Rearrangements of the intermediate filament GFAP in primary human schwannoma cells.

摘要: Loss of the tumor suppressor protein merlin causes a variety benign tumors such as schwannomas, meningiomas, and gliomas in man. We previously reported primary human schwannoma cells to show enhanced integrin-dependent adhesion hyperactivation small RhoGTPase Rac1. Here we that main intermediate filament Schwann cells, glial fibrillary acidic protein, is collapsed perinuclear region instead being well-spread from nucleus cell periphery. This cytoskeletal reorganization accompanied by changes shape increased motility. Moreover, report tyrosine phosphorylation be already described earlier breakdown. Thus, believe Rac activation via kinase stimulation leads GFAP collapse suggest this process plays an important role vivo where become motile, unspecifically ensheathing extracellular matrix forming pseudomesaxons.