Damage to the DNA in our cells can have detrimental consequences. Luckily, most lesions are dealt with by the cellular DNA repair pathways. However, DNA repair pathways are not always accurate and, even worse, might introduce mutations (changes in the DNA code). Here the research of the Bergink lab starts.
Genome instability influencing protein quality control;
Protein quality control influencing DNA repair
- Heat shock proteins as potential targets for protective strategies in neurodegeneration. Kampinga HH, Bergink S. Lancet Neurol. 2016 Jun;15(7):748-59. (pdf)
- DNAJs:more than substrate delivery to HSPA. Dekker SL, Kampinga HH, Bergink S. Front Mol Biosci. 2015 June;2, 35 (pdf)
- Role of Cdc48/p97 as a SUMO-targeted segregase curbing Rad51-Rad52 interaction. Bergink S, Ammon T, Kern M, Schermelleh L, Leonhardt H, Jentsch S. Nat Cell Biol. 2013 May;15(5):526-32. (pdf)
- Principles of ubiquitin and SUMO modifications in DNA repair. Bergink, S., and Jentsch, S. Nature. 2009 Mar 26;458(7237):461-7 (pdf)
- The S/T-rich motif in the DNAJB6 chaperone delays polyglutamine aggregation and the onset of disease in a mouse model. Kakkar V., Månsson C., de Mattos E.P., Bergink S., van der Zwaag M., van Waarde M.A.W.H., Kloosterhuis N.J., Melki R., van Cruchten R.T.P., 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. Mol Cell. 2016 Apr 12 (pdf)
- DNA damage triggers nucleotide excision repair-dependent monoubiquitylation of histone H2A. Bergink, S., Salomons, F.A., Hoogstraten, D., Groothuis, T.A.M., de Waard, H., Wu, J., Yuan, L., Citterio, E., Houtsmuller, A.B., Neefjes, J., Hoeijmakers J.H.J., Vermeulen W., Dantuma N.P. Genes Dev. 2006 May 15;20(10):1343-52. (pdf)
- Recognition of DNA damage by XPC coincides with disruption of the XPC-RAD23 complex. Bergink S., Toussaint W., Luijsterburg M.S., Dinant C., Alekseev S., Hoeijmakers J.H.J., Dantuma N.P., outsmuller A.B., Vermeulen W. J Cell Biol. 2012 Mar 19;196(6):681-8. (pdf)
- Erythropoietic defect associated with reduced cell proliferation in mice lacking the 26S proteasome shuttling factor Rad23b. Bergink S*, Theil AF*, Toussaint W*, De Cuyper IM, Kulu DI, Clapes T, van der Linden R, Demmers JA, Mul EP, van Alphen FP, Marteijn JA, van Gent T, Maas A, Robin C, Philipsen S, Vermeulen W, Mitchell JR, Gutiérrez L. Mol Cell Biol. 2013 Oct;33(19):3879-92 (pdf)
- Versatile DNA damage detection by the global genome nucleotide excision repair protein XPC. Hoogstraten, D., Bergink, S., Ng, J.M.Y., Verbiest, V.H.M., Luijsterburg, M.S., Geverts, B., Raams, A., Dinant, C., Hoeijmakers, J.H.J., Vermeulen, W., Houtsmuller A.B. J Cell Sci. 2008 Sep 1;121(Pt 17):2850-9 (pdf)
- A novel regulation mechanism of DNA repair by damage-induced and RAD23-dependent stabilization of xeroderma pigmentosum group C protein. Ng, J.M.Y., Vermeulen, W., van der Horst, G.T.J., Bergink, S., Sugasawa, K., Vrieling, H., and Hoeijmakers, J.H.J. Genes Dev. 2003 Jul 1;17(13):1630-45. Epub 2003 Jun 18. (pdf)
Suzanne L. Dekker
Anneke Miedema (together with P. Dijkers)
Wouter Huiting (together with E. Nollen)
Joris van der Lienden
Jean Paul Entingh
As DNA encodes for proteins, these mutations might lead to differences in proteins. Apart from these changes in protein composition, the expression level of proteins might also change, when for example the regulatory elements surrounding a gene are affected. Currently it is unclear to what extent DNA damage impacts our proteomes, or how the cellular pathways that deal with protein stress (the protein quality control pathways) respond to DNA damage. My lab investigates this link between genome instability and protein quality control.
My lab investigates this link between genome instability and protein quality control.
Steven Bergink received his MSc in Molecular Biology at the University of Groningen and his PhD at the Erasmus University Rotterdam. As a graduate student he studied the link between Nucleotide Excision Repair and the Ubiquitin Proteasome System under the supervision of Wim Vermeulen and Jan Hoeijmakers.
Following his graduation, he took a postdoctoral position in the lab of Stefan Jentsch in the Max Planck Institute of Biochemistry (Martinsried/Munich, Germany), and deciphered how the AAA-ATPase Cdc48/p97 untangles SUMOylated DNA repair proteins.
In late 2013 he became an assistant professor in the Department of Cell Biology at the UMCG. Here his work focusses on the relationship between genome instability and protein quality control.
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