacetylase and Corepressor ComplexTranscription FactorsDrosophila ProteinsHistone DeacetylasesHistonesNuclear ProteinsPits protein, DrosophilaRepressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexTranscription Factorsttk protein, Drosophila

Identifiers

PMID27622813
PMCPMC5020733
OpenAlexW2520809946

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.