1995 Habilitation in Molecular Biology and Genetics, University of Freiburg, Germany

1985 PhD in Natural Sciences 1985, University of Heidelberg, Germany

Constanze Bonifer studied Biology at the University of Cologne, Germany and graduated 1980 with a first class degree in Biochemistry, Chemistry and Genetics. She then went on to do a PhD in Biochemistry and Molecular Biology, first at the University of Cologne, then at the Centre for Molecular Biology, University of Heidelberg.

This was followed by Postdoctoral training periods at the Karolinska Institute, Stockholm, and the National Institute for Medical Research in London where she started to work on gene regulation. 

1990 she became Assistant Professor and independent group leader at University of Freiburg, Germany, where she worked on gene regulation in the hematopoietic system. 

1997 she went back to the UK and became a group leader at the Molecular Medicine Unit, University of Leeds, where she started to work not only on basic mechanisms controlling blood cell development, but also on epigenetic mechanisms controlling leukemogenesis.

She became a Reader in 2000, a Professor in 2003 and in 2004 became a full Professor and Chair of Experimental Haematology. In 2006 she was appointed Head of Section of Expeirmental Haematology at the Leeds Institute of Molecular Medicine. 

Since August 2011, Constanze is in Birmingham as Chair of Experimental Haematology at the Institute of Biomedical Research. 

Professor Bonifer has only recently moved to the University of Birmingham and has not yet taken up teaching responsibilities.

Constanze has currently two PhD students and is interested in supervising doctoral research in the following areas:

• Basic mechanisms controlling blood cell development
• Molecular mechanisms regulating aberrant gene regulation in leukaemia

For currently advertised studentships visit:

http://www.medicine.bham.ac.uk/pg/grad/Studentships_0910.shtml

The main research interest of the Bonifer lab is to study the mechanism of cell fate decisions at the epigenetic level. All blood cells arise from pluripotent stem cells of the bone marrow and develop via different types of precursor cells, which become progressively committed to the different branches of the blood cell system. 

A number of diseases such as leukaemia affect blood cell development, an understanding of the molecular basis of hematopoietic cell differentiation is therefore of utmost importance for the development of new therapeutic strategies. 

We want to understand how different genetic programs are activated and silenced at specific stages of hematopoiesis and which factors are involved in this process. 

Nature Medicine Podcast (May 2010) 

Member of the Genetics Society, the International Society of Experimental Haematology and the  BBSRC Pool of Experts.

Member on the Leukemia and Lymphoma Career Development Panel.

Serves on the editorial board of Experimental Hematology and Stem Cell Research.

Leddin, M., Perrod, C. , Hoogenkamp, M., Ghani, S., Ass, S., Heinz,S., Wilson, N.K., Follows, G., Schönheit,J., Vockentanz,L., Mosamam,A., Chen, W., Tenen, D.G., Westhead, D.R., Göttgens, B., Bonifer, C*. and Rosenbauer, F*. (2011) (*joint corr. authors). Two distinct auto-regulatory loops operate at the Pu.1 locus in B cells and myeloid cells. Blood 117(10):2827-38

Lamprecht, B., Walter, K., Kreher, S., Kumar, R., Hummel, M., Lenze, D., Köchert, K., Bouhlel, M.A., Richter, J., Soler, E., Stadhouders, R., Jöhrens, C., Wurster, K.D., Callen, C., Harte, M.F., Giefing, M., Barlow, R., Stein, H., Anagnostopoulos, I., Janz, M., Cockerill, P.N., Siebert, R., Dörken, B., Bonifer, C.*, and Mathas, S.* (2010). (*Joint corresponding authors). De–repression of an endogenous long terminal repeat activates the CSF1R proto–oncogene in human lymphoma. Nature Medicine. 16, 571 – 579

Hoogenkamp, H.; Lichtinger, M.; Krysinska, H.; Lancrin, C.; Clarke, D.; Williamson, A.; Mazzarella,L.; Ingram, R.; H. Jorgensen, A. Fisher, D,G. Tenen, Kouskoff, V.; G.Lacaud, and C.Bonifer (2009). Early chromatin unfolding by Runx1 - a molecular explanation for differential requirements during specification versus maintenance of the hematopoietic gene expression program. Blood 114; 299-309. 

Barton, J.L.; Bunka, D.H.J.; Knowling, S.E., Lefevre, P., Warren, A.l, Bonifer, C. and Stockley, P.G. (2009). Isolation and characterization of RNA-aptamers that disrupt the binding of the RUNX1-CBF complex to DNA. Nucleic Acids Res. 37, 6818 - 6830

Lefevre, P., Lacroix, C., Witham, J.,Cockerill, P.N. and Bonifer, C (2008). The LPS-induced transcriptional upregulation of the chicken lysozyme locus involves CTCF eviction and non-coding RNA transcription. Molecular Cell 32, 129 – 139

Ebralidze, A., Guibal, Steidel, U., Zhang, P., Lee, S., Rosenbauer, F., Huang, G., Petkova, V., Dayaram, T., Klupp, J., Hoogenkamp, M., Bonifer, C.*, Tenen, D.G.* (.* joint last authors ). 2008. PU.1 expression is modulated by the balance of functional sense and antisense RNAs regulated by a shared cis-regulatory element. Genes & Development. 22, 2085-2092

M.Hoogenkamp, A. Krysinska, R.Ingram, G. Huang, R. Barlow, D. Clarke, A. Ebralidze, P. Zhang, H. Tagoh, P. Cockerill, D.G.Tenen and C.Bonifer. (2007). The Pu.1 locus is differentially regulated at the level of chromatin structure and non-coding transcription by alternate mechanisms at distinct developmental stages of hematopoiesis. Mol. Cell. Biol. 27, 7425 – 7438

Krysinska, H., Hoogenkamp, M., Ingram, R., Wilson, N., Tagoh, H., Laslo, P., Singh, H. and Bonifer, C. (2007). A two-step, PU.1 dependent, mechanism for developmentally regulated chromatin remodelling and transcription of the c-fms gene. Mol. Cell. Biol.: 27:878-87