News from the Institute

As reported in this month’s issue of Molecular Cell and Cell Host & Microbe, an international team of researchers led by Prof. Ivan Dikic has shed light on the molecular function of the protein PLEKHM1, that has previously been shown to regulate bone density in humans and rats.

The team has identified two novel functions for the protein that are important for human disease; firstly, facilitating the removal of toxic protein aggregates and preventing their accumulation, which is relevant for diseases such as Parkinson’s. Secondly, controlling the intracellular growth of invading pathogens such as Salmonella.

Alexandra Stolz, postdoctoral researcher at IBCII, received a grant from the Fritz Thyssen Foundation to fund her proposed project on targeting the autophagy system.

The research program is supported with 150.000 Euro over the next two years.

The Fritz Thyssen Foundation is an active supporter of basic science since more than 50 years, focusing especially on support for junior researchers.

Cells convert the energy extracted from foodstuff into ATP, the universal currency of cellular energy. Mitochondrial oxidative phosphorylation is carried out by five large enzyme complexes.

The Zickermann group from Institute of Biochemistry 2 together with colleagues from the Cluster of Excellence Macromolecular Complexes in Frankfurt and from Freiburg University solved the 3D structure of mitochondrial complex I, the largest and most complex enzyme of this fundamental metabolic pathway.

EMBO will fund her work that is focused on understanding the role of linear ubiquitylation in tumor stromal crosstalk.

A multidisciplinary, international team led by C. Kubisch (Ulm University), K. Ramadan (Oxford University), J. Terzic (Split University), D. Amor (University of Melbourne) and I. Dikic (Goethe University in Frankfurt) reports in today's online issue of Nature Genetics the discovery of a hitherto unknown mutation causing early onset liver cancer.

Individuals carrying this mutation are highly likely to develop liver cancer during childhood, and also show multiple signs of premature aging. The mutation disrupts the function of a gene called SPRTN, resulting in accumulation of DNA damage during each cell division and subsequent chromosome instability.