Evidence map›Paper›PMID 21528155›Full record

ArticleMolecular medicine (Cambridge, Mass.)2011

All-trans retinoic acid upregulates reduced CD38 transcription in lymphoblastoid cell lines from Autism spectrum disorder.

Mathias Riebold, David Mankuta, Elad Lerer, Salomon Israel, Songfa Zhong, Luba Nemanov, Mikhail V Monakhov, Shlomit Levi, Nurit Yirmiya, Maya Yaari and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Effects of a common variant in the CD38 gene on social processing in an oxytocin challenge study: possible links to autism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
    Trial
  3. Article
  4. Association ofCurrent issues in molecular biology · 2023
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  8. Review
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  13. The Role of Vitamins in Autism Spectrum Disorder: What Do We Know?Journal of molecular neuroscience : MN · 2019
    Review
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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

12 authors at 4 institutions in 3 countries.

Mathias RieboldDepartment of Human Genetics, Hebrew University, Jerusalem, Israel. rpebstein@gmail.com
David Mankuta
Elad Lerer
Salomon Israel
Songfa Zhong
Luba Nemanov
Mikhail V Monakhov
Shlomit Levi
Nurit Yirmiya
Maya Yaari
Fabio Malavasi
Richard P Ebstein
Hebrew University of Jerusalem · ILNational University of Singapore · SGHadassah Medical Center · ILUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deficits in social behavior in mice lacking the CD38 gene have been attributed to impaired secretion of oxytocin. In humans, similar deficits in social behavior are associated with autistic spectrum disorder (ASD), for which genetic variants of CD38 have been pinpointed as provisional risk factors. We sought to explore, in an in vitro model, the feasibility of the theory that restoring the level of CD38 in ASD patients could be of potential clinical benefit. CD38 transcription is highly sensitive to several cytokines and vitamins. One of these, all-trans retinoic acid (ATRA), a known inducer of CD38, was added during cell culture and tested on a large sample of N = 120 lymphoblastoid cell (LBC) lines from ASD patients and their parents. Analysis of CD38 mRNA levels shows that ATRA has an upmodulatory potential on LBC derived from ASD patients as well as from their parents. The next crucial issue addressed in our study was the relationship between levels of CD38 expression and psychological parameters. The results obtained indicate a positive correlation between CD38 expression levels and patient scores on the Vineland Adaptive Behavior Scale. In addition, analysis of the role of genetic polymorphisms in the dynamics of the molecule revealed that the genotype of a single-nucleotide polymorphism (rs6449182; C>G variation) in the CpG island of intron 1, harboring the retinoic-acid response element, exerts differential roles in CD38 expression in ASD and in parental LBC. In conclusion, our results provide an empirical basis for the development of a pharmacological ASD treatment strategy based on retinoids.

Indexed as

AdolescentADP-ribosyl Cyclase 1AdultCell LineChildChild Development Disorders, PervasiveChild, PreschoolCpG IslandsFemaleGene Expression RegulationGenotypeHumansIntelligenceIntronsLymphocytesMaleADP-ribosyl Cyclase 1RNA, MessengerTretinoin

Identifiers

PMID21528155
PMCPMC3146614
OpenAlexW2121367992

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.