Characterization of mouse tGolgin-1 (golgin-245/trans-golgi p230/256 kD golgin) and its upregulation during oligodendrocyte development
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Updated: Sep 30, 2026

Rapid and Specific Immunomagnetic Isolation of Mouse Primary Oligodendrocytes
Published on: May 21, 2018
David A Cowan1, Denise Gay, Bert M Bieler
1Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6082, USA.
Abstract:
As part of an effort to identify gene products that are differentially regulated during oligodendrocyte development, we isolated a mouse cDNA that encodes tGolgin-1, a homolog of the human protein known as golgin-245, trans-golgi p230, or 256 kD golgin. Human tGolgin-1 is the target of autoantibodies in patients with Sjögren's syndrome, and is thought to be involved in vesicular transport processes at the trans-Golgi network. Sequencing of cDNAs and EST clones comprising the full-length tGolgin-1 transcript predict marked homology with the amino- and carboxy-terminal regions of the human protein, but more limited homology within the central predicted coiled-coil region. Epitope tagged, truncated forms of mouse tGolgin-1, like those of its human homolog, were localized at steady state to the Golgi/trans-Golgi network in transfected cells. The tGolgin-1 message was expressed in all tissues examined, but was highly upregulated in oligodendrocyte precursors at a stage just prior to myelination. This expression pattern suggests that tGolgin-1 may play a role in specialized transport processes associated with maturation and/or differentiation of oligodendrocyte precursors.

