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Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction

Taskin, Eylem; Guven, Celal; Kaya, Salih Tunc; Sariman, Melda; Emrence, Zeliha; Ekmekci, Sema Sirma; Abaci, Neslihan; Sevgiler, Yusuf; Akcakaya, Handan


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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Taskin, Eylem</dc:creator>
  <dc:creator>Guven, Celal</dc:creator>
  <dc:creator>Kaya, Salih Tunc</dc:creator>
  <dc:creator>Sariman, Melda</dc:creator>
  <dc:creator>Emrence, Zeliha</dc:creator>
  <dc:creator>Ekmekci, Sema Sirma</dc:creator>
  <dc:creator>Abaci, Neslihan</dc:creator>
  <dc:creator>Sevgiler, Yusuf</dc:creator>
  <dc:creator>Akcakaya, Handan</dc:creator>
  <dc:date>2020-01-01</dc:date>
  <dc:description>Purpose: Adriamycin (APR) is a commonly used anti-cancer drug. ADR has toxic effects on cardiomyocytes and leads to heart failure. However, the underlying mechanism(s) by which ADR causes heart failure is still not clarified exactly. The aim of present study is to investigate whether ADR-induced heart failure is mediated via HMGB1/TLR4 to initiate the apoptosis through MAPK/AMPK pathways.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/7853</dc:identifier>
  <dc:identifier>oai:zenodo.org:7853</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>JOURNAL OF BUON 25(1) 554-565</dc:source>
  <dc:title>Silencing HMGB1 expression inhibits adriamycin's heart toxicity via TLR4 dependent manner through MAPK signal transduction</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>
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