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AuthorSalem, Hebadc.contributor.author
Date of accession2016-03-15T09:05:14Zdc.date.accessioned
Available in OPARU since2016-03-15T09:05:14Zdc.date.available
Year of creation2013dc.date.created
AbstractInflammation has been reported to be involved in obesity and insulin resistance as well as type 1 and type 2 Diabetes (T1D, T2D). In the course of both T1D and T2D, insulin-producing beta-cells in pancreatic islets are known to be finally destroyed by different molecular mechanisms. The IKK2/NF-kappa B system is the master regulator of inflammatory processes. The contribution of IKK/NF-kappa B signaling in this context is controversially discussed and ranges from pro- to anti-apoptotic functions in the regulation of beta-cell survival. To address this issue we generated conditional loss- and gain-of-function mouse models to manipulate IKK activity specifically in beta-cells. Both, inhibition and constitutive activation of IKK2/NF-kappa B signaling results in hyperglycemia and reduction of beta-cell mass indicating a critical role of balanced IKK signaling in beta-cell homeostasis.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseStandarddc.rights
Link to license texthttps://oparu.uni-ulm.de/xmlui/license_v3dc.rights.uri
KeywordB signalingdc.subject
Keywordbeta-cellsdc.subject
KeywordIKK/NF-kappadc.subject
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHDiabetes mellitusdc.subject.mesh
MeSHInflammationdc.subject.mesh
TitleModulation of IKK/NF-B signaling iin pancreatic ß-cells induces diabetesdc.title
Resource typeDissertationdc.type
DOIhttp://dx.doi.org/10.18725/OPARU-2629dc.identifier.doi
PPN1653083530dc.identifier.ppn
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-vts-87134dc.identifier.urn
GNDB-Zelledc.subject.gnd
GNDNuklearfaktor Kappa Bdc.subject.gnd
FacultyFakultät für Naturwissenschaftenuulm.affiliationGeneral
Date of activation2013-11-19T13:42:54Zuulm.freischaltungVTS
Peer reviewneinuulm.peerReview
Shelfmark print versionW: W-H 13.436uulm.shelfmark
DCMI TypeTextuulm.typeDCMI
VTS-ID8713uulm.vtsID
CategoryPublikationenuulm.category
University Bibliographyjauulm.unibibliographie


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