• Funding

    Anne Hamacher-Brady is fully supported by

    Federal Ministry of Education and Research (BMBF)


    Nathan Brady is supported by

    The Helmholtz Alliance on Systems Biology (SBCancer)


    The German Cancer Research Center (DKFZ)




    The University of Heidelberg Medical Faculty


         
  • Anne's Research

    Lysosomal Systems Biology (LysoSys)

    Head: Dr. Anne Hamacher-Brady

    Programmed cell death (PCD) is regulated by the interplay of genetically-defined signaling pathways. The understanding of PCD is of central importance, in that its successful execution is the key to cancer therapy. As fundamental discoveries concerning PCD machineries, or even new modes of PCD are still being reported, addressing the complexity of PCD signaling is a growing challenge. Systems biology offers tools to utilize such biological complexity, through full data integration and mathematically-derived non-intuitive hypothesis generation. Intriguingly, PCD undergoes substantial positive and negative regulation by the endo-lysosomal compartment. This group is dedicated to the elucidation of lysosomal control of PCD in cancer and non-cancer cells, with an emphasis on testing theoretical model predictions, derived from cell culture experiments, in C. elegans. Primary goals are the systemic identification of regulatory mechanisms governing lysosomal and PCD signaling pathways, and confirmation of in vivo functionality.

    This independent junior research group is funded by the German Federal Ministry of Education and Research (BMBF) within the program 'e:Bio - Innovation Competition Systems Biology' (project #0316191, project start: 03/2012).  

    LysoSys Group members
  • Scientific Activities


    TEACHING

    Molecular Biotechnology, B.Sc. and M.Sc., University of Heidelberg 
    DKFZ Ph.D. Program Lecture - Progress in Cancer Research



    SCIENTIFIC COMMUNITY


    Anne Hamacher-Brady & Nathan Brady : Guest editors for "CELLS" special issue "Autophagy" (2014)
    Nathan Brady & Charley Choe : Guest editors for "CELLS" special issue "Systems Biology" (2013)
    Anne Hamacher-Brady : Guest editor for "CELLS" special issue "Autophagy" (2012)
    Nathan Brady: Guest editor for "ANTIOXIDANTS & REDOX SIGNALING" Autophagy Forum 2012



    IN THE NEWS


    Anne Hamacher-Brady : Featured on German Radio Network "SWR2 CAMPUS" in a report on the anti-cancer effects of artesunate (based on our publication (J BIOL CHEM. 2011 FEB 25;285(8):6587-601)
     
    Press release of DKFZ and University Heidelberg on J BIOL CHEM. 2011 FEB 25;285(8):6587-601    
  • Research

    Since 10+ years Anne and Nathan have investigated mitochondria and autophagy in the context of programmed cell death, while located in Amsterdam, Brussels, La Jolla, and currently Heidelberg.  
    Our two independent research groups are both located at the BioQuant Center for Quantitative Analysis of Molecular and Cellular Biosystems.  The Nathan Brady group is affiliated with both the German Cancer Research Center (DKFZ, research unit B170) and the University Hospital Heidelberg. The Anne Hamacher-Brady group is fully funded through the ‘e:Bio Innovation Competition Systems Biology’ awarded by the German Federal Ministry of Education and Research (BMBF) and part of the German Cancer Research Center (DKFZ, research unit B190).

    Research Description

    Programmed cell death (PCD) occurs when pro-death signaling pathways outperform pro-survival pathways.  Apoptosis (Type I PCD) is the best characterized mode of PCD and is executed by caspase proteases which become activated by either the death receptor or the mitochondrial pathways.  Autophagy, on the other hand, is a degradative process involving proteases contained within sequestration vesicles, the lysosomes, and can function to either protect from apoptosis, enhance apoptosis, or act as a mode of cell death distinct from apoptosis (Type II PCD).
    The overall goal of our research is to investigate the interplay of autophagy and apoptosis signaling pathways with the ultimate goal of unraveling the optimal strategy to selectively kill cancer cells.  On the premise that mitochondria are targets and participants of both autophagy and apoptosis, we are focusing on mitochondria as point of convergence of PCD signaling pathways.
    To that end we focus on the autophagy receptor integration within cell signaling, including Bnip3. Molecular-level deconvolution of the spatially- and temporally-coordinated crosstalk between these pro-survival and pro-death pathways requires both the manipulation and quantification of cellular events. We have established novel, high-content, high-sampling and quantitative approaches to measure global and specific modes of autophagy, as well as specific apoptotic events within cancer cell populations.  To integrate knowledge derived from experiments, and explore emergent behavior we utilize pathway, data-driven, and agent-based mathematical modeling. Finally, to address the in vivo relevance of these cell-based findings, we are focusing on homologous pathways in the worm C. elegans.
  • Nathan's Research

