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当内分泌研究室にて、ポスドク研究員/テクニカルスタッフ(Research associate)を募集いたします。 Keratinocyteの増殖分化における転写調節因子coactivatorの役割を研究しています。表皮特異的遺伝子改変マウスを用いて解析しています。当研究室はカリフォルニア大学サンフランシスコ校(UCSF) に属し研究環境・研究費ともに全米有数の研究機関です。サンフランシスコは生活しやすく恵まれた環境の中で研究できます。サンフランシスコでの生活面は日本語でサポートします。意欲の高い方の応募をお待ちしています。2011年4月までの着任を希望します。
応募資格 ポスドク研究員:生物・医学・理学分野にて最近博士号取得または取得見込みの方;テクニカルスタッフ:同分野で修士号取得または取得見込みの方
Yuko Oda PhD Endocrine Research University of California San Francisco / VA Medical Center San Francisco / Northern California Institute of Research and Education.
E-mail: yuko.oda2@gmail.com

A postdoctoral/research associate position (NIH funded) Endocrinology/Dermatology is available to participate in a research program to investigate transcriptional coactivators regulating keratinocyte proliferation and differentiation. The project focuses on the role of the transcriptional coactivators, DRIP/Mediator or steroid receptor coactivator (SRC) in mouse models. Candidates should hold a recent PhD (less than 2 years or PhD candidates), or hold a MS (for research associate) in cellular and/or molecular biology with working experience in gene transcription (QPCR, western, microarray or ChIP assay), in histochemisty or in transgenic mouse studies.

The transcriptional coactivator and corepressor should be involved in temporal or special specific transcriptional regulation through nuclear receptors or transcription factors. These coactivators or corepressors are not interchangeable in their regulation in cell proliferation and differentiation. We found that the DRIP/Mediator complex is the main coactivator for vitamin D receptor (VDR) in the proliferating keratinocytes, whereas steroid receptor coactivator (SRC) is the major coactivator in differentiated keratinocytes. Moreover, we have found a specific role for DRIP in the regulation of Wnt/catenin signaling pathways regulating keratinocyte proliferation, whereas SRC uniquely induce more differentiated functions such as lipid synthesis and processing required for permeability barrier formation and the innate immune response triggered by disruption of the barrier in the skin. These findings provide a basis by which we can understand how one receptor or factor can regulate a large number of genes in a sequential and differentiation specific fashion. We hypothesized that the two main coactivators, DRIP and SRC, differentially modulate keratinocyte proliferation regulated by Wnt/catenin signaling to be involved in epidermal carcinogenesis, and differentiation leading to a protective epidermal barrier formation and normal hair follicle cycling in the skin. We developed mouse model where either DRIP or SRC is deleted. We determine the selective roles of DRIP and SRC in regulation of epidermal and hair follicle proliferation, differentiation, and protective barrier formation using these mouse models.


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