<?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>2026-10-09T01:50:55Z</responseDate><request verb="GetRecord" identifier="oai:riubu.ubu.es:10259/12244" metadataPrefix="marc">https://riubu.ubu.es/oai/request</request><GetRecord><record><header><identifier>oai:riubu.ubu.es:10259/12244</identifier><datestamp>2026-10-08T00:05:39Z</datestamp><setSpec>com_10259_6168</setSpec><setSpec>com_10259_5086</setSpec><setSpec>com_10259_2604</setSpec><setSpec>col_10259_12236</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dcterms="http://purl.org/dc/terms/" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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<subfield code="a">dc</subfield>
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<datafield tag="720" ind1=" " ind2=" ">
<subfield code="a">Fuente Vivas, Dalia de la</subfield>
<subfield code="e">author</subfield>
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<subfield code="a">Casar, Berta</subfield>
<subfield code="e">author</subfield>
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<datafield tag="720" ind1=" " ind2=" ">
<subfield code="a">Crespo, Pedro</subfield>
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<datafield tag="260" ind1=" " ind2=" ">
<subfield code="c">2018</subfield>
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<subfield code="a">An overwhelming body of data unquestionably links the Ras-ERK&#xd;
pathway to the upbringing and progression of human malignancies.&#xd;
About 40% of human cancers harbor activating mutations in proteins&#xd;
involved in this signaling cascade, in particular Ras and Braf. In addition&#xd;
to the main proteins of this signaling pathway, there are several&#xd;
regulatory proteins known as scaffold proteins, that modulate the&#xd;
intensity, amplitude and duration of ERK signals. Interestingly, it can&#xd;
propose the scaffold proteins as antitumoral targets. Considering the&#xd;
hypothesis that scaffold proteins interact and regulate the signal&#xd;
transduction through the Ras-ERK pathway in a coordinated manner&#xd;
we try to find out how these interactions are regulated. Ras proteins&#xd;
are distributed in different types of plasma membrane: microdomains&#xd;
and endomembranes. We have previously demonstrated that&#xd;
compartmentalization dictates Ras utilization of effectors, the intensity&#xd;
of its signals and the biological response of the cells. Cell migration is&#xd;
critical for many physiological processes and is often misregulated in&#xd;
developmental disorders and pathological conditions including cancer.&#xd;
MAPK signaling are known regulators of cytoskeletal dynamics during&#xd;
cellular processes such as cell adhesion and migration. Our hypothesis&#xd;
is that localized ERK signaling mediated through recently identified&#xd;
scaffold proteins and its interactions with the cytoskeleton may&#xd;
regulate specific cellular responses. Here we propose that associations&#xd;
among different scaffold proteins and cytoskeleton will add one further&#xd;
degree of regulation for an already tightly regulated cascade and could&#xd;
provide a novel means for manipulating ERK signals, even with&#xd;
therapeutic purposes.</subfield>
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<subfield code="a">https://hdl.handle.net/10259/12244</subfield>
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<datafield tag="245" ind1="0" ind2="0">
<subfield code="a">Scaffold proteins and cytoskeletal dynamics as modulators of Ras-ERK pathway in cancer</subfield>
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