    Systems Biology of Cell Death Mechanisms
    Head: Dr. Nathan Brady

    We are investigating the control and crosstalk between programmed cell death (PCD) mechanisms of apoptosis, autophagy and necrosis in pancreatic, breast and brain cancer cells. Apoptosis, the most studied PCD mode (Type I), is activated by either the death receptor or the mitochondrial pathway. Autophagy is a process by which intracellular components are sequestered by autophagosomes, which then fuse with and are degraded by lysosomes. In the cancer cell autophagy can paradoxically act as either an alternative cell death pathway (Type II PCD) or as a potent survival response to stress, e.g. hypoxia and chemotherapies. Although considered a passive cell death, many pathways are common to necrosis and PCD modes. In contrast to apoptosis, necrosis is inflammatory due to the rupture of the plasma membrane and the release of specific cytosolic components. As apoptosis does not generate an immune response, the strict focus on apoptosis-inducing therapies may not be fully productive. Our research is aimed at revealing how individual pathway activities and crosstalk between PCD pathways can be tuned to optimize intrinsic and extrinsic pancreatic cancer cell death.  
  • Lab tour

  • Publications

    2014

    ◊ Hamacher-Brady A, Choe SC, Krijnse-Locker J, Brady NR. "Intramitochondrial recruitment of endolysosomes mediates Smac degradation and constitutes a novel intrinsic apoptosis antagonizing function of XIAP E3 ligase." Cell Death Differ. 2014  Aug 1. doi: 10.1038/cdd.2014.101

    ◊ Bhattacharya N, Reichenzeller M, Caudron-Herger M, Haebe S, Brady N, ..., Mertens D. "Loss of cooperativity of secreted CD40L and increased dose-response to IL4 on CLL cell viability correlates with enhanced activation of NF-kB and STAT6." Int J Cancer. 2014 May 15. doi: 10.1002/ijc.28974.
     

    2013

    ◊ Oehme I., Lodrini M., Brady N.R., and O. Witt. “Histone deacetylase 10-promoted autophagy as a druggable point of interference to improve the treatment response of advanced neuroblastomas.” Autophagy2013, October 8, 2013 

    ◊ Oehme I., ..., Hamacher-Brady A., Brady N.R., Deubzer H.E., and O. Witt. “Histone deacetylase 10 promotes autophagy-mediated cell survival.” Proc Natl Acad Sci U S A. 2013, June 25, 2013, doi: 10.1073

    ◊ Chiramel A.I.,  Brady N.R., and Bartenschlager R. “Divergent roles of autophagy in virus infection.” Cells. 2013, 2(1), 83-104. Review.

    ◊ Zhu Y., Massen S., Terenzio M., Lang V., Chen-Lindner S., ... , Hamacher-Brady A. and N.R. Brady. “Modulation of serines 17 and 24 in the LC3-interacting region of BNIP3 determines pro-survival mitophagy vs. apoptosis.” J Biol Chem. 2013 Jan 11;288(2):1099-113. doi: 10.1074

    2012

    ◊ Klionsky D.J., ...,  Brady N.R., et al. “Guidelines for the use and interpretation of assys for monitoring autophagy.” Autophagy. 2012;8Apr;8(4):445-544.
    ◊ Zhai Z., HAan., Papagiannouli F., Hamacher-Brady A., Brady N., Sorge S., Bezdan D., and I. Lohmann. “Antagonistic regulation of differentiation and apoptosis by the CUT transcription factor represents a tumor suppressing mechanism in Drosophila.” PLoS Genetics. 2012;8(3):E1002582. ePub 2012 MAR 15.
    See also commentary: MacCarthy N. “Tumorigenesis: CUT here for differentiation.” Nat Rev Cancer. 2012 Apr 5;12(5):320.
    ◊ A. Hamacher-Brady. "Autophagy regulation and integration with cell signaling." Antiox Redox Signal. Review. 2012 Sep 1;17(5):756-65. ePub 2012 JAN 25.
    ◊ Y. Reis, M. Bernardo-Faura, D. Richter, T. Wolf, B. Brors, A. Hamacher-Brady, R. Eils, and N.R. Brady. "Multi-parametric analysis and modeling of relationships between mitochondrial morphology and apoptosis." PLoS One. 2012;7(1):E28694. ePub 2012 Jan 17.

