Evidence map›Paper›PMID 23494546›Full record

ArticleTransgenic research2013

Generation of mice encoding a conditional allele of Nkx2.2.

Teresa L Mastracci, Chyuan-Sheng Lin, Lori Sussel

Abstract read
In one paragraph

Article in Transgenic research, 2013. 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
2.9field-weighted citation impact, top 10% 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, 26 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Evidence ThatFrontiers in cellular neuroscience · 2021
    Article
  9. Interactive Repression of MYRF Self-Cleavage and Activity in Oligodendrocyte Differentiation by TMEM98 Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Mammalian Nkx2.2+ perineurial glia are essential for motor nerve development.Developmental dynamics : an official publication of the American Association of Anatomists · 2014
    Article
  20. Article
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 1 institution in 1 country.

Teresa L MastracciDepartment of Genetics and Development, Russ Berrie Medical Pavilion, Columbia University, 1150 St. Nicholas Ave., New York, NY, 10032, USA.
Chyuan-Sheng Lin
Lori Sussel
Columbia University · US

Funding

Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DOMENICO ACCILI · 2003 to 2026
$36.7M
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
Defining the roles of Nkx2.2 and NeuroD in regulating islet cell fateU01DK072504 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI SUSSEL, LORI · 2005 to 2010
$3.2M
NIDDK NIH HHS P30 DK063608NIDDK NIH HHS P30 DK63608NIDDK NIH HHS R01 DK082590NIDDK NIH HHS U01 DK072504NIDDK NIH HHS U01 DK089523NIDDK NIH HHS U01DK089523
6 · The paper itself

Abstract

Nkx2.2 is a homeobox transcription factor that is expressed in the pancreas, intestine and central nervous system (CNS) during embryogenesis and in the adult. In mice, global deletion of Nkx2.2 results in cell mis-specification in each of the tissues where it is expressed, and the null mice die as neonates with severe hyperglycemia. Although a whole body knockout demonstrates the importance of Nkx2.2 in cell specification and postnatal viability, it precludes assessment of the cell-autonomous and postnatal functions of Nkx2.2. In this study we report the generation and functional characterization of mice encoding a conditional allele of Nkx2.2. We demonstrate the functional integrity of the conditional Nkx2.2 allele and report successful in vivo deletion using a pancreas-specific Cre recombinase. The pancreas-specific deletion of Nkx2.2 results in similar defects found in the Nkx2.2 null pancreas and the mice die shortly after birth, demonstrating that the neonatal lethality associated with the null allele is caused by pancreatic islet dysfunction. The generation of a conditional Nkx2.2 allele provides an important tool for identifying the cell-autonomous and postnatal activities of Nkx2.2 in establishing and maintaining cell type identities and functions in the pancreas, intestine and CNS.

Indexed as

AnimalsDNA PrimersFluorescent Antibody TechniqueGene DeletionHomeobox Protein Nkx-2.2Homeodomain ProteinsIn Situ HybridizationIntegrasesMiceMice, TransgenicPancreasReal-Time Polymerase Chain ReactionTranscription FactorsZebrafish ProteinsCre recombinaseDNA PrimersHomeobox Protein Nkx-2.2Homeodomain ProteinsIntegrasesnkx2.2b protein, zebrafishNkx2-2 protein, mouseTranscription FactorsZebrafish Proteins

Identifiers

PMID23494546
PMCPMC3713092
OpenAlexW2016010735

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.