Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At higher doses of cytochalasin (e.g. 3 micrograms/ml for 3-20 hr), cells of the rat fibroblastoid line, Hmf, undergo extreme retraction, arborization, and subsequent rounding, and develop big cystic vacuoles. These vacuoles are always closely invested by microfilamentous masses, the CD-induced derivatives of the actin-based cytoskeleton, which aggregate in the endoplasm. Vacuolation is progressive (e.g. 12% cells at 6 hr; greater than 80% at 18 hr), related to total dose (concentration X time); and to congener (CD greater than CB). Vacuole membranes have the same dimension (85 A), surface marker 5'-nucleotidase, and junctional specializations as those found at the cell surface; they lack the membrane markers associated with endomembrane systems (e.g. AcPase, TPPase, IDPase) and are not lysosomal. Vacuoles represent internalized plasma membrane; they apparently result from retention in the endoplasm, and fusion, of pinocytotic vesicles originating at the cell surface. Vacuole membrane is always in intimate relation to the actin-based microfilament aggregates that surround the vacuoles, and actin-membrane linker proteins fodrin and vinculin are localized at the vacuole boundaries. Vacuoles and their enveloping actin-filament aggregates are surrounded by arrays of vimentin-based intermediate filaments. A new membranous compartment with characteristics of plasma membrane is thus formed within the cell under the influence of CD. Rounding brought about by other means causes no vacuolization. Macrovacuolation, like the other changes caused by CD, is completely reversible on restoration of cells to normal medium.
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PMID:Macrovacuolation induced by cytochalasin: its relation to the cytoskeleton; morphological and cytochemical observations. 643 32

The localization of proteases to cell surfaces via receptors may facilitate cell migration, invasion, and matrix degradation. Since vascular smooth muscle cell (SMC) migration may be an important event in atherosclerosis and in intimal thickening after vascular injury, we studied the cell surface expression of a receptor for urokinase-type plasminogen activator (u-PAR) in cultured human vascular SMC. Using immunofluorescence microscopy, we demonstrated several staining patterns of SMC u-PAR: at the periphery of the cell membrane, at the leading edge, and at cell-cell contact sites. When migration experiments were performed using a wound assay, one-third of the SMC at the wound edge demonstrated polarization of cell surface u-PAR toward the leading edge of the cell membrane (32 +/- 2%, +/- SEM, n = 7). A similar pattern was seen with an antibody to caveolin, a transmembrane protein found in caveolae, but not with an antibody to 5'-nucleotidase, another cell surface glycophosphatidylinositol-anchored protein, which was homogeneously expressed on the cell surface. Low-density lipoprotein receptor-related protein, which mediates internalization of u-PAR bound ligands, was distributed in a diffuse punctate pattern, not polarized to the leading edge. Double immunofluorescent studies demonstrated codistribution of SMC u-PAR with vinculin and caveolin in migrating SMC at the leading edge in a wound assay. Polarization of cell surface u-PAR was not observed in either nonwounded or subconfluent cultures, despite random migratory behavior. These studies suggest that in response to wounding, human vascular SMC polarize and concentrate cell surface u-PAR to their leading edge, perhaps facilitating directional migration.
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PMID:Migrating vascular smooth muscle cells polarize cell surface urokinase receptors after injury in vitro. 786 16