Evidence map›Paper›PMID 36255617›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2023

Development of a Cellular Model Mimicking Specific HDAC Inhibitors.

Lena Hess, Verena Moos, Christian Seiser

Abstract read
PubMed Publisher
In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

3 authors.

Lena HessCenter for Anatomy and Cell Biology, Division for Cell and Developmental Biology, Medical University of Vienna, Vienna, Austria.
Verena MoosCenter for Anatomy and Cell Biology, Division for Cell and Developmental Biology, Medical University of Vienna, Vienna, Austria.
Christian SeiserCenter for Anatomy and Cell Biology, Division for Cell and Developmental Biology, Medical University of Vienna, Vienna, Austria. christian.seiser@meduniwien.ac.at.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Class I histone deacetylases (HDACs) are important regulators of cellular functions in health and disease. HDAC1, HDAC2, HDAC3, and HDAC8 are promising targets for the treatment of cancer, neurological, and immunological disorders. These enzymes have both catalytic and non-catalytic functions in the regulation of gene expression. We here describe the generation of a genetic toolbox by the CRISPR/Cas9 methodology in nearly haploid human tumor cells. This novel model system allows to discriminate between catalytic and structural functions of class I HDAC enzymes and to mimic the treatment with specific HDAC inhibitors.

Indexed as

Histone Deacetylase InhibitorsNeoplasmsHistone Deacetylase 1Histone DeacetylasesHumansRepressor ProteinsHDAC8 protein, humanHistone Deacetylase 1Histone Deacetylase InhibitorsHistone DeacetylasesRepressor ProteinsCRISPR/Cas9HDAC inactivationHDAC inhibitionKnock-inKnockoutTransgenic cells

Identifiers

PMID36255617

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.