    2011

    ◊ Wild, P., H. Farhan, D. G. McEwan, S. Wagner, V. V. Rogov, N. R. Brady, B. Richter, J. Korac, O. Waidmann, C. Choudhary, V. Dotsch, D. Bumann, and I. Dikic. 2011. Phosphorylation of the autophagy-receptro optineurin restricts salmonella growth. Science 333:228-233.
    ◊ Balteau, M., ..., N.R. Brady, ..., L. Hue, L. Bertrand, and C. Beauloye. 2011. NADPH oxidase activation by hyperglycaemia in cardiomyocytes is independent of glucose metabolism but requires SGLT1. Cardiovasc Res. 92:237-246.
    ◊  S.C. Choe, G. Zhao, Z. Zhao, J.D. Rosenblatt, H.-M. Choe, S.-U. Shin, N.F. Johnson. Model for in vivo progression of tumors based on co-evolving cell population and vasculature. Scientific Reports 1, 31 (2011)
    ◊ P. Hundeshagen, A. Hamacher-Brady, R. Eils, and N.R. Brady. "Concurrent detection of autolysosome formation and lysosomal degradation by flow cytometry in a high-content screen for inducers of autophagy." BMC Biol., 2011 June 9(1): 38.
    See Also Commentary: Hansen T.E., Johansen T. "Following Autophagy Step-By-Step." BMC Biol. 2011 June 2;9:39.
    ◊ Hamacher-Brady A., ..., and N.R. Brady. "Artesunate Activates Mitochondrial Apoptosis In Breast Cancer Cells Via Iron-Catalysed Lysosomal Reactive Oxygen Species Production." J Biol Chem. 2011 Feb 25;285(8):6587-601.

    2010


    ◊ Mora, R., I. Dokic, T. Kees, C. M. Huber, D. Keitel, R. Geibig, B. Brugge, H. Zentgraf, N. R. Brady, And A. Regnier-Vigouroux. 2010. Sphingolipid Rheostat Alterations Related To Transformation Can Be Exploited For Specific Induction Of Lysosomal Cell Death In Murine And Human GLIOMA. GLIA 58:1364-1383.

    ◊ Huang C., Liu W., Perry C.N., Yitzhaki S., Lee Y., Yuan H., Tsukada Y.T., Hamacher-Brady A., Mentzer R.M. Jr., And R.A. Gottlieb. "Autophagy And Protein Kinase C Are Required For Cardioprotection By Sulfaphenazole." Am J Physiol Heart Circ Physiol. 2010 Feb
     

    2009

    ◊ Schmidt-Glenewinkel, H., E. Reinz, R. Eils, And N. R. Brady. 2009. Systems Biological Analysis Of Epidermal Growth Factor Receptor Internalization Dynamics For Altered Receptor Levels. J Biol Chem 284:17243-17252.

    2008

    ◊ Alirezaei, M., W. B. Kiosses, C. T. Flynn, N. R. Brady, And H. S. Fox. 2008. Disruption Of Neuronal Autophagy By Infected Microglia Results In Neurodegeneration. Plos One 3:E2906.

    2007

    Brady N.R., Hamacher-Brady A., Yuan H., And R.A. Gottlieb. "The Autophagic Response To Nutrient Deprivation In The Hl-1 Cardiac Myocyte Is Modulated By Bcl-2 And Sarco/Endoplasmic Reticulum Calcium Stores." Febs J. 2007 Jun
    Hamacher-Brady A., Brady N.R., Logue S.E., Sayen M.R., Jinno M., Gottlieb R.A., And Gustafsson A.B.  Response To Myocardial Ischemia/Reperfusion Injury Involves Bnip3 And Autophagy. Cell Death Differ. 2007 Jan;14(1):146-57. Epub 2006 Apr 28.

    2006


    ◊ Hamacher-Brady A., Brady N.R., And R.A. Gottlieb.  "The Interplay Between Pro-Death And Pro-Survival Signaling Pathways In Myocardial Ischemia/Reperfusion: Apoptosis Meets Autophagy." Cardiovasc Drugs Ther. 2006 Sept. Review.

    ◊ Hamacher-Brady A.Brady N.R., Gottlieb R.A., And Ab Gustafsson.  "Autophagy As A Protective Response To Bnip3-Mediated Apoptotic Signaling In The Heart."  Autophagy. 2006 Oct 25;2(4)

    ◊ Brady N.R., Hamacher-Brady A., Westerhoff H.V., And R.A. Gottlieb. "A Wave Of Reactive Oxygen Species (Ros)-Induced Ros Release In A Sea Of Excitable Mitochondria." Antioxid Redox Signal. 2006 Sep-Oct. Review.

