Evidence map›Paper›PMID 17416750›Full record

ArticleGenome research2007

X chromosome cDNA microarray screening identifies a functional PLP2 promoter polymorphism enriched in patients with X-linked mental retardation.

Lilei Zhang, Chunfa Jie, Cassandra Obie, Fatima Abidi, Charles E Schwartz, Roger E Stevenson, David Valle, Tao Wang

Open access · bronzeAbstract readValidation Study
In one paragraph

Article in Genome research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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  10. Mutations in ionotropic AMPA receptor 3 alter channel properties and are associated with moderate cognitive impairment in humans.Proceedings of the National Academy of Sciences of the United States of America · 2007
    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

8 authors at 2 institutions in 1 country.

Lilei ZhangMcKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Chunfa Jie
Cassandra Obie
Fatima Abidi
Charles E Schwartz
Roger E Stevenson
David Valle
Tao Wang
Johns Hopkins University · USGreenwood Genetic Center · US

Funding

NICHD MENTAL RETARDATION RESEARCH CENTER CORE GRANTP30HD024061 · NICHD · KENNEDY KRIEGER CHILDRENS HOSPITAL · PI CATALDO, MICHAEL F · 1988 to 2013
$15.8M
X-LINKED MENTAL RETARDATION: LINKAGE &CLINICAL STUDIESR01HD026202 · NICHD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SCHWARTZ, CHARLES E · 1990 to 2006
$7.9M
ID of Genes Responsible for X-Linked Mental RetardationK23HD044789 · NICHD · JOHNS HOPKINS UNIVERSITY · PI WANG, TAO · 2003 to 2007
$671k
NICHD NIH HHS HD24061NICHD NIH HHS HD26202NICHD NIH HHS K23 HD044789NICHD NIH HHS K23HD044789NICHD NIH HHS P30 HD024061NICHD NIH HHS R01 HD026202
6 · The paper itself

Abstract

X-linked Mental Retardation (XLMR) occurs in 1 in 600 males and is highly genetically heterogeneous. We used a novel human X chromosome cDNA microarray (XCA) to survey the expression profile of X-linked genes in lymphoblasts of XLMR males. Genes with altered expression verified by Northern blot and/or quantitative PCR were considered candidates. To validate this approach, we documented the expected changes of expression in samples from a patient with a known X chromosome microdeletion and from patients with multiple copies of the X chromosome. We used our XCA to survey lymphoblast RNA samples from 43 unrelated XLMR males and found 15 genes with significant (>or=1.5-fold) reduction in expression in at least one proband. Of these, subsequent analysis confirmed altered expression in 12. We followed up one, PLP2, at Xp11.23, which exhibits approximately fourfold decreased expression in two patients. Sequencing analysis in both patients revealed a promoter variant, -113C>A, that alters the core-binding site of the transcription factor ELK1. We showed that PLP2-(-113C>A) is sufficient to cause reduced expression using a luciferase reporter system and is enriched in a cohort of males with probable XLMR (14 of 239, 5.85%) as compared to normal males (9 of 577, 1.56%) (chi2=11.07, P<0.001). PLP2 is expressed abundantly in the pyramidal cells of hippocampus and granular cells of the cerebellum in the brain. We conclude that our XCA screening is an efficient strategy to identify genes that show significant changes in transcript abundance as candidate genes for XLMR.

Indexed as

Oligonucleotide Array Sequence AnalysisPolymorphism, GeneticAnimalsBase SequenceCell LineCell Line, TransformedChromosomes, Human, XDNA, ComplementaryFemaleHumansMaleMARVEL Domain-Containing ProteinsMembrane ProteinsMiceMolecular Sequence DataPoint MutationDNA, ComplementaryMARVEL Domain-Containing ProteinsMembrane ProteinsPLP2 protein, humanProteolipids

Identifiers

PMID17416750
PMCPMC1855181
OpenAlexW2140990867

What OpenQuestion holds

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Registered trials

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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.