Evidence map›Paper›PMID 15466398›Full record

ArticleThe American journal of pathology2004

Pbx3 deficiency results in central hypoventilation.

Joon Whan Rhee, Akiko Arata, Licia Selleri, Yakop Jacobs, Satoru Arata, Hiroshi Onimaru, Michael L Cleary

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
1.9field-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

48 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. The regulation of PBXs and their emerging role in cancer.Journal of cellular and molecular medicine · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

7 authors at 3 institutions in 2 countries.

Joon Whan RheeDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Akiko Arata
Licia Selleri
Yakop Jacobs
Satoru Arata
Hiroshi Onimaru
Michael L Cleary
Stanford University · USShowa University · JPRIKEN Center for Brain Science · JP

Funding

MOLECULAR PATHOLOGY OF LYMPHOID MALIGNANCIESR37CA042971 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1999 to 2006
$3.6M
Role of PBX Proteins in Hematopoiesis and Growth ControlR01CA090735 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 2001 to 2010
$3.1M
TRANSCRIPTIONAL REGULATORS IN CANCERP01CA070404 · NCI · STANFORD UNIVERSITY · PI LIPSICK, JOSEPH STEVEN · 1996 to 2001
$1.2M
MOLECULAR PATHOLOGY OF LYMPHOID MALIGNANCIESR01CA042971 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 1986 to 1998
–
NCI NIH HHS CA42971NCI NIH HHS CA70404NCI NIH HHS CA90735NCI NIH HHS R01 CA090735NCI NIH HHS R37 CA042971
6 · The paper itself

Abstract

Pbx proteins comprise a family of TALE (three amino acid loop extension) class homeodomain transcription factors that are implicated in developmental gene expression through their abilities to form hetero-oligomeric DNA-binding complexes and function as transcriptional regulators in numerous cell types. We demonstrate here that one member of this family, Pbx3, is expressed at high levels predominantly in the developing central nervous system, including a region of the medulla oblongata that is implicated in the control of respiration. Pbx3-deficient mice develop to term but die within a few hours of birth from central respiratory failure due to abnormal activity of inspiratory neurons in the medulla. This partially phenocopies the defect in mice deficient for Rnx, a metaHox homeodomain transcription factor, that we demonstrate here is capable of forming a DNA-binding complex with Pbx3. Rnx expression is unperturbed in Pbx3-deficient mice, but its ability to enhance transcription in vitro as a complex with TALE proteins is compromised in the absence of Pbx3. Thus, Pbx3 is essential for respiration and, like its DNA-binding partner Rnx, is critical for proper development of medullary respiratory control mechanisms. Pbx3-deficient mice provide a model for congenital central hypoventilation syndrome and suggest that Pbx3 mutations may promote the pathogenesis of this disorder.

Indexed as

Respiratory Physiological PhenomenaAnimalsEmbryo, MammalianGenotypeHomeodomain ProteinsHypoventilationImmunohistochemistryMedulla OblongataMiceNeuronsProto-Oncogene ProteinsTranscription, GeneticHomeodomain Proteinsproto-oncogene protein Pbx3Proto-Oncogene ProteinsTlx3 protein, mouse

Identifiers

PMID15466398
PMCPMC1618620
OpenAlexW2121074186

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.