<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-01T08:01:15Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/34538" metadataPrefix="qdc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/34538</identifier><datestamp>2026-02-03T11:25:45Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><qdc:qualifieddc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:qdc="http://dspace.org/qualifieddc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
   <dc:title>Absence of LPA1 signaling results in defective cortical development</dc:title>
   <dc:creator>Estivill-Torrús, Guillermo</dc:creator>
   <dc:creator>Llebrez Zayas, Pedro</dc:creator>
   <dc:creator>Matas-Rico, Elisa</dc:creator>
   <dc:creator>Rodriguez-de-Fonseca, Fernando</dc:creator>
   <dc:creator>Chun, Jerold</dc:creator>
   <dc:creator>Santín-Núñez, Luis Javier</dc:creator>
   <dc:creator>Pedraza-Benítez, María del Carmen</dc:creator>
   <dc:creator>De-Diego-Barbado, Isabel</dc:creator>
   <dc:creator>Del Arco-Herrera, Ignacio</dc:creator>
   <dc:creator>Fernández-Llebrez, Pedro</dc:creator>
   <dc:subject>Cerebro - Evolución</dc:subject>
   <dcterms:abstract>Lysophosphatidic acid (LPA) is a simple phospholipid with extracellular signaling properties mediated by specific G protein-coupled receptors. At least 2 LPA receptors, LPA(1) and LPA(2), are expressed in the developing brain, the former enriched in the neurogenic ventricular zone (VZ), suggesting a normal role in neurogenesis. Despite numerous studies reporting the effects of exogenous LPA using in vitro neural models, the first LPA(1) loss-of-function mutants reported did not show gross cerebral cortical defects in the 50% that survived perinatal demise. Here, we report a role for LPA(1) in cortical neural precursors resulting from analysis of a variant of a previously characterized LPA(1)-null mutant that arose spontaneously during colony expansion. These LPA(1)-null mice, termed maLPA(1), exhibit almost complete perinatal viability and show a reduced VZ, altered neuronal markers, and increased cortical cell death that results in a loss of cortical layer cellularity in adults. These data support LPA(1) function in normal cortical development and suggest that the presence of genetic modifiers of LPA(1) influences cerebral cortical development.</dcterms:abstract>
   <dcterms:dateAccepted>2024-10-09T08:03:53Z</dcterms:dateAccepted>
   <dcterms:available>2024-10-09T08:03:53Z</dcterms:available>
   <dcterms:created>2024-10-09T08:03:53Z</dcterms:created>
   <dcterms:issued>2008-04</dcterms:issued>
   <dc:type>journal article</dc:type>
   <dc:identifier>Guillermo Estivill-Torrús, Pedro Llebrez-Zayas, Elisa Matas-Rico, Luis Santín, Carmen Pedraza, Isabel De Diego, Ignacio Del Arco, Pedro Fernández-Llebrez, Jerold Chun, Fernando Rodríguez De Fonseca, Absence of LPA1 Signaling Results in Defective Cortical Development, Cerebral Cortex, Volume 18, Issue 4, April 2008, Pages 938–950, https://doi.org/10.1093/cercor/bhm132</dc:identifier>
   <dc:identifier>https://hdl.handle.net/10630/34538</dc:identifier>
   <dc:identifier>10.1093/cercor/bhm132</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
   <dc:rights>open access</dc:rights>
   <dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 Internacional</dc:rights>
   <dc:publisher>Oxford academy</dc:publisher>
</qdc:qualifieddc>
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