Evidence map›Paper›PMID 27256286›Full record

ArticleNeurotoxicity research2016

A Small Molecule Activator of p300/CBP Histone Acetyltransferase Promotes Survival and Neurite Growth in a Cellular Model of Parkinson's Disease.

Shane V Hegarty, Eimear O'Leary, Franziska Solger, Joanna Stanicka, Aideen M Sullivan, Gerard W O'Keeffe

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In one paragraph

Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

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  20. Inhibition ofNeuronal signaling · 2018
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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

6 authors at 2 institutions in 1 country.

Shane V HegartyDepartment of Anatomy and Neuroscience, Biosciences Institute, University College Cork, Cork, Ireland. shane.hegarty@ucc.ie.
Eimear O'LearyDepartment of Anatomy and Neuroscience, Biosciences Institute, University College Cork, Cork, Ireland.
Franziska SolgerDepartment of Anatomy and Neuroscience, Biosciences Institute, University College Cork, Cork, Ireland.
Joanna StanickaSchool of Biochemistry and Cell Biology, Biosciences Institute, University College Cork, Cork, Ireland.
Aideen M SullivanDepartment of Anatomy and Neuroscience, Biosciences Institute, University College Cork, Cork, Ireland.
Gerard W O'KeeffeDepartment of Anatomy and Neuroscience, Biosciences Institute, University College Cork, Cork, Ireland.
University College Cork · IECork University Hospital · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease characterised by motor and non-motor symptoms, resulting from the degeneration of nigrostriatal dopaminergic neurons and peripheral autonomic neurons. Given the limited success of neurotrophic factors in clinical trials, there is a need to identify new small molecule drugs and drug targets to develop novel therapeutic strategies to protect all neurons that degenerate in PD. Epigenetic dysregulation has been implicated in neurodegenerative disorders, while targeting histone acetylation is a promising therapeutic avenue for PD. We and others have demonstrated that histone deacetylase inhibitors have neurotrophic effects in experimental models of PD. Activators of histone acetyltransferases (HAT) provide an alternative approach for the selective activation of gene expression, however little is known about the potential of HAT activators as drug therapies for PD. To explore this potential, the present study investigated the neurotrophic effects of CTPB (N-(4-chloro-3-trifluoromethyl-phenyl)-2-ethoxy-6-pentadecyl-benzamide), which is a potent small molecule activator of the histone acetyltransferase p300/CBP, in the SH-SY5Y neuronal cell line. We report that CTPB promoted the survival and neurite growth of the SH-SY5Y cells, and also protected these cells from cell death induced by the neurotoxin 6-hydroxydopamine. This study is the first to investigate the phenotypic effects of the HAT activator CTPB, and to demonstrate that p300/CBP HAT activation has neurotrophic effects in a cellular model of PD.

Indexed as

Antiparkinson AgentsBenzamidesCell Line, TumorCell SurvivalDose-Response Relationship, DrugDrug Evaluation, PreclinicalE1A-Associated p300 ProteinHistone AcetyltransferasesHumansNeuronal OutgrowthNeuronsNeuroprotective AgentsOxidopamineParkinson DiseaseAntiparkinson AgentsBenzamidesE1A-Associated p300 ProteinEP300 protein, humanHistone AcetyltransferasesN-(4-chloro-3-trifluoromethylphenyl)-2-ethoxy-6-pentadecylbenzamideNeuroprotective AgentsOxidopamineCTPBEpigenetic regulationNeuronal survival and growthNeurotrophic therapyp300/CBP histone acetyltransferaseParkinson’s disease

Identifiers

PMID27256286
OpenAlexW2417877112

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.