清华大学医学院Charles David实验室2018招聘癌症生物学博士后

清华大学医学院 Charles David实验室招聘癌症生物学博士后(2-3名) 时间：2018-01-03

清华大学医学院 Charles David实验室招聘癌症生物学博士后(2-3名)

Charles David(戴超)实验室具有清华北大联合中心的支持。本实验室运用多种新颖的实验手段鉴定主宰癌症细胞和组织干细胞命运的转录因子以及转录网络。研究鉴定癌信号通路如何通过挟持干细胞的转录网络诱导癌症发生 。

清华博士后享受有竞争力的待遇。实验室支持申请各类博士后基金如CLS博士后基金、大学博士后支持计划等.

招聘条件

1.具有分子和细胞生物学, 生物化学, 或者癌症学相关专业博士学位，获得博士学位2年以内；

2.近3年以来，以第一作者身份在国际知名学术期刊发 （IF > 5) 表过研究论文；

3.具有较高的英语写作及口语交流能力.

申请材料及申请方式 ：

1个人简历；

2个人陈述 （研究背景，个人事业目标等；中英均可）；

3两名推荐人的联系方式。

请将申请材料发至：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.