     Hamacher-Brady A., Brady N.R., And R.A. Gottlieb.  "Enhancing Macroautophagy Protects Against Ischemia/Reperfusion Injury In Cardiac Myocytes."  J Biol Chem. 2006 Oct 6;281(40):29776-87. Epub 2006 Aug 1.

    ◊ Brady N.R., Hamacher-Brady A., & R.A. Gottlieb.  Proapoptotic Bcl-2 Family Members And Mitochondrial Dysfunction During Ischemia/Reperfusion Injury, A Study Employing Cardiac Hl-1 Cells And GFP Biosensors.  Biochim Biophys Acta. 2006 May-Jun

    2004

    ◊ Brady, N. R., S. P. Elmore, J. J. Van Beek, K. Krab, P. J. Courtoy, L. Hue, And H. V. Westerhoff. 2004. Coordinated Behavior Of Mitochondria In Both Space And Time: A Reactive Oxygen Species-Activated Wave Of Mitochondrial Depolarization. Biophys J 87:2022-2034.  
  • About us

    Since 10 years Anne and Nathan have together investigated mitochondria and autophagy in the context of programmed cell death, while located in Amsterdam, Brussels, La Jolla, and currently Heidelberg.  
    At present, we have the exciting opportunity to combine our two independent research groups as a joint unit located at the BioQuant Center for Quantitative Analysis of Molecular and Cellular Biosystems.  The Nathan Brady group is affiliated with both the German Cancer Research Center (DKFZ, research unit B170) and the University Hospital Heidelberg. The Anne Hamacher-Brady group is fully funded through the ‘e:Bio Innovation Competition Systems Biology’ awarded by the German Federal Ministry of Education and Research (BMBF) and part of the German Cancer Research Center (DKFZ, research unit B190).

    Research Description

    Programmed cell death (PCD) occurs when pro-death signaling pathways outperform pro-survival pathways.  Apoptosis (Type I PCD) is the best characterized mode of PCD and is executed by caspase proteases which become activated by either the death receptor or the mitochondrial pathways.  Autophagy, on the other hand, is a degradative process involving proteases contained within sequestration vesicles, the lysosomes, and can function to either protect from apoptosis, enhance apoptosis, or act as a mode of cell death distinct from apoptosis (Type II PCD).
    The overall goal of our research is to investigate the interplay of autophagy and apoptosis signaling pathways with the ultimate goal of unraveling the optimal strategy to selectively kill cancer cells.  On the premise that mitochondria are targets and participants of both autophagy and apoptosis, we are focusing on mitochondria as point of convergence of PCD signaling pathways.
    To that end we focus on the autophagy receptor integration within cell signaling, including Bnip3. Molecular-level deconvolution of the spatially- and temporally-coordinated crosstalk between these pro-survival and pro-death pathways requires both the manipulation and quantification of cellular events. We have established novel, high-content, high-sampling and quantitative approaches to measure global and specific modes of autophagy, as well as specific apoptotic events within cancer cell populations.  To integrate knowledge derived from experiments, and explore emergent behavior we utilize pathway, data-driven, and agent-based mathematical modeling. Finally, to address the in vivo relevance of these cell-based findings, we are focusing on homologous pathways in the worm C. elegans.    
  • Theses

    Scientific supervision of the following works:

     

    Defended doctoral students (Ph.D.)

    Silu Chen-Lindner (2014) – BACH1 as a novel target for ROS-induced cell death in pancreatic cancer cells
    Yanyan Zhu (2013) – Regulation of BH3-only proteins Bnip3- and Nix-induced mitophagy and role of mitophagy in apoptosis
    Yara Reis (2011) – Mitochondrial dynamics dynamics during apoptosis – an integrated modeling approach
    Phillip Hundeshagen (2011) – Quantitative studies on autophagy
     

    Medical doctoral students (Dr. med.)

    Henning Stein (2012) – Artesunate activates mitochondrial apoptosis in breast cancer cells via iron-catalyzed lysosomal reactive oxygen species production
     

    Master student theses (M.Sc.)

