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University Medical Center Groningen

Transgenic Mouse Clinic for Ageing Research

The mouse is one of the most useful animal models to study the biological function of proteins in living organisms. The mouse model is an established animal model to increase our knowledge on the pathophysiology of human diseases and to develop or improve treatment of these diseases. Many researchers at the UMCG are using transgenic mice to answer their research questions. To improve our sources for fundamental and biomedical research at the UMCG, we started a state-of-the-art mouse facility that will generate innovative mouse models. All techniques (recombineering, CRISPR/Cas9, ES cell culture, zygote injection) and equipment involved in the generation of new mouse models have been in implemented in our laboratory or in the animal facility (CDP Groningen).

We generate conditional knock-out (KO) mice by homologous recombination in embryonic stem (ES) cells followed by injection into blastocysts to create chimeric mice. In addition, full KO or knock-in (KI) mice can be generated by CRISPR/Cas9 technology. Transgenic mice expressing “new” proteins or protein variants can be made by different techniques, including microinjection of DNA into the pronuclei of fertilized eggs or by electroporation of ES cells followed by selection, injection into blastocysts to create eventually chimeric mice. Recently, we are using CRISPR/Cas9 technology to edit genes in somatic cells, for example in hepatocytes of living mice. Prof. Jan van Deursen (Mayo Clinic, Rochester, MN, USA) will advice our team in the different transgenic technologies.


  • Dr. Bart van de Sluis (Project leader)
  • Daphne Dekker (Technician: molecular techniques, ES cell culture)
  • Nicolette Huijkman (Technician: molecular techniques, ES cell culture)
  • Marieke Smit (Technician: mouse handeling, microinjection)
  • Niels Kloosterhuis (Technician: mouse handeling, microinjection)
  • Prof. Jan van Deursen (Advisor)

Published genetically engineered mouse models (GEMMs)

  • Riedlinger T, Dommerholt MB, Wijshake T, Kruit JK, Huijkman N, Dekker D,Koster M, Kloosterhuis N, Koonen DPY, de Bruin A, Baker D, Hofker MH, van Deursen J, Jonker JW, Schmitz ML, van de Sluis B. NF-kB p65 serine 467 phosphorylation sensitizes mice to weight gain and TNF-a or diet-induced inflammation. Biochim Biophys Acta. 2017 Jul 16. pii: S0167-4889(17)30191-X. [PubMed]
  • Booij HG., Yu H., de Boer RA., van de Kolk CW., van de Sluis B., van Deursen JM., Van Gilst WH., Silje HH., Westerbrink RD. (2016) Overexpression of A kinase interacting protein 1 attenuates myocardial ischaemia/reperfusion injury but does not influence heart failure development. Cardiovasc. Res., 111, 217-26. [PubMed]
  • Kakkar V., Månsson C., de Mattos E., Bergink S., van der Zwaag M., van Waarde M.A.W.H., Kloosterhuis N.J., Melki R., van Cruchten R., Al-Karadaghi S., Arosio P., Dobson C.M., Knowles T.P.J., Bates G.P., van Deursen J., Linse S., van de Sluis B., Emanuelsson C., Kampinga H.H. (2016) The S/T-rich motif in the DNAJB6 chaperone delays polyglutamine aggregation and the onset of disease in a mouse model. Molecular Cell . April 12. Pii:S1097(16)00227-6. [PubMed]
  • Li H., Koo Y., Mao X., Sifuentes-Dominguez L., Morris L.L., Jia D., Miyata N., Faulkner R.A., van deursen J.M., Vooijs M., Billadeau D.D., van de Sluis B., Cleaver B., Burstein E. (2015) Endosomal sorting of Notch receptors through COMMD9-dependent pathways modulates Notch signalling. J. Cell Biol. 211, 605-17. [PubMed]
  • Smeets C.J., Jezierska J., Watanabe H., Duarri A., Fokkens M.R., Meijer M., Zhou Q., Yakovleva T., Boddeke E., den Dunnen W., van Deursen J., Bakalkin G., Kampinga H.H., van de Sluis B., Verbeek (2015) Elevated mutanat dynorphin A cause Purkinje cell loss and motor dysfunction in spinocerebellar ataxia type 23. Brain. 138, 2537-52. [PubMed]
  • Cannon M.V., Silke H.H., Sijbesma J.W., Vreeswijk-Bausoin I., Ciapaite J., van de Sluis B., van Deursen J., Silva G.J., de Windt L.J., Gustafsson J.A., van der Harst P., van Gilst W.H., de Boer R.A. (2015) Cardiac LXR a protects against pathological cardia hypertrophy and dysfunction by enhancing glucose uptake and utilization. EMBO Mol. Med. 7, 1229-43. [PubMed]
  • Mahmud H., Candido W.M., van Genne L., Vreeswijk-Baudoin I., Yu H., van de Sluis B., van Deursen J., van Gilst W.H., Silje H.H., de Boer R.A. (2014). Cardiac function and architecture are maintained in a model of cardiorestricted overexpression of the prorenin-renin receptor. PLoS ONE, 25;9:e89929 [PubMed]

At this moment, the following GEMMs are being characterized: 5x conditional knockout models; 4x transgenic models, 4x CRISPR-mediated knockout models, and 2x CRISPR-mediated somatic genome edited models.

Laatst gewijzigd:24 juli 2017 10:48