Evidence map›Paper›PMID 12215548›Full record

ArticleMolecular and cellular biology2002

Characterization of lpa(2) (Edg4) and lpa(1)/lpa(2) (Edg2/Edg4) lysophosphatidic acid receptor knockout mice: signaling deficits without obvious phenotypic abnormality attributable to lpa(2).

James J A Contos, Isao Ishii, Nobuyuki Fukushima, Marcy A Kingsbury, Xiaoqin Ye, Shuji Kawamura, Joan Heller Brown, Jerold Chun

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
5.6field-weighted citation impact, top 3% 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

130 citing papers in PubMed, 313 citations in OpenAlex.

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  12. Autotaxin Has a Negative Role in Systemic Inflammation.International journal of molecular sciences · 2022
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70 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 2 countries.

James J A ContosDepartment of Pharmacology, Neurosciences and Biomedical Sciences Programs, School of Medicine, University of California, San Diego, La Jolla 92093-0636, USA.
Isao Ishii
Nobuyuki Fukushima
Marcy A Kingsbury
Xiaoqin Ye
Shuji Kawamura
Joan Heller Brown
Jerold Chun
University of California, San Diego · US

Funding

ROLES FOR LPA SIGNALING IN CEREBRAL CORTICAL DEVELOPMENTK02MH001723 · NIMH · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI CHUN, JEROLD · 1999 to 2005
$465k
NIMH NIH HHS K02 MH001723NIMH NIH HHS K02MH01723
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA), a bioactive lipid produced by several cell types including postmitotic neurons and activated platelets, is thought to be involved in various biological processes, including brain development. Three cognate G protein-coupled receptors encoded by lpa(1)/lp(A1)/Edg-2/Gpcr26, lpa(2)/lp(A2)/Edg-4, and lpa(3)/lp(A3)/Edg-7 mediate the cellular effects of LPA. We have previously shown that deletion of lpa(1) in mice results in craniofacial dysmorphism, semilethality due to defective suckling behavior, and generation of a small fraction of pups with frontal hematoma. To further investigate the role of these receptors and LPA signaling in the organism, we deleted lpa(2) in mice. Homozygous knockout (lpa(2)((-/-))) mice were born at the expected frequency and displayed no obvious phenotypic abnormalities. Intercrosses allowed generation of lpa(1)((-/-)) lpa(2)((-/-)) double knockout mice, which displayed no additional phenotypic abnormalities relative to lpa(1)((-/-)) mice except for an increased incidence of perinatal frontal hematoma. Histological analyses of lpa(1)((-/-)) lpa(2)((-/-)) embryonic cerebral cortices did not reveal obvious differences in the proliferating cell population. However, many LPA-induced responses, including phospholipase C activation, Ca(2+) mobilization, adenylyl cyclase activation, proliferation, JNK activation, Akt activation, and stress fiber formation, were absent or severely reduced in embryonic fibroblasts derived from lpa(1)((-/-)) lpa(2)((-/-)) mice. Except for adenylyl cyclase activation [which was nearly abolished in lpa(1)((-/-)) fibroblasts], these responses were only partially affected in lpa(1)((-/-)) and lpa(2)((-/-)) fibroblasts. Thus, although LPA(2) is not essential for normal mouse development, it does act redundantly with LPA(1) to mediate most LPA responses in fibroblasts.

Indexed as

Protein Serine-Threonine KinasesReceptors, G-Protein-CoupledAdenylyl CyclasesAnimalsCalciumCell DivisionCells, CulturedCerebral CortexCrosses, GeneticEnzyme ActivationFemaleFibroblastsGene TargetingHematomaHomozygoteLysophospholipidsAdenylyl CyclasesCalciumLysophospholipidsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptors, Cell SurfaceReceptors, G-Protein-CoupledReceptors, Lysophosphatidic AcidType C Phospholipases

Identifiers

PMID12215548
PMCPMC134025
OpenAlexW2156303710

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.