    Silu Chen (2011) - Quantitative investigation and analysis of p62-regulated crosstalk between Keap1-Nrf2 signaling pathway and autophagy
    Kathrin Nussbaum (2010) – Quantitative population level analysis of apoptosis and autophagy activities in cancer cells
    Andreas Kuehne (2010) – An integrative experimentnal and computational systems biology approach to investigate crosstalk between autophagy and Keap1-Nrf2 reactive oxygen species regulatory system
    Simon Turschner (2009) – Quantitative systems level investigation into artesunate-triggered programmed cell death in cancer cells
    Marko Müller (2009) – Modeling Bcl-2 regulation of calcium
    Marti Bernardo (2008) – Understanding crosstalk between apoptosis and autophagy using data driven modeling
    Martin Schultz (2007) – Systematic approach to the role of Bid in programmed cell death

     

    Bachelor student theses (B.Sc.)

    Carsten Beese (2012) - Scaffold protein p62 modifies TNF receptor activities in pro-survival and pro-death signaling in cancer cells
    Nils Eling (2012) - Modelling the Nrf2-Keap1 signalling pathway in human pancreatic carcinoma cells
    Stephen Krämer (2010) - Conceptual limitations and potential solutions for frugal dynamic network modeling
    Nadezhda Abazova (2010) – Role of ceramide pathway on gemcitabine robustness in pancreatic cancer  
  • Contact

    How to find us

    Email


    Nathan Brady:  n.brady@dkfz.de
    Anne Hamacher-Brady:  a.brady@dkfz.de
     

    Postal Address


    Im Neuenheimer Feld 267
    Bioquant
    69120 Heidelberg
    Germany
  • p5rn7vb
  • Lab members// who we are

    Dr. Anne Hamacher-Brady ← back

    About me

    Name

    Anne Hamacher-Brady, PhD

    Position

    Independent Group Leader

    Research Interests

    • Lysosomal regulation of programmed cell death in cancer cells ______________________ • In vivo consequences of specific autophagy (C. elegans) ____________________ • Multi-scale modeling of cellular and in vivo responses

    Awards

    2012: BMBF 'e:Bio - Innovation Competition Systems Biology', 1.32 Million EURO funding over five years for independent research group (LysoSys, Foerderkennzeichen 0316191)

    Short Vitae

    2012 – present: Head of Independent Research Group funded by the ‘e:Bio – Innovation Competition Systems Biology’ Award of the German Federal Ministry of Education and Research (BMBF)

    2010-2012 : Group leader at the German Cancer Research Center, within Division of Theoretical Bioinformatics

    2006 – 2010*: PostDoc, at the German Cancer Research Center, Division of Theoretical Bioinformatics (*incl. maternity leaves, in 2006 and 2008)

    2003 – 2006: PhD thesis, lab of Prof. Robbie Gottlieb at The Scripps Research Institute, Department of Molecular and Experimental Medicine, La Jolla, California (under the auspices of the RWTH Aachen, Germany)

    ‘The interplay between pro-death and pro-survival pathways converging at mitochondria in myocardial ischemia/reperfusion: apoptosis meets autophagy’

    2003: Diploma Thesis (Dipl.-Biol. equiv. MSc), lab of Prof. Hans Westerhoff at the Vrije Universiteit Amsterdam, Department of Molecular Cell Physiology, The Netherlands (under the auspices of the RWTH Aachen, Germany)

    ‘Dynamics of mitochondrial organization and communication in the adult cardiomyocyte – a study employing laser scanning confocal microscopy’

    Publication List

  • Lab members// who we are

    Dr. Nathan Brady ← back

    About me

    Name

    Nathan Ryan Brady, PhD

    Position

    Independent Group Leader

    Research Interests

    Molecular mechanisms of crosstalk between apoptosis and autophagy ___________________ Biosensor development and high-content screening ___________________ Data-driven mathematical modeling of survival and death pathway

    Short Vitae

    2010 – Current: Head of Independent Research Group, The German Cancer Research Center (DKFZ) and University Hospital Heidelberg, Germany

    2006 – 2009: Group Leader in Division of Theoretical Bioinformatics, The German Cancer Research Center (DKFZ), Heidelberg, Germany

    2005 – 2006: PostDoc, The Scripps Research Institute, La Jolla, California

    2004 – 2005: PostDoc, The Burnham Medical Research Institute, La Jolla, California

    2000 – 2004: Ph.D., Free University of Amsterdam, The Netherlands;  Christian de Duve Institute of Cellular Pathology, Bruxelles, Belgium

    2000: M.Sc., ‘Endocrinologie et interactions cellulaires‘  CNRS/University of Paris VI, France

    Publications

    Quote

    Do it! - Starsky and Hutch

    The reward for work well done is the opportunity to do more – Jonas Salk

     

  • Lab members// who we are

    Dr. Charley Sehyo Choe ← back

    About me

    Name

    Charley Sehyo Choe, D.Phil.

