Contact information

Prof. Dr. rer. nat. Hamid Kashkar

Institute for Molecular Immunology

CECAD - Cluster of Excellence at the University of Cologne

Joseph-Stelzmann-Straße 26

50931 Cologne



Academic education

2000 - 2002 Graduate studies in Biology/Genetics, University of Cologne (Dissertation), Mentor: Dr. Juliane Jürgensmeier / Prof. Dr. Jonathan C. Howard
1997 - 2000 Studies in Biology, University of Cologne (Diploma), Mentor: Prof. Dr. Jonathan C. Howard
1987 - 1991 Studies in Biology, University of Orumieh, Iran (Bachelor of Science)


Scientific degrees

2022 W3 Professor, Molecular Immunology, University of Cologne
2015 Extraordinary Professorship (Apl. Prof.), University of Cologne
2008 Habilitation in Immunology, University of Cologne, Mentor: Prof. Dr. M. Krönke
2002 Promotion (with “distinction”) in Biology, University of Cologne, Thesis supervisor: Prof. Dr. J. C. Howard


Scientific career

2022 Chair, Institute for Molecular Immunology, University of Cologne
2014 - 2021    Independent Research Group Leader, CECAD, University of Cologne
2011 - 2013 Independent Research Group Leader, Center for Molecular Medicine Cologne (CMMC), University of Cologne
2005 - 2011 Senior Investigator with an own research group, Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne
2002 - 2005 Postdoctoral Research Fellow, Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne


Honors/ Awards/ Memberships

since 2008 Reviewer: Mol Cell, Immunity, Cell Host Microbe, Cell Rep., Nat. Cell Biol., Nat. Microbiol., Nat. Comm., EMBO Journal, EMBO Rep, Cell Death & Differentiation, Cancer Research, Oncogene, Blood
since 2002 Member of the Deutsche Gesellschaft für Immunologie
2011 Career Development Award of the CMMC, University of Cologne
2009 Award for the Best Habilitation 2009, Medical Faculty, University of Cologne


  • cIAPs control RIPK1 kinase activity-dependent and -independent cell death and tissue inflammation

    Cellular inhibitor of apoptosis proteins (cIAPs) are RING-containing E3 ubiquitin ligases that ubiquitylate receptor-interacting protein kinase 1 (RIPK1) to regulate TNF signalling. Here, we established mice simultaneously expressing enzymatically inactive cIAP1/2 variants, bearing mutations in the…

  • Aberrant expansion of spontaneous splenic germinal centers induced by hallmark genetic lesions of aggressive lymphoma

    Unique molecular vulnerabilities have been identified in the aggressive MCD/C5 genetic subclass of diffuse large B-cell lymphoma (DLBCL). However, the premalignant cell-of-origin exhibiting MCD-like dependencies remains elusive. In this study, we examined animals carrying up to 4 hallmark genetic…

  • Deregulation and epigenetic modification of BCL2-family genes cause resistance to venetoclax in hematologic malignancies

    The BCL2 inhibitor venetoclax has been approved to treat different hematological malignancies. Because there is no common genetic alteration causing resistance to venetoclax in chronic lymphocytic leukemia (CLL) and B-cell lymphoma, we asked if epigenetic events might be involved in venetoclax…

  • An Autochthonous Mouse Model of Myd88- and BCL2-Driven Diffuse Large B-cell Lymphoma Reveals Actionable Molecular Vulnerabilities

    Based on gene expression profiles, diffuse large B-cell lymphoma (DLBCL) is subdivided into germinal center B-cell–like (GCB) and activated B-cell–like (ABC) DLBCL. Two of the most common genomic aberrations in ABC-DLBCL are mutations in MYD88 as well as BCL2 copy-number gains. Here, we employ…

  • Mitochondrial respiration controls neoangiogenesis during wound healing and tumour growth

    The vasculature represents a highly plastic compartment, capable of switching from a quiescent to an active proliferative state during angiogenesis. Metabolic reprogramming in endothelial cells (ECs) thereby is crucial to cover the increasing cellular energy demand under growth conditions. Here we…

  • CHIP ubiquitylates NOXA and induces its lysosomal degradation in response to DNA damage

    The BH3-only protein NOXA is a regulator of mitochondrial apoptosis by specifically antagonizing the anti-apoptotic protein MCL-1. Here we show that the E3 ubiquitin ligase CHIP controls NOXA stability after DNA damage. Our findings reveal that CHIP and MCL-1 are binding partners of NOXA and…

  • Caspase-8 is the molecular switch for apoptosis, necroptosis and pyroptosis

    Caspase-8 is the initiator caspase of extrinsic apoptosis1,2 and inhibits necroptosis mediated by RIPK3 and MLKL. Accordingly, caspase-8 deficiency in mice causes embryonic lethality3, which can be rescued by deletion of either Ripk3 or Mlkl4-6. Here we show that the expression of enzymatically…

  • BCL-2-family protein tBID can act as a BAX-like effector of apoptosis

    During apoptosis, the BCL-2-family protein tBID promotes mitochondrial permeabilization by activating BAX and BAK and by blocking anti-apoptotic BCL-2 members. Here, we report that tBID can also mediate mitochondrial permeabilization by itself, resulting in release of cytochrome c and mitochondrial…