Nijman

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	[http://www.wi.mit.edu/research/fellows/brummelkamp.html Thijn Brummelkamp] (MIT, Whitehead Institute)		[http://www.wi.mit.edu/research/fellows/brummelkamp.html Thijn Brummelkamp] (MIT, Whitehead Institute)
-	[http://www.biomedicalgenetics.nl/Members/Bernards/bernards.html Rene Bernards ] (Netherlands Cancer Institute)	+	[http://www.nki.nl/Research/Faculty+and+Research/Divisions/Molecular+Carcinogenesis/Bernards.htm Rene Bernards ] (Netherlands Cancer Institute)
	[http://www.broad.mit.edu/about/bios/bio-golub.html Todd Golub] (Broad Institute, MIT/Harvard)		[http://www.broad.mit.edu/about/bios/bio-golub.html Todd Golub] (Broad Institute, MIT/Harvard)

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Revision as of 14:45, 20 December 2009

Contents 1 Ce-M-M- 2 Research scope 3 Projects 3.1 Synthetic lethal interactions in mammalian cells 3.2 Cell circuits and cancer 3.2.1 Ubiquitin dynamics 3.2.2 Genetic screens 4 Collaborations 5 In the news

Ce-M-M-

The Nijman lab is the latest addition to CeMM. CeMM is a novel, international, independent and interdisciplinary research Center in Molecular Medicine of the Austrian Academy of Sciences. “From the clinic to the clinic”: Driven by medical needs, CeMM integrates basic research and clinical expertise to pursue innovative diagnostic and therapeutic approaches. A particular focus of CeMM includes cancer research and as such is a significant addition to the research community in Vienna (Austria). At the center of CeMM’s interest are patients and associated diseases. CeMM’s mission is to combine insight obtained from basic and clinical research and use it to implement the development of innovative therapeutic and diagnostic strategies – from the clinic to the clinic. Located at the Vienna General Hospital (AKH), Austria’s largest medical research complex, CeMM functions as bidirectional channel between basic research and clinical applications. CeMM provides access to post-genomic technologies for the biomedical community and is a training and teaching center for a new generation of researchers in molecular medicine. CeMM’s innovative approaches are based on a novel, post-genomic, molecular understanding of biological and pathological systems.The goal of CeMM is to assist in preparing the predictive, preventive and personalized medicine of the future.

Research scope

In the post-genomic era, a major challenge is to understand the molecular networks that allow the cell perform it's physiological function. Within the Nijman lab the aim is to contribute to the understanding of the cellular circuitry in health and disease with a particular focus on cancer. In addition, we try to find new angles for cancer therapy. In order to achieve these goals, the lab employs state-of-the-art technology, genomics and bioinformatics.

Figure (right). Breast cancer in a mastectomy specimen (top). The cancerous tumour (pale yellow) resembles the figure of a crab, giving the disease its name.

Projects

Synthetic lethal interactions in mammalian cells

During the last 5 years, in vitro human cell genetics has become within reach for many laboratories around the world. One of the challenges for the coming years is to use the available tools in new and creative ways to fully exploit the power of experimental genetics. In this context, a major focus of the lab is the high-throughput assessment of synthetic lethal/sick (SSL) interactions using chemical compounds and RNAi. In particular we are trying to identify genotype-specific cancer vulnerabilites or "Achilles' heels". However, the identification of SSL interactions can be useful for the study of any cell biological process and is thus not limited to the study of cell growth.

Cell circuits and cancer

Ubiquitin dynamics

Other projects in the lab are generally focussed on cancer-relevant pathways and signaling dynamics, such as ubiquitination/deubiquitination. To identify deubiquitinating enzymes (DUBs) in pathways or processes of interest we employ RNAi libraries directed against all DUBs in the human genome. Using this approach we have previously identifid DUBs in NF-kappaB signaling, DNA repair and hypoxia signaling.

Figure (right). Ribbon representation of ubiquitin protein, highlighting the secondary structure. α-helices are coloured in blue and the β-sheet in green. The typical attachment point for a further ubiquitin molecule in polyubiquitin chain formation, lysine 48, is shown in pink.

Genetic screens

The lab also employs genome wide gain-of-function and loss-of-function screens using cDNA and shRNA libraries.

Figure (left). Colony formation assay showing that overexpression of TFE3 can by-pass the temperature sensitive growth arrest induced by pRB. Figure taken from Nijman et. al. JBC (2006) Free access.

For instance, we identified the transcription factor TFE3 as a regulator of cell-cycle arrest induced by the Retinoblastoma tumor suppressor gene (pRB).

Collaborations

Collaborations are crucial for modern day science!

Listed here are some (science) friends and collaborators:

Tony Huang (NYU)

Thijn Brummelkamp (MIT, Whitehead Institute)

Rene Bernards (Netherlands Cancer Institute)

Todd Golub (Broad Institute, MIT/Harvard)

Dave Root (Broad Institute, MIT/Harvard)

In the news

Die Presse

Medical News

Sebastian Nijman wins "Future of Vienna award" (Wiener Zukunftspreis) See also CeMM News