Evidence map›Paper›PMID 28401685›Full record

ArticleGenesis (New York, N.Y. : 2000)2017

Characterization of new bone morphogenetic protein (Bmp)-2 regulatory alleles.

Tapan A Shah, Youhua Zhu, Nadia N Shaikh, Marie A Harris, Stephen E Harris, Melissa B Rogers

Abstract read
In one paragraph

Article in Genesis (New York, N.Y. : 2000), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. The Role of Bmp- and Fgf Signaling Modulating Mouse Proepicardium Cell Fate.Frontiers in cell and developmental biology · 2021
    Article
  3. 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

6 authors at 2 institutions in 1 country.

Tapan A ShahDepartment of Microbiology, Biochemistry, and Molecular Genetics, Rutgers NJMS, Newark, New Jersey.
Youhua ZhuDepartment of Microbiology, Biochemistry, and Molecular Genetics, Rutgers NJMS, Newark, New Jersey.
Nadia N ShaikhDepartment of Microbiology, Biochemistry, and Molecular Genetics, Rutgers NJMS, Newark, New Jersey.
Marie A HarrisDepartment of Periodontics, University of Texas Health Science Centre, San Antonio, Texas.
Stephen E HarrisDepartment of Periodontics, University of Texas Health Science Centre, San Antonio, Texas.
Melissa B RogersDepartment of Microbiology, Biochemistry, and Molecular Genetics, Rutgers NJMS, Newark, New Jersey.ORCID 0000-0003-2258-9365
Rutgers, The State University of New Jersey · USThe University of Texas Health Science Center at San Antonio · US

Funding

BMP2 Gene Regulation in Calcific Aortic Valve DiseaseR01HL114751 · NHLBI · VANDERBILT UNIVERSITY · PI MORTLOCK, DOUGLAS P, ROGERS, MELISSA B · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL114751
6 · The paper itself

Abstract

Bone morphogenetic protein 2 (BMP2, HGNC:1069, GeneID: 650) is a classical morphogen; a molecule that acts at a distance and whose concentration influences cell proliferation, differentiation, and apoptosis. Key events requiring precise Bmp2 regulation include heart specification and morphogenesis and neural development. In mesenchymal cells, the concentration of BMP2 influences myogenesis, adipogenesis, chondrogenesis, and osteogenesis. Because the amount, timing, and location of BMP2 synthesis influence pattern formation and organogenesis, the mechanisms that regulate Bmp2 are crucial. A sequence within the 3'UTR of the Bmp2 mRNA termed the "ultra-conserved sequence" (UCS) has been largely unchanged since fishes and mammals diverged. Cre-lox mediated deletion of the UCS in a reporter transgene revealed that the UCS may repress Bmp2 in proepicardium, epicardium, and epicardium-derived cells (EPDC) and in tissues with known epicardial contributions (coronary vessels and valves). The UCS also repressed the transgene in the aorta, outlet septum, posterior cardiac plexus, cardiac and extra-cardiac nerves, and neural ganglia. We used homologous recombination and conditional deletion to generate three new alleles in which the Bmp2 3'UTR was altered as follows: a UCS flanked by loxP sites with or without a neomycin resistance targeting vector, or a deleted UCS. Deletion of the UCS was associated with elevated Bmp2 mRNA and BMP signaling levels, reduced fitness, and embryonic malformations.

Indexed as

3' Untranslated RegionsAnimalsBone Morphogenetic Protein 2Conserved SequenceCoronary VesselsGene DeletionMiceMice, Inbred C57BLPericardiumRNA, Messenger3' Untranslated RegionsBmp2 protein, mouseBone Morphogenetic Protein 2RNA, Messengerbirth defectsgeneticsmammalmutagenesisneuraltranscription

Identifiers

PMID28401685
PMCPMC5509488
OpenAlexW2605838243

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.