Prof. Dr. Daniel Krappmann
Head of Research Unit Signaling and Translation“My research is dedicated to decipher molecular machineries controlling immune activation and to translate this findings into the development of new therapies to fight immune diseases and cancer.”
“My research is dedicated to decipher molecular machineries controlling immune activation and to translate this findings into the development of new therapies to fight immune diseases and cancer.”
Academic Pathway and Research Area
He started his academic career as a PhD student and continued his studies on signal transduction in cancer cells as a postdoctoral fellow and junior group leader at the Max-Delbrück-Center (MDC) for Molecular Medicine in Berlin. His Research Unit at Helmholtz Munich is dedicated to study physiological and pathological signaling pathways in the immune system and in cancer.
The identification of the pro-proliferative and anti-apoptotic function of signaling networks in human tumor cells inspired his long-standing efforts to bridge the gap between basic science and clinical translation. He has been leading a successful drug discovery program and the pre-clinical development of new immune modulatory drugs. Candidate drugs from this program are currently tested in the clinic for their ability to boost our immune defence to fight cancer.
Skills and Expertise
Immunology OncologyCancer
Cell Signaling T cell Biology Target Identification Drug Discovery
Professional Career
Director of Research Unit Signaling and Translation
Head of Research Unit ‘Cellular Signal Integration’
Adjunct Professor Faculty of Biology, Ludwig-Maximilians-Universität München
Group Leader Helmholtz Munich
Head Junior Research Group at MDC Berlin
Postdoctoral Fellow at Max-Delbrück-Center (MDC) Berlin
Honors and Awards
Delbrück Fellowship Award (MDC Berlin)
2002
Publication Highlights
Complete list of publication2022 Science Advances
Modulation of pre-mRNA structure by hnRNP proteins regulates alternative splicing of MALT1.
2021 Science Immunology
TRAF6 prevents fatal inflammation by homeostatic suppression of MALT1 protease.