Evidence map›Paper›PMID 27546286›Full record

ArticleScientific reports2016

Immune cell-specific transcriptional profiling highlights distinct molecular pathways controlled by Tob1 upon experimental autoimmune encephalomyelitis.

Alessandro Didonna, Egle Cekanaviciute, Jorge R Oksenberg, Sergio E Baranzini

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. A pathogenic and clonally expanded B cell transcriptome in active multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. TopoDB: a novel multifunctional management system for laboratory animal colonies.Database : the journal of biological databases and curation · 2020
    Article
  6. Article
  7. Association between the SNPs of theJournal of Cancer · 2018
    Article
  8. HyperpolarizedProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. 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

4 authors at 1 institution in 1 country.

Alessandro DidonnaDepartment of Neurology, University of California San Francisco, San Francisco, California 94158, USA.
Egle CekanaviciuteDepartment of Neurology, University of California San Francisco, San Francisco, California 94158, USA.
Jorge R OksenbergDepartment of Neurology, University of California San Francisco, San Francisco, California 94158, USA.
Sergio E BaranziniDepartment of Neurology, University of California San Francisco, San Francisco, California 94158, USA.
University of California, San Francisco · US

Funding

UCSF IRACDA Scholars ProgramK12GM081266 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Raymond M. Esquerra, HOLLY A. INGRAHAM · 2007 to 2026
$19.4M
Post GWAS approach to identify cell-specific genetic pathways underlying MS riskR01NS088155 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BARANZINI, SERGIO E · 2014 to 2018
$2.2M
NIGMS NIH HHS K12 GM081266NINDS NIH HHS R01 NS088155
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system characterized by focal lymphocytic infiltration, demyelination and neurodegeneration. Despite the recent advances in understanding MS molecular basis, no reliable biomarkers have been identified yet to monitor disease progression. Our group has previously reported that low levels of TOB1 in CD4(+) T cells are strongly associated with a higher risk of MS conversion in individuals experiencing an initial demyelinating event. Consistently, Tob1 ablation in mice exacerbates the clinical phenotype of the MS model experimental autoimmune encephalomyelitis (EAE). To shed light on Tob1 molecular functions in the immune system, we have conducted the first cell-based transcriptomic analysis in Tob1(-/-) and wildtype mice upon EAE. Next-generation sequencing was employed to characterize the changes in gene expression in T and B cells at pre- and post-symptomatic EAE stages. Remarkably, we found only modest overlap among the different genetic signatures, suggesting that Tob1 may control distinct genetic programs in the different cytotypes. This hypothesis was corroborated by gene ontology and global interactome analyses, which highlighted specific cellular pathways in each cellular subset before and after EAE induction. In summary, our work pinpoints a multifaceted activity of Tob1 in both homeostasis and disease progression.

Indexed as

Gene Expression ProfilingAnimalsB-LymphocytesCarrier ProteinsCD4-Positive T-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMultiple SclerosisNIH 3T3 CellsSignal TransductionCarrier ProteinsIntracellular Signaling Peptides and ProteinsTob1 protein, mouse

Identifiers

PMID27546286
PMCPMC4992865
OpenAlexW2510586930

What OpenQuestion holds

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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.