    Position

    Postdoctoral researcher

    Research Interests

    • Agent-based modeling to reveal emergent behavior of autophagy and apoptosis pathway interactions ___________________ • Micro-environmental influence on spatio-temporal dynamics ___________________ • Multi-scale, data-driven modeling of subcellular cellular processes

    Short Vitae

    2012- present : Post-doctoral research fellow, German Cancer Research Center (DKFZ), Systems Biology of Cell Death Mechanisms

    2009 – 2012: Post-doctoral research fellow, University Of Heidelberg, Department Of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology (Ipmb), Theoretical Systems Biology Group

    2007 – 2009: Post-doctoral research fellow, University Of Miami, Department Of Physics, Complex Systems Group (Prof. Neil F. Johnson)

    2006 – 2007: Research assistant fellowship, University Of Oxford, Department Of Physics, Theoretical Condensed Matter Physics Group (Prof. Neil F. Johnson)

    2003: Research assistant fellowship, Nasa Ames Research Center, California, USA, Collective Intelligence Group (Dr. Kagan Tumer)

    2002-2007: D.Phil., University Of Oxford, Modelling Complex Adaptive Systems with Underlying Network Structure, Theoretical Condensed Matter Physics

    2001 – 2002: M.A.St., University Of Cambridge, Can Evolution Be Modeled Using Self-Organized Criticality?, Applied Mathematics And Theoretical Physics

    1998 – 2001: B.Sc., Imperial College London, Universality Of Omori’s Law In Earthquakes, Physics With Theoretical Physics

    Publications

    ◊  S.C.Choe, G. Zhao, Z. Zhao, J.D. Rosenblatt, H.-M. Choe, S.-U. Shin, N.F. Johnson, Model For In Vivo Progression Of Tumors Based On Co-Evolving Cell Population And Vasculature, In Scientific Reports 1, 31 (2011)

    ◊  S.C. Choe, S. Gourley, N.F. Johnson, P.M. Hui, Theoretical Analysis Of Local Information Transmission In Competitive Populations, In The Complex Networks Of Economic Interactions567, A. Namatame, T. Kaizouji, Y. Aruka (Eds.), Springer Verlag (2005)

    ◊  K.E. Mitman, S.C. Choe, N.F. Johnson, A Competitive Advantage For Mixed-Memory Strategies In An Artificial Market (2005), In Proceedings Of Spie: Noise And Fluctuations In Econophysics And Finance5848, 225–232 The International Society For Optical Engineering, May 2005

    ◊  N.F. Johnson, S.C. Choe, S. Gourley, T. Jarrett, P.M. Hui, Crowd Effects In Competitive, Multi-Agent Populations And Networks, In Non-Linear Dynamics And Heterogeneous Interacting Agents550, 55-70, T. Lux, S. Reitz, E. Samanidou (Eds.), Springer Verlag Berlin Heidelberg, (2005)

    ◊  S.C. Choe, N.F. Johnson, P.M. Hui, Error-Driven Global Transition In A Competitive Population On A Network, Phys. Rev. E70, 055101(R), (2004). Also Selected For The November 15, 2004 Issue Of Virtual Journal Of Biological Physics

    ◊  S.C. Choe, S. Gourley, P.M. Hui, N. F. Johnson, Effects Of Local Connectivity In A Competitive Population With Limited Resources, Europhys. Lett.67 (6), Pp. 867-873, (2004)

    ◊  N.F. Johnson, S.C. Choe, S. Gourley, T. Jarrett, P.M. Hui, Theory Of Collective Dynamics In Multi-Agent Complex Systems, Advances In Solid State Physics44, 427-438, Springer Verlag, (2004)

    Quote

    “Physicist. Theoretical Physicist. Oh, And I Like To Wear Lab Coats.”

  • Lab members// who we are

    Dr. Rakesh Bodhicharla ← back

    About me

    Name

    Rakesh Bodhicharla, PhD

    Position

    Postdoc

    Short Vitae

    2013- Present: Post-doctoral research Scientist, German Cancer Research Center (DKFZ). Consequences of mitophagy receptor engagement in Caenorhabditis elegans. (Dr. Anne Hamacher-Brady).

     

    2011 – 2013: Post-doctoral research fellow, RJRT-Duke Leon Golberg Postdoctoral Program, Nicholas school of environment, Duke University, USA. Investigation of single and combined effects of a representative tobacco-specific nitrosamine (NNK) and a representative polycyclic aromatic hydrocarbon (BaP) in the model organism Caenorhabditis elegans. (Dr. Joel Meyer)

     

    2007 – 2011:  PhD Genetics, School of Biology, University of Nottingham, United Kingdom.

