Evidence map›Paper›PMID 23996959›Full record

ArticleGenesis (New York, N.Y. : 2000)2013

Nkx2.2:Cre knock-in mouse line: a novel tool for pancreas- and CNS-specific gene deletion.

Dina A Balderes, Mark A Magnuson, Lori Sussel

Open access · greenAbstract read
In one paragraph

Article in Genesis (New York, N.Y. : 2000), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  11. Review
  12. Nkx2.2 is expressed in a subset of enteroendocrine cells with expanded lineage potential.American journal of physiology. Gastrointestinal and liver physiology · 2015
    Article
  13. Pancreatic islet cell development and regeneration.Current opinion in endocrinology, diabetes, and obesity · 2015
    Review
  14. Review
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 1 country.

Dina A BalderesDepartment of Genetics and Development, Columbia University, New York, New York, 10032.
Mark A Magnuson
Lori Sussel
Columbia University · USVanderbilt University · US

Funding

Coordinating Center for Beta Cell Biology ConsortiumU01DK072473 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2005 to 2014
$61.0M
Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DOMENICO ACCILI · 2003 to 2026
$36.7M
RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
Regulation of Pancreatic Islet Cell FateR01DK082590 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LORI SUSSEL · 2009 to 2026
$7.3M
Genetic control of pancreatic endocrine cell developmentU01DK089523 · NIDDK · VANDERBILT UNIVERSITY · PI MAGNUSON, MARK A · 2010 to 2014
$5.3M
NIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30 DK063608NIDDK NIH HHS R01 DK082590NIDDK NIH HHS U01 DK072473NIDDK NIH HHS U01 DK089523
6 · The paper itself

Abstract

Nkx2.2 is a homeodomain-containing transcriptional regulator necessary for the appropriate differentiation of ventral neuronal populations in the spinal cord and hindbrain, and endocrine cell populations in the pancreas and intestine. In each tissue, Nkx2.2 inactivation leads to reciprocal cell fate alterations. To confirm the cell fate changes are due to respecification of Nkx2.2-expressing progenitors and to provide a novel tool for lineage tracing in the pancreas and CNS, we generated an Nkx2.2:Cre mouse line by knocking in a Cre-EGFP cassette into the Nkx2.2 genomic locus and inactivating endogenous Nkx2.2. The R26R-CAG-LSL-tdTomato reporter was used to monitor the specificity and efficiency of Nkx2.2:Cre activity; the tomato reporter faithfully recapitulated endogenous Nkx2.2 expression and could be detected as early as embryonic day (e) 9.25 in the developing CNS and was initiated shortly thereafter at e9.5 in the pancreas. Lineage analyses in the CNS confirmed the cell populations thought to be derived from Nkx2.2-expressing progenitor domains. Furthermore, lineage studies verified Nkx2.2 expression in the earliest pancreatic progenitors that give rise to all cell types of the pancreas; however they also revealed more robust Cre activity in the dorsal versus ventral pancreas. Thus, the Nkx2.2:Cre line provides a novel tool for gene manipulations in the CNS and pancreas.

Indexed as

Gene Knock-In TechniquesSequence DeletionAnimalsCentral Nervous SystemHomeobox Protein Nkx-2.2Homeodomain ProteinsIntegrasesMiceMice, TransgenicOrgan SpecificityPancreasTranscription FactorsZebrafish ProteinsCre recombinaseHomeobox Protein Nkx-2.2Homeodomain ProteinsIntegrasesnkx2.2b protein, zebrafishNkx2-2 protein, mouseTranscription FactorsZebrafish ProteinsCNSCre-loxlineageNkx2.2pancreas

Identifiers

PMID23996959
PMCPMC3902634
OpenAlexW1580155637

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.