University Medical Center Utrecht
Room KC.03.139.2
Lundlaan 6
3584 EA Utrecht
The Netherlands
phone: 088 - 75 542 58
e-mail:
E.Kalkhoven@umcutrecht.nl Date and place of birth: 15 August 1967, Eindhoven
Scientific education 1985-1991:
Biology degree, Utrecht University. Research projects Molecular Cell Biology (Dr. P.J. Rijken) and Developmental Biology (Dr. F. Meijlink).
Research experience May 1991-Sept 1995
phD project entitled "Progestin action in human breast tumor cells"at the Hubrecht Laboratory, Utrecht. Promotor Prof. Dr. S.W. de Laat, co-promotors Dr. B. van der Burg and Dr. P.T. van der Saag.
Oct 1995-Nov 1997
Post-doctoral fellow, Imperial Cancer Research Fund, London. Molecular Endocrinology Laboratory headed by Dr. M.G. Parker.
Dec 1997-Dec 2001
Post-doctoral fellow, LUMC, Leiden. Department of Molecular Cell Biology initially headed by Prof. Dr. A.J. van der Eb, later succeeded by Prof. Dr. C.P. Verrijzer.
Jan 2002-July 2003
KNAW research fellow, LUMC, Leiden. Department of Molecular Cell Biology headed by Prof. Dr. C.P. Verrijzer.
Aug 2003-present
KNAW research fellow and staff member, UMC Utrecht. Department of Metabolic and Endocrine Diseases headed by Prof. R. Berger.
Since the start of his PhD project Dr. Kalkhoven has been interested in signalling through nuclear hormone receptors. His research activities have focussed on the structure and function of several members of this transcription factor superfamily (PR, ER, PPAR) and their associated coactivator proteins (SRC1, CBP/p300).
During his PhD project (Hubrecht laboratory, Utrecht) he investigated the mechanism of growth inhibition of human breast cancer cells by the steroid hormone progesterone and the role of TGF-ƒÒ in this process. In addition, a study on the mechanism of transcriptional interference between the progesterone receptor and the transcription factor NFƒÛ-B was performed. After finishing his PhD he went to the ICRF (London) to work in the laboratory of Dr. M.G. Parker on nuclear receptor coactivators, a class of proteins that interacts with hormone-activated receptors and is required to elicit a transcriptional response. Besides studies on various estrogen receptor mutants, he studied the structure-function relationships between two different isoforms of the coactivator SRC1. He was also involved in the discovery of the LXXLL motif in coactivators, which is required for nuclear receptor binding. After that he went to the LUMC (Leiden) to work on the function of the coactivators CBP and p300 in the laboratory of Dr. A. Zantema and Prof. Dr. A.J. van der Eb, who was succeeded by Prof. C.P Verrijzer in that period. CBP and p300 are two related coactivators that harbour the ability to acetylate histones, which is regarded as an important step in transcription regulation. Mutational analysis of a PHD-type zinc finger in CBP revealed that this region is indispensable for its acetyltransferase activity. In collaboration with the Department of Human Genetics he found that PHD finger mutations that abolish the acetyltransferase activity of CBP are sufficient to cause Rubinstein-Taybi syndrome, a congenital developmental disorder. He was also involved in studies on the activation of the collagenase promoter and the role of CBP and p300 therein.
In August 2003 Eric Kalkhoven moved to the Department of Metabolic and Endocrine Diseases to start in new line of research into gene regulation during adipocyte differentiation (adipogenesis). His research focuses on the role of acetyltransferases in adipogenesis (PhD student Olivier van Beekum) and the function of several key transcription factors, including the nuclear hormone receptors PPAR-gamma and -delta, in this differentiation process (PhD student vacancy).