The Seventh Affiliated Hospital of Sun Yat-sen University (SYSU), located in Shenzhen city, China, is a brand-new research hospital. While building up a 100,000m2 research centre, the hospital currently runs a 1,300m2 laboratory and has established six science and technology platforms and one clinical big data centre. The central laboratory in our hospital has integrated molecular and cellular biology, imaging, analytical, and histology facilities, and other critical equipment.
Recently, the hospital started a close collaboration with Tomas Lindahl (Nobel Price 2015; https://www.crick.ac.uk/about-us/who-we-are/how-we-got-here/notable-alumni/tomas-lindahl) and Axel Behrens (https://www.crick.ac.uk/research/labs/axel-behrens) at The Francis Crick Institute (London, UK). Led by Prof. Lindahl, and by Prof. Behrens, a Laboratory focused on “DNA Repair and Treatment”, will be established at the Seventh Affiliated Hospital SYSU in Shenzhen starting next March.
Repair of damaged DNA is tightly regulated to preserve genome integrity and prevent development of cancer and other diseases. The signalling network that detects, signals and repairs DNA lesions is known as DNA damage response (DDR). Cancer cells with impaired DDR often become dependent on other DNA repair pathways for survival. Therefore, identification and characterization of DDR proteins and signalling pathways can provide valuable targets for cancer therapy. Ataxia telangiectasia-mutated (ATM), the protein kinase that is mutated in patients with ataxia telangiectasia (A-T), is a central player in the cellular response to DNA damage (Derheimer et al., 2010; Lukas et al., 2011). ATM is activated following double-strand breaks (DSB) by MRE11-RAD50-NBS1 complex (MRN), which acts as an initial sensor of DSB (Lee et al., 2007; Uziel et al., 2003). ATM is also activated by stimuli that change chromatin structure such as chloroquine and hypotonic shock, which depends on the ATM-interactor protein (ATMIN) as a cofactor (Kanu et al., 2007). ATMIN and NBS1 directly compete for ATM, thereby determining ATM pathway choice (Zhang et al., 2012), and ATM/ATMIN signalling is also controlled by ATMIN ubiquitylation by UBR5 (Zhang et al., 2014). ATMIN promotes ATM signalling in response to replication stress (Kanu et al., 2015) and oxidative stress. ATMIN appears to be required for tumour suppression by ATM, as ATMIN-deficiency leads to B cell lymphoma (Loizou et al., 2011). Yet, in glioblastoma, ATMIN-dependent ATM signaling has a pro-tumourigenic role (Blake et al., 2016). The lab employs mouse models and a diversity of advanced molecular and cell biology techniques to understand and characterise the complex regulation of ATMIN-mediated ATM signaling and its role in the DDR and cancer.
Currently, the Seventh Affiliated Hospital SYSU (Shenzhen, China) will recruit ONE postdoctoral fellow, who will focus on the regulation and function of ATMIN-dependent ATM signalling. The excellent candidates would be offered opportunities to directly study at Dr. Behrens’ Lab at the Francis Crick Institute for 2–3 years (starting in Jan. 2019), and are expected to carry on and lead such research as an independent PI at the Nobel Prize Laboratory at the Seventh Affiliated Hospital SYSU (Shenzhen, China).
A good candidate should meet the following qualifications:
Salary and Eligibility
Education degree: PhD
Salary （pre-tax, insurance and house fee）& Apartment: ￥350,000 -￥450,000 & apartment provided for living in Shenzhen
Inquiries or application (CV and a personal statement) should be sent to Dr. Ningning Li email@example.com.
|Location:||Shenzhen - China|
£42,431.56 to £46,898.04 converted salary*
|Placed On:||1st January 2019|
|Expires:||28th February 2019|
Type / Role: