KIAA1199 expression and hyaluronan degradation colocalize in multiple sclerosis lesions
Author:
Affiliation:
1. Drug Discovery Department, Halozyme Therapeutics, Inc., San Diego, CA, USA
2. F1 Oncology, West Palm Beach, FL, USA
3. Biologics21.NET Consulting, San Diego, CA, USA
Funder
Halozyme Therapeutics, Inc
Publisher
Oxford University Press (OUP)
Subject
Biochemistry
Link
http://academic.oup.com/glycob/article-pdf/28/12/958/26649416/cwy064.pdf
Reference33 articles.
1. Mutations in the gene encoding KIAA1199 protein, an inner-ear protein expressed in Deiters’ cells and the fibrocytes, as the cause of nonsyndromic hearing loss;Abe;J Hum Genet,2003
2. Hyaluronan deficiency due to Has3 knock-out causes altered neuronal activity and seizures via reduction in brain extracellular space;Arranz;J Neurosci,2014
3. Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation;Back;Nat Med,2005
4. Temporal oligodendrocyte lineage progression: In vitro models of proliferation, differentiation and myelination;Barateiro;Biochim Biophys Acta,2014
5. Cutting edge: High molecular weight hyaluronan promotes the suppressive effects of CD4+CD25+ regulatory T cells;Bollyky;J Immunol,2007
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