Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The MOCH-1 glial cell line, which was derived from a glioblastoma taken from the brain of a MBP/c-neu transgenic mouse, was used as a model for studying the plastic nature of gliomas in culture. Fifteen MOCH-1 clones were derived and characterized under different growth conditions via Western blot analysis and immunocytochemical staining using a panel of antibodies specific for major myelin markers and glial fibrillary acidic protein. In low serum conditions, the clones resemble immature oligodendrocytes and express only immature oligodendrocyte markers. When placed in serum-free chemically defined medium (CDM), nine clones do not change their phenotypes, while five variably express myelin markers. One clone, 4C8, differentiates into mature, membrane sheet-bearing oligodendrocyte-like cells and expresses major myelin markers in amounts and distributions similar to cultured primary oligodendrocytes. Our data show that 4C8 can reversibly switch from an oligodendrocyte-like phenotype to a reactive astrocyte-like phenotype, depending upon the presence of serum and other factors in different growth media. Our data indicate that serum "pushes" 4C8 into the astrocyte-like phenotype, while serum-free CDM "pushes" 4C8 into the oligodendrocyte-like phenotype. Furthermore, a population of mixed phenotypes results when the astrocyte-like 4C8 cells are placed in serum-free CDM. To our knowledge, this is the first report to show that by altering environment, a "mixed glioma" can arise from a homogeneous population of glial tumor cells. It is therefore possible that glial tumor cells in vivo may be induced to undergo similar phenotypic changes when they are exposed to different environmental signals in the central nervous system.
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PMID:A clone of the MOCH-1 glial tumor in culture: multiple phenotypes expressed under different environmental conditions. 759 58

Oligodendrocyte precursor cells (OPCs) differentiate during postnatal development into myelin-forming oligodendrocytes, in a process distinguished by substantial changes in morphology and the onset of myelin gene expression. A mammalian-specific CNS myelin gene, tmem10, also called Opalin, encodes a type 1 transmembrane protein that is highly upregulated during early stages of OPC differentiation; however, a function for TMEM10 has not yet been identified. Here, consistent with previous studies, we detect TMEM10 protein in mouse brain beginning at ~P10 and show that protein levels continue to increase as oligodendrocytes differentiate and myelinate axons in vivo. We show that constitutive TMEM10 overexpression in the Oli-neu oligodendroglial cell line promotes the expression of the myelin-associated genes MAG, CNP and CGT, whereas TMEM10 knock down in primary OPCs reduces CNP mRNA expression and decreases the percentage of MBP-positive oligodendrocytes that differentiate in vitro. Ectopic TMEM10 expression evokes an increase in process extension and branching, and blocking endogenous TMEM10 expression results in oligodendrocytes with abnormal cell morphology. These findings may have implications for human demyelinating disorders, as oligodendrocytes expressing TMEM10 are detected in human remyelinating multiple sclerosis lesions. Together, our findings provide evidence that TMEM10 promotes oligodendrocyte terminal differentiation and may represent a novel target to promote remyelination in demyelinating disorders.
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PMID:TMEM10 Promotes Oligodendrocyte Differentiation and is Expressed by Oligodendrocytes in Human Remyelinating Multiple Sclerosis Plaques. 3083 46