Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
 More search options
Prof Robin Ketteler
Gower Street
Tel: 02031084063
Prof Robin Ketteler profile picture
  • Professor of Translational Cell Biology
  • Lab for Molecular Cell Bio MRC-UCL
  • Faculty of Life Sciences
Research Groups
Research Themes
Research Summary

My lab is
interested in the regulation of cancer signaling pathways. We employ
high-throughput screening and novel biomolecular tools to investigate growth
factor signaling cascades and to identify therapeutic targets for anti-cancer
strategies. The two main research projects are:

Identification of novel Grb2
mediated signaling pathways

The small
adaptor molecule Grb2 links growth receptor signaling to intracellular signal
transduction cascades such as the MAP kinase pathway. In order to identify
novel growth factor receptors and mediators, we use whole genome
high-throughput screening approaches utilizing cDNA expression vectors and
siRNA knockdown libraries. Grb2 tagged with the green fluorescent protein
serves as a cellular marker for functional translocation upon activation of
surface receptors or direct binding to Grb2. This approach enabled
us to identify several novel binding partners for Grb2 that we currently
characterize in further detail. In order to better characterize image-based
screening data, we are designing bioinformatic tools to classify molecular
translocations with respect to the cellular localization.

Identification of signaling cascades
that regulate autophagy as therapeutic opportunity

Autophagy is an
evolutionary conserved protein degradation pathway that is essential for
cellular homeostasis and cell viability. Autophagy is enhanced under
nutrient-limiting conditions such as amino acid starvation and can be induced
by treatment with rapamycin, an inhibitor of the mammalian TOR complex.
Autophagy has been implicated in tumour suppressive, as well as tumour
promoting mechanisms. The molecular regulation of autophagy is not very well

We have recently developed a cell-based assay
for autophagy that is amenable to high-throughput screening. The method
measures proteolytic cleavage of a tripartite sensor protein by the autophagy
protease ATG4B. Activation of ATG4B by overexpression or treatment
with rapamycin results in release of Gaussia luciferase from cells that can be
non-invasively harvested from cellular supernatants.

In order to better understand the signaling cascades involved in the
activation of autophagy, we are screening whole genome siRNA libraries for
factors that enhance or reduce the activity of ATG4B. In addition, we are
performing small molecule library screening to identify potential therapeutic
lead compounds.



01-SEP-2009 Group Leader/Manager MRC LMCB UCL, United Kingdom
01-SEP-2002 – 30-AUG-2009 Postdoctoral Research Fellow Molecular Biology Massachusetts General Hospital, United States
01-SEP-1998 – 30-AUG-2002 PhD student Max-Planck-Institute for Immunobiology Albrecht-Ludwigs University Freiburg, Germany
Some IRIS profile information is sourced from HR data as explained in our FAQ. Please report any queries concerning HR data shown on this page to hr-services@ucl.ac.uk.
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by