Evidence map›Paper›PMID 24933366›Full record

ArticleJournal of proteome research2014

Quantitative proteomic analysis identifies targets and pathways of a 2-aminobenzamide HDAC inhibitor in Friedreich's ataxia patient iPSC-derived neural stem cells.

Bing Shan, Chunping Xu, Yaoyang Zhang, Tao Xu, Joel M Gottesfeld, John R Yates

Open access · bronzeAbstract read
In one paragraph

Article in Journal of proteome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Perspectives on current models of Friedreich's ataxia.Frontiers in cell and developmental biology · 2022
    Article
  4. Review
  5. Article
  6. Histone deacetylase-3: Friend and foe of the brain.Experimental biology and medicine (Maywood, N.J.) · 2020
    Review
  7. Mechanism of Action for HDAC Inhibitors-Insights from Omics Approaches.International journal of molecular sciences · 2019
    Review
  8. Article
  9. Targeting HDAC3 Activity with RGFP966 Protects Against Retinal Ganglion Cell Nuclear Atrophy and Apoptosis After Optic Nerve Injury.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2018
    Article
  10. Modeling simple repeat expansion diseases with iPSC technology.Cellular and molecular life sciences : CMLS · 2016
    Review
  11. Review
  12. Review
  13. Translating HDAC inhibitors in Friedreich's ataxia.Expert opinion on orphan drugs · 2016
    Article
  14. Review
  15. 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

6 authors at 1 institution in 1 country.

Bing ShanDepartment of Chemical Physiology, ‡Department of Cell and Molecular biology, The Scripps Research Institute , La Jolla, California 92037, United States.
Chunping Xu
Yaoyang Zhang
Tao Xu
Joel M Gottesfeld
John R Yates
Scripps Research Institute · US

Funding

TrainingP41GM103533 · NIGMS · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2012 to 2021
$20.7M
Proteogenetics of Autism Spectrum DisordersR01MH100175 · NIMH · SCRIPPS RESEARCH INSTITUTE, THE · PI MUOTRI, ALYSSON R., YATES III, JOHN R · 2013 to 2025
$7.4M
Mechanisms of Gene Silencing of Friedreich's AtaxiaR01NS062856 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI GOTTESFELD, JOEL M. · 2009 to 2018
$4.1M
NHLBI NIH HHS HHSN268201000035CNIGMS NIH HHS P41 GM103533NIMH NIH HHS R01 MH068770NIMH NIH HHS R01 MH100175NIMH NIH HHS R01MH100175NINDS NIH HHS R01 NS062856
6 · The paper itself

Abstract

Members of the 2-aminobenzamide class of histone deacetylase (HDAC) inhibitors show promise as therapeutics for the neurodegenerative diseases Friedreich's ataxia (FRDA) and Huntington's disease (HD). While it is clear that HDAC3 is one of the important targets of the 2-aminobenzamide HDAC inhibitors, inhibition of other class I HDACs (HDACs 1 and 2) may also be involved in the beneficial effects of these compounds in FRDA and HD, and other HDAC interacting proteins may be impacted by the compound. To this end, we synthesized activity-based profiling probe (ABPP) versions of one of our HDAC inhibitors (compound 106), and in the present study we used a quantitative proteomic method coupled with multidimensional protein identification technology (MudPIT) to identify the proteins captured by the ABPP 106 probe. Nuclear proteins were extracted from FRDA patient iPSC-derived neural stem cells, and then were reacted with control and ABPP 106 probe. After reaction, the bound proteins were digested on the beads, and the peptides were modified using stable isotope-labeled formaldehyde to form dimethyl amine. The selectively bound proteins determined by mass spectrometry were subjected to functional and pathway analysis. Our findings suggest that the targets of compound 106 are involved not only in transcriptional regulation but also in posttranscriptional processing of mRNA.

Indexed as

Friedreich AtaxiaHistone Deacetylase InhibitorsHumansInduced Pluripotent Stem CellsMass SpectrometryMolecular ProbesNeural Stem CellsNuclear Proteinsortho-AminobenzoatesProteomicsPyrazolesPyridinium CompoundsRNA Processing, Post-Transcriptionalanthranilamidecompound 106Histone Deacetylase InhibitorsMolecular ProbesNuclear Proteinsortho-AminobenzoatesPyrazolesPyridinium Compoundsdimethyl labelingFRDAHDAC inhibitorMudPIT

Identifiers

PMID24933366
PMCPMC4227551
OpenAlexW2325985150

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.