Evidence map›Paper›PMID 23935514›Full record

ArticlePLoS genetics2013

Hepatocyte growth factor signaling in intrapancreatic ductal cells drives pancreatic morphogenesis.

Ryan M Anderson, Marion Delous, Justin A Bosch, Lihua Ye, Morgan A Robertson, Daniel Hesselson, Didier Y R Stainier

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Met regulates endoderm migration in zebrafish.bioRxiv : the preprint server for biology · 2026
    Article
  2. A Novel Zebrafish Liver-Specific Metastasis Model Reveals c-Met as a Driver of Liver Tropism.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
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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

7 authors at 3 institutions in 1 country.

Ryan M AndersonDepartment of Biochemistry and Biophysics, Programs in Developmental and Stem Cell Biology, Genetics and Human Genetics, Liver Center and Diabetes Center, University of California San Francisco, San Francisco, California, United States of America. ryanande@iu.edu
Marion Delous
Justin A Bosch
Lihua Ye
Morgan A Robertson
Daniel Hesselson
Didier Y R Stainier
University of California, San Francisco · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jennifer Y. Chen · 1986 to 2026
$30.7M
MOLECULAR GENETICS OF LIVER DEVELOPMENTR01DK060322 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STAINIER, DIDIER Y · 2001 to 2012
$3.8M
MOLECULAR GENETICS OF PANCREAS DEVELOPMENTR01DK075032 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STAINIER, DIDIER Y · 2007 to 2011
$1.5M
NIDDK NIH HHS DK060322NIDDK NIH HHS DK075032NIDDK NIH HHS P30 DK026743NIDDK NIH HHS R01 DK060322NIDDK NIH HHS R01 DK075032
6 · The paper itself

Abstract

In a forward genetic screen for regulators of pancreas development in zebrafish, we identified donut(s908) , a mutant which exhibits failed outgrowth of the exocrine pancreas. The s908 mutation leads to a leucine to arginine substitution in the ectodomain of the hepatocyte growth factor (HGF) tyrosine kinase receptor, Met. This missense mutation impedes the proteolytic maturation of the receptor, its trafficking to the plasma membrane, and diminishes the phospho-activation of its kinase domain. Interestingly, during pancreatogenesis, met and its hgf ligands are expressed in pancreatic epithelia and mesenchyme, respectively. Although Met signaling elicits mitogenic and migratory responses in varied contexts, normal proliferation rates in donut mutant pancreata together with dysmorphic, mislocalized ductal cells suggest that met primarily functions motogenically in pancreatic tail formation. Treatment with PI3K and STAT3 inhibitors, but not with MAPK inhibitors, phenocopies the donut pancreatic defect, further indicating that Met signals through migratory pathways during pancreas development. Chimera analyses showed that Met-deficient cells were excluded from the duct, but not acinar, compartment in the pancreatic tail. Conversely, wild-type intrapancreatic duct and "tip cells" at the leading edge of the growing pancreas rescued the donut phenotype. Altogether, these results reveal a novel and essential role for HGF signaling in the intrapancreatic ducts during exocrine morphogenesis.

Indexed as

MorphogenesisSignal TransductionAnimalsHepatocyte Growth FactorMitogen-Activated Protein Kinase KinasesMutation, MissensePancreatic DuctsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-metSTAT3 Transcription FactorZebrafishHepatocyte Growth FactorMitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-metSTAT3 Transcription Factor

Identifiers

PMID23935514
PMCPMC3723531
OpenAlexW2003768812

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.