Publikationsserver der Universitätsbibliothek Marburg
Titel:TAF4B begleitet die Differenzierung von humanen Makrophagen und bindet nach inflammatorischer Stimulation zusammen mit NFkappaB an den Promotor von tumor necrosis factor alpha
Autor:Schipper, Michael
Weitere Beteiligte: Renkawitz-Pohl, Renate (Prof. Dr.)
Veröffentlicht:2013
URI:https://archiv.ub.uni-marburg.de/diss/z2013/0077
URN: urn:nbn:de:hebis:04-z2013-00771
DOI: https://doi.org/10.17192/z2013.0077
DDC:570 Biowissenschaften, Biologie
Titel (trans.):TAF4B accompanies the differentiation of human macrophages and binds together with NFkappaB on the promoter of tumor necrosis factor alpha
Publikationsdatum:2013-02-20
Lizenz:https://rightsstatements.org/vocab/InC-NC/1.0/

Dokument

Schlagwörter:
Tumorassoziierter Makrophage, TAF TBP associated Factors, TATA Box Binding protein associated Factor, Transkription, Transkription <Genetik>, TATA-Box, TAF TBP assoziierte Faktoren, Int, Makrophage, TATA Box Bindeprotein assoziierte Faktoren, Interleukin 13, Interleukin 10, Interleukin 4, Macrophage, Transcription

Zusammenfassung:
Die TATA-Box-Bindeprotein-assoziierten Faktoren (TAFs) des TFIID-Komplexes bilden zahlreiche Funktionen aus, welche essentiell sind für die Regulation der Transkriptionsinitiation. Unter anderem interagieren verschiedene der TAFs mit Enhancer-gebundenen Aktivatoren. Dies ist notwendig für die Bildung des Transkriptionskomplexes und die Aktivierung der Transkription durch die RNA-Polymerase II an zahlreichen Genen. Das gewebespezifische TAF4B stellt ein Paralog des ubiquitär exprimierten TAF4 dar. TAF4B interagiert in verschiedenen Zelltypen spezifisch mit Transkriptionsaktivatoren, u.a. mit NFkappaB RelA und cRel. Der Koaktivator TAF4B ist dadurch notwendig für die Vermittlung der NFkappaB-induzierten Aktivierung der Transkription durch die RNA-Polymerase II. Bisher war eine Rolle von TAF4B im Immunsystem nur für T-und B-Lymphozyten aufgezeigt. Die Zielsetzung dieser Arbeit war es, eine Funktion von TAF4B in der Reifung und Funktion von Makrophagen als Zellen des angeborenen Immunsystems aufzuzeigen. Die Ergebnisse deuten darauf hin, dass die Translation von TAF4B in primären humanen Monozyten inhibiert ist. Mit einsetzender Adhärenz und Differenzierung wird das TAF4B-Protein in Makrophagen exprimiert. In dieser Phase der Makrophagen-Entwicklung kolokalisiert nukleäres TAF4B zudem partiell mit aktiver RNA Polymerase II, was auf eine transkriptionelle Funktion von TAF4B in der Zelldifferenzierung hindeutet. In reifen Makrophagen induziert die Stimulation mit bakteriellen Lipopolysacchariden die Anreicherung von TAF4B in den Nukleus. Diese Stimulation der Makrophagen induziert zudem die spezifische Bindung von TAF4B an den Promotor von tumor necrosis factor alpha, zusammen mit den Trankriptions-Aktivatoren RelA und cRel. Auch die Stimulation der Makrophagen mit inflammatorischen Cytokinen wie Interferon gamma oder Interleukin 4, 10 und 13 bedingt darüber hinaus eine distinkte Lokalisation des TAF4B-Proteins in reifen Makrophagen, was auf eine Regulation von TAF4B durch diese Cytokine hindeutet.

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