Evidence map›Paper›PMID 16847320›Full record

ArticleMolecular and cellular biology2006

Hypomorphic mutation of the TALE gene Prep1 (pKnox1) causes a major reduction of Pbx and Meis proteins and a pleiotropic embryonic phenotype.

Elisabetta Ferretti, J Carlos Villaescusa, Patrizia Di Rosa, Luis C Fernandez-Diaz, Elena Longobardi, Roberta Mazzieri, Annarita Miccio, Nicola Micali, Licia Selleri, Giuliana Ferrari and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

58 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Gene dosage effects of poly(A) track-engineered hypomorphs.Molecular therapy. Nucleic acids · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. The Role of Prep1 in the Regulation of Mesenchymal Stromal Cells.International journal of molecular sciences · 2019
    Article
  9. Article
  10. Review
  11. Article
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  13. Review
  14. Article
  15. Review
  16. 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

11 authors at 4 institutions in 2 countries.

Elisabetta FerrettiLaboratory of Molecular Genetics, DIBIT, via Olgettina 58, 20132 Milano, Italy.
J Carlos Villaescusa
Patrizia Di Rosa
Luis C Fernandez-Diaz
Elena Longobardi
Roberta Mazzieri
Annarita Miccio
Nicola Micali
Licia Selleri
Giuliana Ferrari
Francesco Blasi
Vita-Salute San Raffaele University · ITCornell University · USIFOM · ITThe San Raffaele Telethon Institute for Gene Therapy · IT

Funding

Mechanisms of Pbx-directed Genetic &Transcriptional Control of Limb DevelopmentR01HD043997 · NICHD · WEILL MEDICAL COLL OF CORNELL UNIV · PI SELLERI, LICIA · 2004 to 2016
$3.7M
NICHD NIH HHS HD43997NICHD NIH HHS R01 HD043997Telethon GGP02031
6 · The paper itself

Abstract

The interaction of Prep1 and Pbx homeodomain transcription factors regulates their activity, nuclear localization, and likely, function in development. To understand the in vivo role of Prep1, we have analyzed an embryonic lethal hypomorphic mutant mouse (Prep1(i/i)). Prep1(i/i) embryos die at embryonic day 17.5 (E17.5) to birth with an overall organ hypoplasia, severe anemia, impaired angiogenesis, and eye anomalies, particularly in the lens and retina. The anemia correlates with delayed differentiation of erythroid progenitors and may be, at least in part, responsible for intrauterine death. At E14.5, Prep1 is present in fetal liver (FL) cMyb-positive cells, whose deficiency causes a marked hematopoietic phenotype. Prep1 is also localized to FL endothelial progenitors, consistent with the observed angiogenic phenotype. Likewise, at the same gestational day, Prep1 is present in the eye cells that bear Pax6, implicated in eye development. The levels of cMyb and Pax6 in FL and in the retina, respectively, are significantly decreased in Prep1(i/i) embryos, consistent with the hematopoietic and eye phenotypes. Concomitantly, Prep1 deficiency results in the overall decrease of protein levels of its related family member Meis1 and its partners Pbx1 and Pbx2. As both Prep1 and Meis interact with Pbx, the overall Prep1/Meis-Pbx DNA-binding activity is strongly reduced in whole Prep1(i/i) embryos and their organs. Our data indicate that Prep1 is an essential gene that acts upstream of and within a Pbx-Meis network that regulates multiple aspects of embryonic development.

Indexed as

Embryo, MammalianMutationPhenotypeAllantoisAnemiaAnimalsCells, CulturedEyeFemaleGene TargetingGestational AgeHematopoietic Stem CellsHomeodomain ProteinsMiceMice, Inbred C57BLMyeloid Ecotropic Viral Integration Site 1 ProteinHomeodomain ProteinsMeis1 protein, mouseMyeloid Ecotropic Viral Integration Site 1 ProteinNeoplasm ProteinsPbx1 protein, mousePknox1 protein, mousePlatelet Endothelial Cell Adhesion Molecule-1Pre-B-Cell Leukemia Transcription Factor 1RNA, MessengerTranscription Factors

Identifiers

PMID16847320
PMCPMC1592771
OpenAlexW2114286710

What OpenQuestion holds

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Registered trials

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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.