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AuthorSchütz, Stefaniedc.contributor.author
Date of accession2016-03-15T06:23:25Zdc.date.accessioned
Available in OPARU since2016-03-15T06:23:25Zdc.date.available
Year of creation2010dc.date.created
AbstractAs PCa is one of the most serious diseases in elderly man, current research focuses on the development of effective new therapies for PCa. Although most patients suffering from PCa initially respond to androgen withdrawal therapy, PCa almost invariably progresses to a hormone refractory state of the disease within 18 - 24 months. In recent years, it has become obvious that cell growth and survival of HRPCa largely depend on the cellular content of the AR protein as well as on AR function. Alterations in the AR protein, AR expression, and/or AR activity by protein kinases are some of the most common factors leading to hormone-independent PCa. The present work highlights important roles of the protein kinases glycogen GSK-3 and IKK in AR signalling of PCa cells. Both kinases have been shown to modulate AR transactivation and AR phosphorylation. In addition, GSK-3 and IKK are both involved directly or indirectly in PCa cell proliferation and survival. In contrast to IKK, a special feature of GSK-3 is the control of AR localisation, thereby influencing the intracellular fate of the AR protein. On many occasions, pharmacological inhibition of serine/threonine kinases has been shown to have a negative impact on AR signalling. Although, inhibition of GSK-3 as well as IKK downregulates AR transactivation, both kinases affect different levels of AR signalling. Therefore, GSK-3 and IKK inhibitors have potential future roles as therapeutic agents in the treatment of PCa. Some GSK-3 inhibitors have successfully entered clinical trials, showing low cytotoxic side-effects in the treatment of type II diabetes or neurological malignancies, such as Alzheimer’s disease and bipolar disorders. Based on our results, GSK-3 inhibitors appear to be the most promising compounds for the treatment of PCa in the near future.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseStandard (Fassung vom 01.10.2008)dc.rights
Link to license texthttps://oparu.uni-ulm.de/xmlui/license_v2dc.rights.uri
Dewey Decimal GroupDDC 570 / Life sciencesdc.subject.ddc
MeSHGlycogen synthase kinase 3dc.subject.mesh
MeSHI-kappa B kinasedc.subject.mesh
MeSHProstatic neoplasmsdc.subject.mesh
MeSHReceptors, androgendc.subject.mesh
TitleEffects of glycogen synthase kinase-3 and IkappaB kinase on ligand-dependent activation of the androgen receptordc.title
Resource typeDissertationdc.type
DOIhttp://dx.doi.org/10.18725/OPARU-1841dc.identifier.doi
PPN626971993dc.identifier.ppn
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-vts-72701dc.identifier.urn
GNDAndrogen-Rezeptordc.subject.gnd
GNDGlykogensynthasedc.subject.gnd
FacultyFakultät für Naturwissenschaftenuulm.affiliationGeneral
Date of activation2010-05-18T10:14:27Zuulm.freischaltungVTS
Peer reviewneinuulm.peerReview
Shelfmark print versionZ: J-H 13.662; W: W-H 12.138uulm.shelfmark
DCMI TypeTextuulm.typeDCMI
VTS ID7270uulm.vtsID
CategoryPublikationenuulm.category
Bibliographyuulmuulm.bibliographie


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