    Fluorescence Resonance Energy Transfer (FRET) based assay as a biosensor for α-synclein aggregation in transgenic Caenorhabditis elegans strains as a model for Parkinson’s disease. (Dr. David de Pomerai)

     

    2006 – 2007: MRes Genetics, School of Biology, University of Nottingham, United Kingdom.

    The effect of α-synclein over-expression in Caenorhabditis elegans as a model for Parkinson’s disease. (Dr. David de Pomerai)

     

    2002 – 2006: B.Tech Industrial Biotechnology, A.C.Tech, Anna  University, Chennai, India

     

    Publications

     

    Archana Nagarajan, Rakesh Bodhicharla, Jody Winter, Ademola Adenle, Aamir Nazir, Declan Brady, Kelly Vere, Jo Richens, Paul O’Shea, David R. Bell and David de Pomerai. (2013) A FRET assay for monitoring α-synclein aggregation in a Caenorhabditis elegans model for Parkinson’s disease. (Submitted in PLOS one).

     

    Rakesh Bodhicharla, Ian Ryde, Prasad G.L and Joel Meyer. (2013) The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces mitochondrial and nuclear DNA damage in Caenorhabditis elegans. Environmental and Molecular Mutagenesis.

     

    Rakesh Bodhicharla, Archana Nagarajan, Jody Winter, Ademola Adenle, Aamir Nazir, Declan Brady, Kelly Vere, Jo Richens, Paul O’Shea, David R. Bell and David de Pomerai. (2012)The effects of α-synclein over-expression in transgenic Caenorhabditis elegans strains. CNS & Neurological Disorders – Drug Targets.

     

    Dawe AS, Bodhicharla RK, Graham NS, May ST, Reader T, Loader B, Gregory A, Swicord M, Bit-Babik G, de Pomerai.DI. (2009) Low-intensity microwave irradiation does not substantially alter gene expression in late larval and adult Caenorhabditis elegans. Bioelectromagnetics. 30(8):602-12.

  • Lab members// who we are

    Anja Jünger ← back

    About me

    Name

    Anja Jünger

    Position

    Transcriptional regulation of autophagy

    Short Vitae

    2014 – current: Master thesis work at Brady labs

    2012 – present M.Sc., Molecular Biotechnology, University of Heidelberg (Germany)

    2009-2012 : B.Sc., Molecular Biotechnology, University of Heidelberg (Germany)

     

  • Lab members// who we are

    Paula Marin Zapata ← back

    About me

    Name

    Paula Marin Zapata

    Position

    PhD student

    Research Interests

    Mathematical modeling of lysosomal regulation of cell death pathways

    Short Vitae

    2013-present. Ph.D. Student, German Cancer Research Center (DKFZ), Heidelberg, research group  ‘Lysosomal Systems Biology’  (Dr. Anne Hamacher-Brady)

    2010-2013. Consultant, Laboratory for Industrial Mathematics Eindhoven (LIME BV)

    2008-2010. M.Sc., Eindhoven University of Technology, Industrial and Applied Mathematics

    2003-2008. B.Sc., National University of Colombia, Biological Engineering

     

     

  • Lab members// who we are

    Verena Lang ← back

    About me

    Name

    Verena Lang

    Position

    PhD student

    Research Interests

    • Lysosomal regulation of cancer cell death ___________________ • Mitochondrial morphology machinery integration with apoptosis, autophagy and mitophagy

    Short Vitae

    2012 – present: Ph.D. student, German Cancer Research Center (DKFZ) Heidelberg, Division Lysosomal Systems Biology on Lysosomal Control of Programmed Cell Death (Dr. Anne Hamacher-Brady)

    2010 – 2011: Dipl. Biol. (equiv. MSc), German Cancer Research Center (DKFZ) Heidelberg, Division of Molecular Genetics titled Characterization of the Role of Protein Kinase C Iota in the Survival of Brain Cancer Stem-like Cells (Prof. Dr. Peter Lichter)

    Publications

    ◊ Zhu Y., Massen S., Terenzio M., Lang V., … ., Hamacher-Brady A. and N.R. Brady. “Modulation of serines 17 and 24 in the LC3-interacting region of BNIP3 determines pro-survival mitophagy vs. apoptosis.” J Biol Chem. 2012 Dec 3, doi:10.1074

    ◊ V. Voss, C. Senft, V. Lang, M. W. Ronellenfitsch, J. P. Steinbach, V. Seifert und D. Kögel, The Pan-Bcl-2 Inhibitor (-)-Gossypol Triggers Autophagic Cell Death in Malignant Glioma, Mol. Cancer Res. 8, 1002 (2010)

    Quote

    “Big thinking. Smart acting… …when wearing a lab coat.”

