Evidence map›Paper›PMID 23299886›Full record

ArticleNature communications2013

Splicing factor SRSF3 is crucial for hepatocyte differentiation and metabolic function.

Supriya Sen, Hassan Jumaa, Nicholas J G Webster

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  20. SR proteins in cancer: function, regulation, and small inhibitor.Cellular & molecular biology letters · 2024
    Review

36 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Supriya SenMedical Research Service, VA San Diego Healthcare System, 3350 La Jolla Village Drive, San Diego, California 92161, USA.
Hassan Jumaa
Nicholas J G Webster
VA San Diego Healthcare System · USUniversity of Freiburg · DE

Funding

VIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DIANE M SIMEONE · 1985 to 2026
$124.9M
Transgenic & Knock-out MouseP30DK063491 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PETER J TONTONOZ · 2003 to 2026
$40.4M
The Interaction of Neuroendocrine Repro. Function and Metabolic SignalingU54HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1999 to 2013
$18.0M
UCSD Biorepository Shared ResourceU54CA155435 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KERR, JACQUELINE · 2011 to 2015
$9.1M
The Role of FSH in Female InfertilityP50HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1985 to 2020
$7.5M
GnRH signaling in LbetaT2 gonadotrope cellsR01HD047400 · NICHD · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI WEBSTER, NICHOLAS J · 2005 to 2009
$1.3M
Alternative Splicing of the Insulin Receptor GeneI01BX000130 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI WEBSTER, NICHOLAS J · 2011 to 2013
–
BLRD VA I01 BX000130NCI NIH HHS CA23100NCI NIH HHS P30 CA023100NCI NIH HHS U54 CA155435NICHD NIH HHS HD12303NICHD NIH HHS R01 HD047400NICHD NIH HHS U54 HD012303NIDDK NIH HHS DK063491NIDDK NIH HHS P30 DK063491
6 · The paper itself

Abstract

SR family RNA binding proteins regulate splicing of nascent RNAs in vitro but their physiological role in vivo is largely unexplored, as genetic deletion of many SR protein genes results in embryonic lethality. Here we show that SRSF3HKO mice carrying a hepatocyte-specific deletion of Srsf3 (homologous to human SRSF3/SRp20) have a disrupted hepatic architecture and show pre- and postnatal growth retardation. SRSF3HKO mice exhibit impaired hepatocyte maturation with alterations in glucose and lipid homeostasis characterized by reduced glycogen storage, fasting hypoglycemia, increased insulin sensitivity and reduced cholesterol synthesis. We identify various splicing alterations in the SRSF3HKO liver that explain the in vivo phenotype. In particular, loss of SRSF3 causes aberrant splicing of Hnf1α, Ern1, Hmgcs1, Dhcr7 and Scap genes, which are critical regulators of glucose and lipid metabolism. Our study provides the first evidence for a SRSF3-driven genetic programme required for morphological and functional differentiation of hepatocytes that may have relevance for human liver disease and metabolic dysregulation.

Indexed as

Cell DifferentiationAlternative SplicingAnimalsBase SequenceBiomarkersCholesterolExonsGlucoseGrowth HormoneHepatocytesHomeostasisHumansLiverMiceMice, KnockoutModels, BiologicalBiomarkersCholesterolGlucoseGrowth HormoneRNA-Binding ProteinsRNA, MessengerSerine-Arginine Splicing FactorsSrsf3 protein, mouseTriglycerides

Identifiers

PMID23299886
PMCPMC4314219
OpenAlexW2072172413

What OpenQuestion holds

Textmetadata
LicenceTDM
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.