Evidence map›Paper›PMID 24469813›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Genetic dissection of plexin signaling in vivo.

Thomas Worzfeld, Jakub M Swiercz, Aycan Sentürk, Berit Genz, Alexander Korostylev, Suhua Deng, Jingjing Xia, Mikio Hoshino, Jonathan A Epstein, Andrew M Chan and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

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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

14 authors at 8 institutions in 3 countries.

Thomas WorzfeldDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Jakub M Swiercz
Aycan Sentürk
Berit Genz
Alexander Korostylev
Suhua Deng
Jingjing Xia
Mikio Hoshino
Jonathan A Epstein
Andrew M Chan
Brigitte Vollmar
Amparo Acker-Palmer
Rohini Kuner
Stefan Offermanns
Heidelberg University · DEMax Planck Institute for Heart and Lung Research · DEFocus (Germany) · DEUniversity of Rostock · DEIcahn School of Medicine at Mount Sinai · USMax Planck Society · DENational Center of Neurology and Psychiatry · JPUniversity of Pennsylvania · US

Funding

Semaphorin3d and anomalous pulmonary venous returnR01HL118768 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI EPSTEIN, JONATHAN A. · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL118768
6 · The paper itself

Abstract

Mammalian plexins constitute a family of transmembrane receptors for semaphorins and represent critical regulators of various processes during development of the nervous, cardiovascular, skeletal, and renal system. In vitro studies have shown that plexins exert their effects via an intracellular R-Ras/M-Ras GTPase-activating protein (GAP) domain or by activation of RhoA through interaction with Rho guanine nucleotide exchange factor proteins. However, which of these signaling pathways are relevant for plexin functions in vivo is largely unknown. Using an allelic series of transgenic mice, we show that the GAP domain of plexins constitutes their key signaling module during development. Mice in which endogenous Plexin-B2 or Plexin-D1 is replaced by transgenic versions harboring mutations in the GAP domain recapitulate the phenotypes of the respective null mutants in the developing nervous, vascular, and skeletal system. We further provide genetic evidence that, unexpectedly, the GAP domain-mediated developmental functions of plexins are not brought about via R-Ras and M-Ras inactivation. In contrast to the GAP domain mutants, Plexin-B2 transgenic mice defective in Rho guanine nucleotide exchange factor binding are viable and fertile but exhibit abnormal development of the liver vasculature. Our genetic analyses uncover the in vivo context-dependence and functional specificity of individual plexin-mediated signaling pathways during development.

Indexed as

AnimalsMiceMice, TransgenicNerve Tissue ProteinsSignal TransductionNerve Tissue ProteinsPlxnb2 protein, mousecerebellumneural tubeoutflow tract

Identifiers

PMID24469813
PMCPMC3926053
OpenAlexW1999118391

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.