Evidence map›Paper›PMID 20534695›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Neural crest-specific loss of Prkar1a causes perinatal lethality resulting from defects in intramembranous ossification.

Georgette N Jones, Daphne R Pringle, Zhirong Yin, Michelle M Carlton, Kimerly A Powell, Michael B Weinstein, Ramiro E Toribio, Krista M D La Perle, Lawrence S Kirschner

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. 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
1.2field-weighted citation impact, top 21% 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, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Mouse embryo phenotyping using X-ray microCT.Frontiers in cell and developmental biology · 2022
    Review
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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

9 authors at 2 institutions in 1 country.

Georgette N JonesDepartment of Molecular Virology, The Ohio State University, Columbus, Ohio 43210, USA.
Daphne R Pringle
Zhirong Yin
Michelle M Carlton
Kimerly A Powell
Michael B Weinstein
Ramiro E Toribio
Krista M D La Perle
Lawrence S Kirschner
Columbus Center · USThe Ohio State University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
Carney Complex: A Model for PKA-Mediated TumorigenesisR01CA112268 · NCI · OHIO STATE UNIVERSITY · PI KIRSCHNER, LAWRENCE S · 2004 to 2008
$1.3M
NCI NIH HHS CA112268-02NCI NIH HHS CA16058NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA112268
6 · The paper itself

Abstract

The cranial neural crest (CNC) undergoes complex molecular and morphological changes during embryogenesis in order to form the vertebrate skull, and nearly three quarters of all birth defects result from defects in craniofacial development. The molecular events leading to CNC differentiation have been extensively studied; however, the role of the cAMP-dependent protein kinase [protein kinase A (PKA)] during craniofacial development has only been described in palate formation. Here, we provide evidence that strict PKA regulation in postmigratory CNC cells is essential during craniofacial bone development. Selective inactivation of Prkar1a, a regulatory subunit of the PKA holoenzyme, in the CNC results in perinatal lethality caused by dysmorphic craniofacial development and subsequent asphyxiation. Additionally, aberrant differentiation of CNC mesenchymal cells results in anomalous intramembranous ossification characterized by formation of cartilaginous islands in some areas and osteolysis of bony trabeculae with fibrous connective tissue stabilization in others. Genetic interaction studies revealed that genetic reduction of the PKA catalytic subunit C(alpha) was able to rescue the phenotype, whereas reduction in Cbeta had no effect. Overall, these observations provide evidence of the essential role of proper regulation of PKA during the ossification of the bones of the skull. This knowledge may have implications for the understanding and treatment of craniofacial birth defects.

Indexed as

AnimalsCraniofacial AbnormalitiesCyclic AMP-Dependent Protein Kinase RIalpha SubunitMiceMice, KnockoutNeural CrestOssification, HeterotopicX-Ray MicrotomographyCyclic AMP-Dependent Protein Kinase RIalpha SubunitPrkar1a protein, mouse

Identifiers

PMID20534695
PMCPMC2940464
OpenAlexW2153401322

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.