Axel Behrens

Adult Stem Cell Laboratory

Every organ harbours adult stem cells which have the potential for long-term replication, together with the capacities of self-renewal and multi-lineage differentiation. These stem cells function in tissue homeostasis and contribute to regeneration in response to injury. In addition, many cancers are caused by transforming mutations occurring in tissue-specific progenitor cells. Our major focus is to elucidate the molecular mechanisms governing stem cell function. As well as studying tumour development using murine genetic models, we are now also applying our knowledge of stem cells and cellular differentiation mechanisms to diabetes.

Figure 1

Figure 1: Overview of stem cell function. Stem cells have the capacity to self-renew and to give rise to specialised cell types. The balance between proliferation and differentiation is crucial for the development and maintenance of a functional tissue. In most organs, stem cells are responsible for replacing differentiated cells that are lost during ageing, and stem cells also help repair damaged tissue. Oncogenic mutations in stem cells are a common cause of cancer. However, given an appropriate stimulus, differentiated cells may transdifferentiate into a distinct fate, or reprogram to a more stem-like tumour-initiating cell.

Selected publications

Behrens A, van Deursen JM, Rudolph KL, Schumacher B. Impact of genomic damage and ageing on stem cell functionNat Cell Biol. 2014; 16 (3): 201-7 

Diefenbacher ME, Popov N, Blake SM, Schülein-Völk C, Nye E, Spencer-Dene B, Jaenicke LA, Eilers M, Behrens A. The deubiquitinase Usp28 controls intestinal homeostasis and promotes colorectal cancer. Journal of Clinical Investigation.  2014; 124(8):3407-18 

Sancho R, Gruber R, Gu G, Behrens A. Loss of Fbw7 reprograms adult pancreatic ductal cells into α, δ, and β cellsCell Stem Cell. 2014;15(2):139-53 

Zhang T, Cronshaw J, Kanu N, Snijders AP and Behrens A. UBR5-mediated ubiquitination of ATMIN is required for IR-induced ATM signaling and functionProc Natl Acad Sci USA. 2014;111(33):12091-6 

Davies CC, Chakraborty A, Diefenbacher ME, Skehel M, Behrens A.  Arginine methylation of the c-Jun co-activator RACO-1 is required for c-Jun/AP-1 activationEMBO J. 2013:32(11):1556-67 

Sancho R, Blake SM, Tendeng C, Clurman BE, Lewis J, Behrens A. Fbw7 repression by hes5 creates a feedback loop that modulates notch-mediated intestinal and neural stem cell fate decisionsPLoS Biol. 2013;11(6):e1001586 

Fontana X, Hristova M, Da Costa C, Patodia S, Thei L, Makwana M, Spencer-Dene B, Latouche M, Mirsky R, Jessen KR, Klein R, Raivich G, Behrens A. c-Jun in Schwann cells promotes axonal regeneration and motoneuron survival via paracrine signalingJ Cell Biol. 2012;198(1):127-41 

Aguilera C, Nakagawa K, Sancho R, Chakraborty A, Hendrich B, Behrens A. c-Jun N-terminal phosphorylation antagonises recruitment of the Mbd3/NuRD repressor complexNature. 2011;469(7329):231-5 

Loizou JI, Sancho R, Kanu N, Bolland DJ, Yang F, Rada C, Corcoran AE, Behrens A. ATMIN is required for maintenance of genomic stability and suppression of B cell lymphomaCancer Cell. 2011;19(5):587-600 

Davies CC, Chakraborty A, Cipriani F, Haigh K, Haigh JJ, Behrens A. Identification of a co-activator that links growth factor signalling to c-Jun/AP-1 activationNat Cell Biol. 2010;12(10):963-72 

Hoeck JD, Jandke A, Blake SM, Nye E, Spencer-Dene B, Brandner S, Behrens A. Fbw7 controls neural stem cell differentiation and progenitor apoptosis by antagonising Notch and JNK/c-Jun signallingNature Neuroscience. 2010;13(11):1365-72 

Axel Behrens
+44 (0)20 379 61194

  • Qualifications and history
  • 1998 PhD in Biology, Institute of Molecular Pathology, Austria
  • 1998 Postdoctoral Fellow, Institute of Molecular Pathology, Austria
  • 1999 Postdoctoral Fellow, Institute of Neuropathology, Switzerland
  • 2001 Established lab at the Imperial Cancer Research Fund, UK (in 2002 the Imperial Cancer Research Fund became Cancer Research UK)
  • 2015 Group Leader, the Francis Crick Institute, London, UK