Evidence map›Paper›PMID 25568313›Full record

ArticleThe Journal of biological chemistry2015

Deficiency of the chromatin regulator BRPF1 causes abnormal brain development.

Linya You, Jinfeng Zou, Hong Zhao, Nicholas R Bertos, Morag Park, Edwin Wang, Xiang-Jiao Yang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

43 citing papers in PubMed, 60 citations in OpenAlex.

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  14. Mosaicism inCase reports in genetics · 2023
    Article
  15. Review
  16. Article
  17. Reprogramming of the epigenome in neurodevelopmental disorders.Critical reviews in biochemistry and molecular biology · 2022
    Review
  18. Review
  19. Article
  20. Observational
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 2 countries.

Linya YouFrom the Rosalind & Morris Goodman Cancer Research Center, Department of Medicine, McGill University, Quebec H3A 1A3.
Jinfeng Zouthe National Research Council Canada, Montreal, Quebec H4P 2R2, and.
Hong ZhaoFrom the Rosalind & Morris Goodman Cancer Research Center.
Nicholas R BertosFrom the Rosalind & Morris Goodman Cancer Research Center.
Morag ParkFrom the Rosalind & Morris Goodman Cancer Research Center, Department of Medicine, McGill University, Quebec H3A 1A3, the Department of Biochemistry, McGill University and McGill University Health Center, Montreal, Quebec H3A 1A3, Canada.
Edwin Wangthe National Research Council Canada, Montreal, Quebec H4P 2R2, and.
Xiang-Jiao YangFrom the Rosalind & Morris Goodman Cancer Research Center, Department of Medicine, McGill University, Quebec H3A 1A3, the Department of Biochemistry, McGill University and McGill University Health Center, Montreal, Quebec H3A 1A3, Canada xiang-jiao.yang@mcgill.ca.
McGill University · CACancer Research Center · USNational Research Council Canada · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Epigenetic mechanisms are important in different neurological disorders, and one such mechanism is histone acetylation. The multivalent chromatin regulator BRPF1 (bromodomain- and plant homeodomain-linked (PHD) zinc finger-containing protein 1) recognizes different epigenetic marks and activates three histone acetyltransferases, so it is both a reader and a co-writer of the epigenetic language. The three histone acetyltransferases are MOZ, MORF, and HBO1, which are also known as lysine acetyltransferase 6A (KAT6A), KAT6B, and KAT7, respectively. The MORF gene is mutated in four neurodevelopmental disorders sharing the characteristic of intellectual disability and frequently displaying callosal agenesis. Here, we report that forebrain-specific inactivation of the mouse Brpf1 gene caused early postnatal lethality, neocortical abnormalities, and partial callosal agenesis. With respect to the control, the mutant forebrain contained fewer Tbr2-positive intermediate neuronal progenitors and displayed aberrant neurogenesis. Molecularly, Brpf1 loss led to decreased transcription of multiple genes, such as Robo3 and Otx1, important for neocortical development. Surprisingly, elevated expression of different Hox genes and various other transcription factors, such as Lhx4, Foxa1, Tbx5, and Twist1, was also observed. These results thus identify an important role of Brpf1 in regulating forebrain development and suggest that it acts as both an activator and a silencer of gene expression in vivo.

Indexed as

Gene Expression Regulation, DevelopmentalAdaptor Proteins, Signal TransducingAgenesis of Corpus CallosumAnimalsBehavior, AnimalBrainBromodomain Containing ProteinsCarrier ProteinsCorpus CallosumDNA-Binding ProteinsGene DeletionGene SilencingMiceMice, KnockoutNeurogenesisTranscriptional ActivationAdaptor Proteins, Signal TransducingBromodomain Containing ProteinsBRPF1 protein, mouseCarrier ProteinsDNA-Binding ProteinsBrain DevelopmentBromodomainBRPF1Chromatin ModificationGene RegulationHistone AcetylaseHistone AcetyltransferaseMicroarrayPleckstrin Homology Domain Finger

Identifiers

PMID25568313
PMCPMC4358132
OpenAlexW1965261854

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.