清華大學醫(yī)學院 Charles David實驗室招聘癌癥生物學博士后(2-3名) 時間：2018-01-03

清華大學醫(yī)學院 Charles David實驗室招聘癌癥生物學博士后(2-3名)

Charles David(戴超)實驗室具有清華北大聯(lián)合中心的支持。本實驗室運用多種新穎的實驗手段鑒定主宰癌癥細胞和組織干細胞命運的轉錄因子以及轉錄網(wǎng)絡。研究鑒定癌信號通路如何通過挾持干細胞的轉錄網(wǎng)絡誘導癌癥發(fā)生 。

清華博士后享受有競爭力的待遇。實驗室支持申請各類博士后基金如CLS博士后基金、大學博士后支持計劃等.

招聘條件

1.具有分子和細胞生物學, 生物化學, 或者癌癥學相關專業(yè)博士學位，獲得博士學位2年以內(nèi)；

2.近3年以來，以第一作者身份在國際知名學術期刊發(fā) （IF > 5) 表過研究論文；

3.具有較高的英語寫作及口語交流能力.

申請材料及申請方式 ：

1個人簡歷；

2個人陳述 （研究背景，個人事業(yè)目標等；中英均可）；

3兩名推薦人的聯(lián)系方式。

請將申請材料發(fā)至：cdavid@mail.tsinghua.edu

Charles David’s Lab at Tsinghua University School of Medicine recruiting 2-3 postdoctoral fellows

The David laboratory is supported in part by the Peking-Tsinghua Center for Life Sciences (CLS). The laboratory uses cutting-edge approaches to parse essential tumorigenic transcriptional networks in cancer as well as the stem/progenitor cells that can serve as the cell of origin for neoplasms. The laboratory is also focused on understanding the specific molecular interactions between oncogenic signaling pathways and stem/progenitor-derived transcriptional networks.

Tsinghua University postdoctoral fellows enjoy competitive pay and benefits, and are able to apply for a wide range of additional support available at Tsinghua/CLS.

The successful candidate(s) will:

1. have a Ph.D. in the areas of molecular/cellular biology, biochemistry, epigenetics, or cancer biology within the last two years;

2. have published a first author paper in a reputable journal (IF > 5) in the past three years; AND

3. have proficiency in verbal and written English.

Applicants should supply:

1. an up-to-date CV;

2. a personal statement (detailing research experience, career goals etc.); AND

3. contact information for two references.

Please send application materials to: cdavid@mail.tsinghua.edu.

戴超代表成果如下：

1.David CJ, Huang YH, Chen M, Su J, Bardeesy N, Iacobuzio-Donahue CA, Massagué J (2016) TGF-β tumor suppression through a lethal EMT.Cell164(5):1015-30.

2.David CJ, Boyne AB, Millhouse SR, Manley JL (2011). The RNA polymerase II C-terminal domain promotes splicing activation through recruitment of a U2AF65-Prp19 complex.Genes and Development25: 972-83.

3.David CJ, Manley JL (2010). Alternative pre-mRNA splicing regulation in cancer: pathways and programs unhinged.Genes and Development24: 2324-64.

4.David CJ*, Chen M*, Assanah M, Canoll P, Manley JL (2010). HnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer.Nature463: 364-8.*Co-first author

5.David CJ, Manley JL (2008). The search for alternative splicing regulators: new approaches offer a path to a splicing code.Genes and Development22: 279-85.