Dergi makalesi Açık Erişim
Varisli, Lokman; Ozturk, Bilge E.; Akyuz, Gencer K.; Korkmaz, Kemal S.
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<identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/80041</identifier>
<creators>
<creator>
<creatorName>Varisli, Lokman</creatorName>
<givenName>Lokman</givenName>
<familyName>Varisli</familyName>
</creator>
<creator>
<creatorName>Ozturk, Bilge E.</creatorName>
<givenName>Bilge E.</givenName>
<familyName>Ozturk</familyName>
<affiliation>Ege Univ, Dept Bioengn, Canc Biol Lab, Fac Engn, Izmir, Turkey</affiliation>
</creator>
<creator>
<creatorName>Akyuz, Gencer K.</creatorName>
<givenName>Gencer K.</givenName>
<familyName>Akyuz</familyName>
<affiliation>Ege Univ, Dept Bioengn, Canc Biol Lab, Fac Engn, Izmir, Turkey</affiliation>
</creator>
<creator>
<creatorName>Korkmaz, Kemal S.</creatorName>
<givenName>Kemal S.</givenName>
<familyName>Korkmaz</familyName>
<affiliation>Ege Univ, Dept Bioengn, Canc Biol Lab, Fac Engn, Izmir, Turkey</affiliation>
</creator>
</creators>
<titles>
<title>Hn1 Negatively Influences The Beta-Catenin/E-Cadherin Interaction, And Contributes To Migration In Prostate Cells</title>
</titles>
<publisher>Aperta</publisher>
<publicationYear>2015</publicationYear>
<dates>
<date dateType="Issued">2015-01-01</date>
</dates>
<resourceType resourceTypeGeneral="Text">Journal article</resourceType>
<alternateIdentifiers>
<alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/80041</alternateIdentifier>
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<relatedIdentifiers>
<relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1002/jcb.24956</relatedIdentifier>
</relatedIdentifiers>
<rightsList>
<rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
<rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
</rightsList>
<descriptions>
<description descriptionType="Abstract">Previously, it has been reported that HN1 is involved in cytoplasmic retention and degradation of androgen receptor in an AKT dependent manner. As HN1 is a hormone inducible gene, and has been shown that it is upregulated in various cancers, we studied the importance of HN1 function in -catenin signaling in prostate cancer cell line, PC-3 and mammary cancer cell line MDA-MB231. Here, we demonstrated that HN1 physically associates with GSK3/-catenin destruction complex and abundantly localizes to cytoplasm, especially when the GSK3 is phosphorylated on S9 residue. Further, ectopic HN1 expression results an increase in the -catenin degradation leading to loss of E-cadherin interaction, concurrently contributing to actin re-organization, colony formation and migration in cancer cell lines. Thus, we report that HN1 is an essential factor for -catenin turnover and signaling, augments cell growth and migration in prostate cancer cells. J. Cell. Biochem. 116: 170-178, 2015. (c) 2014 Wiley Periodicals, Inc.</description>
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