Evidence map›Paper›PMID 35829845›Full record

ArticleMetabolic brain disease2022

A de novo YY1 missense variant expanding the Gabriele-de Vries syndrome phenotype and affecting X-chromosome inactivation.

Suely Rodrigues Dos Santos, Rafael Mina Piergiorge, Jady Rocha, Bianca Barbosa Abdala, Andressa Pereira Gonçalves, Márcia Mattos Gonçalves Pimentel, Cíntia Barros Santos-Rebouças

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Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Suely Rodrigues Dos SantosGaffrée and Guinle University Hospital, Federal University of Rio de Janeiro State, Rio de Janeiro, Brazil.
Rafael Mina PiergiorgeDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Jady RochaDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Bianca Barbosa AbdalaDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Andressa Pereira GonçalvesDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Márcia Mattos Gonçalves PimentelDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Cíntia Barros Santos-RebouçasDepartment of Genetics, Institute of Biology Roberto Alcantara Gomes, State University of Rio de Janeiro, Rio de Janeiro, Brazil. cbs@uerj.br.ORCID http://orcid.org/0000-0003-4729-2373
Universidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Yin and Yang 1 gene (YY1; MIM#600,013) is recognized as a dual transcriptional activating and repressing factor, RNA-binding protein, and 3D chromatin regulator, with multi roles in neurodevelopmental and maintenance pathways. YY1 haploinsufficiency caused either by heterozygous sequence variants or deletions involving the whole gene has been recently associated with Gabriele-de Vries syndrome (GADEVS), a rare congenital autosomal dominant condition, leading to intellectual disability (ID) and multiple physical/behavioural abnormalities. Herein, we describe clinical and molecular findings from a Brazilian female harbouring a de novo missense pathogenic variant in YY1 gene (NM_003403.5:c.1106A > G; p.Asn369Ser) found by whole exome sequencing with potential implications for protein structure and function. Undescribed or uncommon clinical features in this patient included non-febrile seizures, severe scoliosis, hearing impairment, and chorioretinitis. Further bioinformatics analyses using YY1-other protein interaction networks reinforced the involvement of YY1 interactors in such phenotypes, in exception of chorioretinitis. Moreover, X-chromosome inactivation (XCI) skewing was evidenced in the patient and attributed to the haploinsufficiency of YY1, which direct and indirectly interacts with numerous XCI key regulators. Besides expanding the mutational and phenotype spectrum of GADEVS, our results highlight the role of YY1 as an essential autosomal regulator of XCI epigenetic process.

Indexed as

ChorioretinitisIntellectual DisabilityChromatinFemaleHumansMutation, MissensePhenotypeSyndromeYY1 Transcription FactorChromatinYY1 protein, humanYY1 Transcription FactorGabriele-de Vries syndromeGADEVSWhole exome sequencingX-chromosome inactivationX-chromosome inactivation skewingYY1 gene

Identifiers

PMID35829845
OpenAlexW4285086725

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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.