Biography Ditte Lundvig

2004:   M.Sc. in Molecular Biology, University of Aarhus, Aarhus, Denmark
2007:   PhD in Medicine, University of Aarhus, Aarhus, Denmark
2008:   Postdoctoral Fellow, Department of Neuromedical Genetics, The Netherlands Institute for Neuroscience (NIN), Royal Netherlands Academy of Arts and Sciences (KNAW), Amsterdam, The Netherlands

Publications Ditte Lundvig

Kleinnijenhuis AJ, Hedegaard C, Lundvig D, Sundbye S, Issinger OG, Jensen ON, Jensen PH. Identification of multiple post-translational modifications in the porcine brain specific p25alpha. J Neurochem. 2008 Jul;106(2):925-33.

 

Song YJ, Lundvig DM, Huang Y, Gai WP, Blumbergs PC, Højrup P, Otzen D, Halliday GM, Jensen PH. p25alpha relocalizes in oligodendroglia from myelin to cytoplasmic inclusions in multiple system atrophy. Am J Pathol. 2007 Oct;171(4):1291-303.

 

Skjoerringe T, Lundvig DM, Jensen PH, Moos T. P25alpha/Tubulin polymerization promoting protein expression by myelinating oligodendrocytes of the developing rat brain. J Neurochem. 2006 Oct;99(1):333-42.

 

Otzen DE, Lundvig DM, Wimmer R, Nielsen LH, Pedersen JR, Jensen PH. p25alpha is flexible but natively folded and binds tubulin with oligomeric stoichiometry. Protein Sci. 2005 Jun;14(6):1396-409.

 

Lundvig D, Lindersson E, Jensen PH. Pathogenic effects of alpha-synuclein aggregation. Brain Res Mol Brain Res. 2005 Mar 24;134(1):3-17. Review.

 

Lindersson E, Lundvig D, Petersen C, Madsen P, Nyengaard JR, Højrup P, Moos T, Otzen D, Gai WP, Blumbergs PC, Jensen PH. p25alpha Stimulates alpha-synuclein aggregation and is co-localized with aggregated alpha-synuclein in alpha-synucleinopathies. J Biol Chem. 2005 Feb 18;280(7):5703-15.

 

Personal Interests

During my PhD and master studies I worked in the field of neurodegeneration that is caused by protein aggregation. In the course of this work I familiarized myself with a wide range of classical biochemical techniques. This is now being extended with the acquirement of skills in molecular biology and transgenesis in my current project.
My present project is to generate conditional Crb3 knockout mouse models to study the function of the Crb3 members of the Crb protein family, in which the Crb1 protein is known to be involved in retinitis pigmentosa and Leber congenital amarousis. In mouse and man, two Crb3 transcripts are generated by alternative splicing the Crb3 gene, resulting in the expression of two proteins with distinct intracellular parts that could assign novel functions to this group of Crb proteins and thus contribute to the dissection of the underlying molecular pathology of the Crumbs (Crb1)-related eye disorders.