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Fifty years have passed since the discovery of glial fibrillary acidic protein (GFAP) by Lawrence Eng and colleagues. Now recognized as a member of the intermediate filament family of proteins, it has become a subject for study in fields as diverse as structural biology, cell biology, gene expression, basic neuroscience, clinical genetics and gene ...
Albee Messing
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Properties of astrocytes cultured from GFAP over-expressing and GFAP mutant mice [PDF]
Alexander disease is a fatal leukoencephalopathy caused by dominantly-acting coding mutations in GFAP. Previous work has also implicated elevations in absolute levels of GFAP as central to the pathogenesis of the disease. However, identification of the critical astrocyte functions that are compromised by mis-expression of GFAP has not yet been possible.
Albee Messing
exaly +3 more sources
Role of GFAP in CNS injuries [PDF]
The role of GFAP in CNS injury is reviewed as revealed by studies using GFAP null mice. In order to provide background information for these studies, the effects of absence of GFAP in the uninjured astrocyte are also described. Activities attributable to GFAP include suppressing neuronal proliferation and neurite extension in the mature brain, forming ...
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Progress in Neurobiology, 2011
Glial fibrillary acidic protein (GFAP) is the main intermediate filament protein in mature astrocytes, but also an important component of the cytoskeleton in astrocytes during development. Major recent developments in astrocyte biology and the discovery of novel intermediate filament functions enticed the interest in the function of GFAP. The discovery
Middeldorp, J., Hol, E.M.
openaire +2 more sources
Glial fibrillary acidic protein (GFAP) is the main intermediate filament protein in mature astrocytes, but also an important component of the cytoskeleton in astrocytes during development. Major recent developments in astrocyte biology and the discovery of novel intermediate filament functions enticed the interest in the function of GFAP. The discovery
Middeldorp, J., Hol, E.M.
openaire +2 more sources

