A surprising role for myelin in Williams syndrome.

Lindsay A Osso, Jonah R Chan

Abstract readComment

In one paragraph

Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it

0cells of the map it votes in

3citing 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

3 citing papers in PubMed.

Gtf2i-encoded transcription factor Tfii-i regulates myelination via Sox10 and Mbp regulatory elements.Nature communications · 2025
Article
Williams syndrome.Nature reviews. Disease primers · 2021
Review
Core transcriptional networks in Williams syndrome: IGF1-PI3K-AKT-mTOR, MAPK and actin signaling at the synapse echo autism.Human molecular genetics · 2021
Article

4 · The record

Corrections and comments

Comment on
Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug.2019

5 · Who and what money

Authors and funding

2 authors.

Lindsay A OssoUCSF Weill Neuroscience Graduate Program and Department of Neurology, University of California, San Francisco, San Francisco, CA, USA.

Jonah R ChanUCSF Weill Neuroscience Graduate Program and Department of Neurology, University of California, San Francisco, San Francisco, CA, USA. jonah.chan@ucsf.edu.

Funding

THE ESTABLISHMENT OF SCHWANN CELL POLARITY AND THE INITIATION OF MYELINATIONR01NS062796 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAN, JONAH R · 2008 to 2018

$3.4M

Functional Screening of GPCR Small Molecule Libraries for Remyelination TherapiesR01NS095889 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAN, JONAH R · 2016 to 2020

$1.9M

Somatodendritic Inhibition of Oligodendrocyte MyelinationR01NS097428 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAN, JONAH R, PELES, ELIOR · 2016 to 2020

$1.5M

NINDS NIH HHS R01 NS062796NINDS NIH HHS R01 NS095889NINDS NIH HHS R01 NS097428

6 · The paper itself

Abstract

PubMed holds no abstract for this paper.

Indexed as

Transcription Factors, TFIITranscription Factors, TFIIIWilliams SyndromeHumansMyelin SheathSequence DeletionGTF2I protein, humanTranscription Factors, TFIITranscription Factors, TFIII

Identifiers

PMID31011225

DOI10.1038/s41593-019-0368-5

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.