Evidence map›Paper›PMID 21149718›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Model of pediatric pituitary hormone deficiency separates the endocrine and neural functions of the LHX3 transcription factor in vivo.

Stephanie C Colvin, Raleigh E Malik, Aaron D Showalter, Kyle W Sloop, Simon J Rhodes

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  10. Genome-wide association studies for multiple diseases of the German Shepherd Dog.Mammalian genome : official journal of the International Mammalian Genome Society · 2012
    Article
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  13. 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

5 authors at 2 institutions in 1 country.

Stephanie C ColvinDepartment of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Raleigh E Malik
Aaron D Showalter
Kyle W Sloop
Simon J Rhodes
Indiana University School of MedicineEli Lilly (United States) · US

Funding

Role of LHX3 Protein Isoforms in Pituitary DevelopmentR01HD042024 · NICHD · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI RHODES, SIMON JAMES · 2002 to 2012
$2.6M
Indiana Clinical and Translational Science Institute-T32 Program TL1TL1RR025759 · NCRR · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2008 to 2011
$710k
NCRR NIH HHS TL1 RR025759NCRR NIH HHS TL1RR025759NICHD NIH HHS HD42024NICHD NIH HHS R01 HD042024
6 · The paper itself

Abstract

The etiology of most pediatric hormone deficiency diseases is poorly understood. Children with combined pituitary hormone deficiency (CPHD) have insufficient levels of multiple anterior pituitary hormones causing short stature, metabolic disease, pubertal failure, and often have associated nervous system symptoms. Mutations in developmental regulatory genes required for the specification of the hormone-secreting cell types of the pituitary gland underlie severe forms of CPHD. To better understand these diseases, we have created a unique mouse model of CPHD with a targeted knockin mutation (Lhx3 W227ter), which is a model for the human LHX3 W224ter disease. The LHX3 gene encodes a LIM-homeodomain transcription factor, which has essential roles in pituitary and nervous system development in mammals. The introduced premature termination codon results in deletion of the carboxyl terminal region of the LHX3 protein, which is critical for pituitary gene activation. Mice that lack all LHX3 function do not survive beyond birth. By contrast, the homozygous Lhx3 W227ter mice survive, but display marked dwarfism, thyroid disease, and female infertility. Importantly, the Lhx3 W227ter mice have no apparent nervous system deficits. The Lhx3 W227ter mouse model provides a unique array of hormone deficits and facilitates experimental approaches that are not feasible with human patients. These experiments demonstrate that the carboxyl terminus of the LHX3 transcription factor is not required for viability. More broadly, this study reveals that the in vivo actions of a transcription factor in different tissues are molecularly separable.

Indexed as

Disease Models, AnimalModels, BiologicalAnimalsBlotting, WesternCodon, NonsenseFemaleGene Knock-In TechniquesHistological TechniquesHomeodomain ProteinsHumansHypopituitarismImmunohistochemistryLIM-Homeodomain ProteinsMaleMiceMice, TransgenicCodon, NonsenseHomeodomain ProteinsLhx3 proteinLIM-Homeodomain ProteinsPituitary HormonesTranscription Factors

Identifiers

PMID21149718
PMCPMC3017168
OpenAlexW2013869618

What OpenQuestion holds

Textmetadata
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.