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The Regulation of TiPARP by the Aryl Hydrocarbon Receptor, the Platelet-derived Growth Factor Receptor, and the Estrogen Receptor Alpha

TiPARP is a PARP-like mART that is induced by and negatively regulates AHR transactivation. Despite these insights, not much is known about TiPARP. This study aimed to characterize the regulation of TiPARP by AHR, PDGFR, and ERα, and investigate potential receptor interplay. Gene expression studies revealed that coactivation of AHR and PDGFR can enhance TiPARP expression after 3 h relative to activation of either receptor pathway alone. Gene expression and ChIP studies demonstrated that while co-activation of AHR and ER enhanced AHR, ARNT, and ERα recruitment to the regulatory region of TiPARP, TiPARP mRNA levels were not potentiated by co-activation relative to activation of either pathway. Dissection of the 5’ regulatory region of TiPARP using reporter gene assays revealed that a putative AHRE cluster and an ERE half-site were functional. Lastly, overexpression of TiPARP with an estrogen-responsive reporter revealed that TiPARP can repress ERα signalling and requires its catalytic activity.

Identiferoai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/43310
Date10 December 2013
CreatorsRajendra, Sharanya
ContributorsMatthews, Jason
Source SetsUniversity of Toronto
Languageen_ca
Detected LanguageEnglish
TypeThesis

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