Evidence map›Paper›PMID 24721715›Full record

ArticleDevelopmental biology2014

Distinct requirements for beta-catenin in pancreatic epithelial growth and patterning.

Brett K Baumgartner, Gabriela Cash, Hillary Hansen, Shawn Ostler, L Charles Murtaugh

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  12. Review
  13. Effect of Wnt Signaling on the Differentiation of IsletBioMed research international · 2017
    Article
  14. Article
  15. Notch Signaling in Pancreatic Development.International journal of molecular sciences · 2015
    Review
  16. Neural cells play an inhibitory role in pancreatic differentiation of pluripotent stem cells.Genes to cells : devoted to molecular & cellular mechanisms · 2015
    Article
  17. Article
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Brett K BaumgartnerUniversity of Utah, Department of Human Genetics, 15 N. 2030 E. Rm 2100, Salt Lake City, UT 84112, USA.
Gabriela CashUniversity of Utah, Department of Human Genetics, 15 N. 2030 E. Rm 2100, Salt Lake City, UT 84112, USA.
Hillary HansenUniversity of Utah, Department of Human Genetics, 15 N. 2030 E. Rm 2100, Salt Lake City, UT 84112, USA.
Shawn OstlerUniversity of Utah, Department of Human Genetics, 15 N. 2030 E. Rm 2100, Salt Lake City, UT 84112, USA.
L Charles MurtaughUniversity of Utah, Department of Human Genetics, 15 N. 2030 E. Rm 2100, Salt Lake City, UT 84112, USA. Electronic address: murtaugh@genetics.utah.edu.
University of Utah · US

Funding

Interdisciplinary Training Program in MetabolismT32DK091317 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI SCOTT A SUMMERS · 2011 to 2026
$4.8M
Wnt/beta-catenin signaling in exocrine pancreas developoment and regenerationR01DK075072 · NIDDK · UNIVERSITY OF UTAH · PI MURTAUGH, LEWIS C · 2007 to 2011
$1.6M
NIDDK NIH HHS R01 DK075072NIDDK NIH HHS R01-DK075072NIDDK NIH HHS T32 DK091317NIDDK NIH HHS T32-DK091317
6 · The paper itself

Abstract

Pancreatic exocrine and endocrine lineages arise from multipotent pancreatic progenitor cells (MPCs). Exploiting the mechanisms that govern expansion and differentiation of these cells could enhance efforts to generate β-cells from stem cells. Although our prior work indicates that the canonical Wnt signaling component β-catenin is required qualitatively for exocrine acinar but not endocrine development, precisely how this requirement plays out at the level of MPCs and their lineage-restricted progeny is unknown. In addition, the contribution of β-catenin function to β-cell development remains controversial. To resolve the potential roles of β-catenin in development of MPCs and β-cells, we generated pancreas- and pre-endocrine-specific β-catenin knockout mice. Pancreas-specific loss of β-catenin produced not only a dramatic reduction in acinar cell numbers, but also a significant reduction in β-cell mass. The loss of β-cells is due not to a defect in the differentiation of endocrine precursors, but instead correlates with an early and specific loss of MPCs. In turn, this reflects a novel role for β-catenin in maintaining proximal-distal patterning of the early epithelium, such that distal MPCs resort to a proximal, endocrine-competent "trunk" fate when β-catenin is deleted. Moreover, β-catenin maintains proximal-distal patterning, in part, by inhibiting Notch signaling. Subsequently, β-catenin is required for proliferation of both distal and proximal cells, driving overall organ growth. In distinguishing two distinct roles for β-catenin along the route of β-cell development, we suggest that temporally appropriate positive and negative manipulation of this molecule could enhance expansion and differentiation of stem cell-derived MPCs.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsbeta CateninBody PatterningCell DifferentiationCell ProliferationEpithelial CellsEpitheliumGenotypeInsulin-Secreting CellsIslets of LangerhansMiceMice, KnockoutOrgan SizePancreasReceptors, Notchbeta CateninCTNNB1 protein, mouseReceptors, NotchBeta-cateninBeta-cellsIsletNotchPancreasProgenitors

Identifiers

PMID24721715
PMCPMC4065238
OpenAlexW2068949232

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.