<?xml version="1.0"?><rdf:RDF xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:edm="http://www.europeana.eu/schemas/edm/" xmlns:wgs84_pos="http://www.w3.org/2003/01/geo/wgs84_pos" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:rdaGr2="http://rdvocab.info/ElementsGr2" xmlns:oai="http://www.openarchives.org/OAI/2.0/" xmlns:owl="http://www.w3.org/2002/07/owl#" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:ore="http://www.openarchives.org/ore/terms/" xmlns:skos="http://www.w3.org/2004/02/skos/core#" xmlns:dcterms="http://purl.org/dc/terms/"><edm:WebResource rdf:about="http://www.dlib.si/stream/URN:NBN:SI:doc-RC2FPDFC/b5a9130d-8a45-4fa1-97c4-9cc2d5f37d43/TEXT"><dcterms:extent>0 KB</dcterms:extent></edm:WebResource><edm:WebResource rdf:about="http://www.dlib.si/stream/URN:NBN:SI:doc-RC2FPDFC/db337f8d-9df5-4f5f-9504-e4e4dabc45a3/PDF"><dcterms:extent>119 KB</dcterms:extent></edm:WebResource><edm:TimeSpan rdf:about="1992-2025"><edm:begin xml:lang="en">1992</edm:begin><edm:end xml:lang="en">2025</edm:end></edm:TimeSpan><edm:ProvidedCHO rdf:about="URN:NBN:SI:doc-RC2FPDFC"><dcterms:isPartOf rdf:resource="https://www.dlib.si/details/URN:NBN:SI:spr-FNIFVE9S" /><dcterms:issued>2006</dcterms:issued><dc:creator>Lenassi, Metka</dc:creator><dc:creator>Plemenitaš, Ana</dc:creator><dc:format xml:lang="sl">številka:1</dc:format><dc:format xml:lang="sl">letnik:40</dc:format><dc:format xml:lang="sl">7 strani</dc:format><dc:format xml:lang="sl">str. 51-56</dc:format><dc:identifier>ISSN:1318-2099</dc:identifier><dc:identifier>COBISSID:21116889</dc:identifier><dc:identifier>URN:URN:NBN:SI:doc-RC2FPDFC</dc:identifier><dc:language>en</dc:language><dc:publisher xml:lang="sl">Association of Radiology and Oncology</dc:publisher><dcterms:isPartOf xml:lang="sl">Radiology and oncology (Ljubljana)</dcterms:isPartOf><dc:subject xml:lang="en">Apoptosis</dc:subject><dc:subject xml:lang="sl">Apoptoza</dc:subject><dc:subject xml:lang="en">Calmodulin-Dependent Protein Kinases</dc:subject><dc:subject xml:lang="sl">kemoterapija</dc:subject><dc:subject xml:lang="en">Tumor Cells, Cultured</dc:subject><dc:subject xml:lang="sl">tumorske celice</dc:subject><dc:subject xml:lang="sl">Tumorske celične kulture</dc:subject><dcterms:temporal rdf:resource="1992-2025" /><dc:title xml:lang="sl">The role of p38 MAP kinase in cancer cell apoptosis|</dc:title><dc:description xml:lang="sl">Background. Cellular behaviour in response to many extracellular stimuli is mediated through MAP kinase signalling pathways. p38 MAP kinase that is represented in mammals by four isoforms (p38alfa, p38beta, p38gama and p38delta) is one of the four main subgroups of MAP kinases. Recent studies show that p38 activation is necessary for cancer cell death initiated by variety of anti-cancer agents. This finding connected cancer therapies previously considered to be mechanistically unrelated and raised the possibility of developing anti-cancer agents that lack the side effects causedby events upstream of p38 MAPK Many of the details of p38 induced apoptosis still need to be elucidated. Since most of the past studies rely only on the cell culture models, all the results have to be verified using in vivo models. Also very little is known about the role of p38 mediated apoptosis on non-neoplastic cells in response to anti-cancer agents. Conclusion. Although p38 activation of cancer cell apoptosis is a very complexprocess, recent studies indicate a good starting point for new strategies that would increase the efficiency and decrease the toxicity of proven therapies</dc:description><dc:description xml:lang="sl">Izhodišča. Odzivanje celic na številne zunajcelične signale poteka preko aktivacije MAP kinaznih signalnih poti. Ena od štirih glavnih podskupin MAP kinaz je p38 MAP kinaza, ki je pri sesalcih prisotna v štirih izooblikah: p38alfa, p38beta, p38gama in p38delta. Nedavne raziskave so pokazale, da je zaaktivacijo apoptoze rakavih celic z različnimi kemoterapevtiki nujna aktivacija p38 kinaze. To spoznanje je v eni točki povezalo poti delovanja raznolikih kemoterapevtikov ter s tem nakazalo nove možnosti njihovega razvojabrez stranskih učinkov, ki jih sedaj povzročajo dogodki pred aktivacijop38. Veliko podrobnosti o p38 posredovani apoptozi je potrebno še razjasniti. Dosedanja dognanja je potrebno preveriti v in vivo modelih, saj seta sedaj nanašajo predvsem na celične kulture. Malo je znanega tudi o vlogi p38 pri apoptozi nerakavih celic po aktivaciji s kemoterapevtiki. Zaključki. Čeprav je p38 posredovana aktivacija apoptoze rakavih celic zelo kompleksen proces, novejše študije ponujajo dober začetek za razvoj novih kemoterapevtikov s povečano učinkovitostjo in zmanjšano toksičnostjo</dc:description><edm:type>TEXT</edm:type><dc:type xml:lang="sl">znanstveno časopisje</dc:type><dc:type xml:lang="en">journals</dc:type><dc:type rdf:resource="http://www.wikidata.org/entity/Q361785" /></edm:ProvidedCHO><ore:Aggregation rdf:about="http://www.dlib.si/?URN=URN:NBN:SI:doc-RC2FPDFC"><edm:aggregatedCHO rdf:resource="URN:NBN:SI:doc-RC2FPDFC" /><edm:isShownBy rdf:resource="http://www.dlib.si/stream/URN:NBN:SI:doc-RC2FPDFC/db337f8d-9df5-4f5f-9504-e4e4dabc45a3/PDF" /><edm:rights rdf:resource="http://creativecommons.org/licenses/by/4.0/" /><edm:provider>Slovenian National E-content Aggregator</edm:provider><edm:intermediateProvider xml:lang="en">National and University Library of Slovenia</edm:intermediateProvider><edm:dataProvider xml:lang="sl">Društvo radiologije in onkologije</edm:dataProvider><edm:object rdf:resource="http://www.dlib.si/streamdb/URN:NBN:SI:doc-RC2FPDFC/maxi/edm" /><edm:isShownAt rdf:resource="http://www.dlib.si/details/URN:NBN:SI:doc-RC2FPDFC" /></ore:Aggregation></rdf:RDF>