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Publication : Normal CNS myelination in transgenic mice overexpressing MHC class I H-2L(d) in oligodendrocytes.

First Author  Fuss B Year  2001
Journal  Mol Cell Neurosci Volume  18
Issue  2 Pages  221-34
PubMed ID  11520182 Mgi Jnum  J:71481
Mgi Id  MGI:2150222 Doi  10.1006/mcne.2001.1011
Citation  Fuss B, et al. (2001) Normal cns myelination in transgenic mice overexpressing mhc class i h-2l(d) in oligodendrocytes. Mol Cell Neurosci 18(2):221-34
abstractText  In demyelinating diseases, such as multiple sclerosis, an upregulation of MHC class I expression is thought to contribute to oligodendrocyte/myelin damage. In order to investigate potential physiological consequences of upregulated MHC class I expression in oligodendrocytes, we generated transgenic mice that overexpress H-2L(d) under the control of the proteolipid protein (PLP) promoter (PLP-L(d) mice). We focused our studies on the MHC class I molecule H-2L(d), because of its unique intracellular transport characteristics. In the CNS of PLP-L(d) mice, H-2L(d) was expressed by oligodendrocytes. Furthermore, H-2L(d) protein was transported to and expressed on the surface of oligodendrocytes. Most importantly, this upregulation of MHC class I expression in the CNS of PLP-L(d) mice did not by itself result in a de- or dysmyelinating phenotype. These transgenic mice are likely to provide a unique and novel tool for the analysis of potential roles of MHC class I-mediated mechanisms in demyelinating pathologies. Copyright 2001 Academic Press.
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