  • Lab members// who we are

    Nadia Rodrigues De Sousa ← back

    About me

    Name

    Nadia Rodrigues De Sousa

    Position

    HiWi/Student Assistant

    Research Interests

    In vivo study of mitophagy in C. elegans

    Short Vitae

    From 2013 Oct. M.Sc. in Molecular Biosciences, Major in Systems Biology, University of Heidelberg, Heidelberg, Germany

    2013 – present. Student Assistant at German Cancer Research Center (DKFZ)/BioQuant in the Lysosomal Systems Biology Group, Heidelberg, Germany

    2012 – present. Internship and temporary help activity at Boehringer Ingelheim GmbH – Biopharmaceuticals, Depart. Marketing, Communications & Business Intelligence, Ingelheim am Rhein, Germany

    2009 – 2012. B. Sc. in Marine Biology and Biotechnology, School of Tourism and Maritime Technology, Polytechnic Institute of Leiria, Peniche, Portugal

    Awards:

    Lotaçor Annual Academic Award 2010/2011 – Innovation and Research in Fisheries and Sea Resources

    German Academic Exchange Service (DAAD) Study Scholarship (2013)

  • Lab members// who we are

    Silu Chen-Lindner ← back

    About me

    Name

    Silu Chen-Lindner

    Position

    PhD student

    Research Interests

    • Redox regulation of genes and pathways in pancreatic cancer ___________________ • Keap1-Nrf2 system

    Short Vitae

    Short Vitae

    2011 – Present: Ph.D. Student, German Cancer Research Center (DKFZ) Heidelberg, in group Systems Biology Of Cell Death Mechanisms (Dr. Nathan Brady)

    2008 – 2011: M.Sc.,University Of Heidelberg (Germany), Molecular Biotechnology

    2003 – 2007: B.Sc., University Of Beijing Agriculture (China), Food Science And Technology 

    Publications

    Zhu Y., Massen S., Terenzio M., Lang V., Chen-Lindner S., … , Hamacher-Brady A. and N.R. Brady. “Modulation of serines 17 and 24 in the LC3-interacting region of BNIP3 determines pro-survival mitophagy vs. apoptosis.” J Biol Chem. 2012 Dec 3, doi:10.1074

    Quote

  • Lab members// who we are

    Ashik Pari ← back

    About me

    Name

    Ashik Pari

    Position

    PhD student

    Research Interests

    Interaction between innate immune response and autophagy

    Short Vitae

    September 2013- Present: PhD student, German Cancer Research institute (DKFZ), Systems Biology of Cell Death Mechanisms (Dr. Nathan Brady)

    September 2011-July 2013: MASTERS in Life sciences and Technology with specialization in Molecular Medicine, École polytechnique fédérale de Lausanne, Switzerland.

    September 2007- June 2011: B.TECH Biotechnology, Anna University, Chennai

    Master Thesis(July 2012- June 2013):- “Validation of autophagy-related proteins as targets in oncology using inducible shRNA” at Merck, Darmstadt, Germany under the supervision of Dr. Vladimir Kirkin ,Senior Scientist, Merck-Serono.

     

  • Lab members// who we are

    Carsten Beese ← back

    About me

    Name

    Carsten Beese

    Position

    HiWi/Student Assistant

    Research Interests

    • C elegans

    Short Vitae

    2012 – M.Sc.,University Of Heidelberg (Germany), Molecular Biotechnology (Student Assistant)

    200x-2012 :B.Sc., B.Sc.,University Of Heidelberg (Germany), Molecular Biotechnology

    Quote

  • Lab members// who we are

    Nils Eling ← back

    About me

    Name

    Nils Eling

    Position

    Rotation student

    Research Interests

    • Autophagy receptors

    Awards

    Team Awesomeness

    Short Vitae

    06/2014 – 12/2014 – M.Sc. thesis, Brady labs

    2012 – M.Sc.,University Of Heidelberg (Germany), Molecular Biotechnology (Student Assistant)

    200x-2012 :B.Sc., B.Sc.,University Of Heidelberg (Germany), Molecular Biotechnology

    Quote

    It is a miracle that curiosity survives formal education.
    - Albert Einstein