Evidence map›Paper›PMID 24844212›Full record

ArticleMolecular biology reports2014

Histone post-translational modifications induced by histone deacetylase inhibition in transcriptional control units of NIS gene.

Federica Baldan, Elisa Lavarone, Carla Di Loreto, Sebastiano Filetti, Diego Russo, Giuseppe Damante, Cinzia Puppin

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Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Federica BaldanDepartment of Medical and Biological Sciences, University of Udine, Piazzale Kolbe 4, 33100, Udine, Italy.
Elisa Lavarone
Carla Di Loreto
Sebastiano Filetti
Diego Russo
Giuseppe Damante
Cinzia Puppin
University of Udine · ITMagna Graecia University · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone post-translational modifications (HPTMs) play a major role in control of gene transcription. Among them, histone acetylation and methylation have been extensively investigated. Histone acetylation at different residues is generally associated to active gene transcription. In contrast, histone methylation can be associated either to transcriptional activation or repression, depending primarily on the histone residue that is subjected to the modification. Herein, effects of the histone deacetylase inhibitor SAHA on the sodium-iodide symporter (NIS) gene expression were investigated in breast cancer cells (MDA157 and MDA468). SAHA treatment induces high increase of NIS mRNA levels in MDA468 cells (300-fold), but moderate increase in MDA157 cells (fivefold). Histone H3 HPTMs (acetylation and methylations) on transcriptional units of NIS gene were investigated in these cell lines upon SAHA treatment. Our data indicate that HPTMs, particularly the H3 lysine 27 trimethylation, may operate in contrast to current models that relate epigenetic modifications with transcriptional activity.

Indexed as

Protein Processing, Post-TranslationalAcetylationAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCell SurvivalChromatin ImmunoprecipitationGene Expression RegulationHistone Deacetylase InhibitorsHistonesHumansHydroxamic AcidsMethylationSodium-Iodide SymportersSymportersAntineoplastic AgentsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsSodium-Iodide SymportersSymportersVorinostat

Identifiers

PMID24844212
OpenAlexW2092103249

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.