Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.4.4 (kinesin)
 5,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neisseria gonorrhoeae interact with polarized T84 epithelial cells by engaging carcinoembryonic antigen-related cellular adhesion molecule (CEACAM) receptors. Adherent bacteria that are taken up by the cells are able to traverse the epithelial layer from the apical to the basal side. Herein, we demonstrate that the actin cytoskeleton of the cells is not required for the initial adherence of the bacteria, however, it is essential for invasion into and traversal through T84 cells. Furthermore, microtubule inhibitors blocked the traversal, but not the adherence and invasion of the bacteria. Inhibition of the motor activity of myosins reduced invasion and traversal, but not bacterial adherence. Immunofluorescence confocal laser scanning microscopy revealed the colocalization of the microtubule-based kinesin and dynein motors, and the actin-based motor myosin with adherent and intracellular gonococci. Transcytosis was reduced by blocking kinesin and myosin with specific antibodies. This underlines the importance of these motor proteins for the transcytosis of epithelial monolayers by N. gonorrhoeae.
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PMID:Cytoskeleton and motor proteins are required for the transcytosis of Neisseria gonorrhoeae through polarized epithelial cells. 1768 82

Leukocyte migration across endothelial cell borders (paracellular) and through endothelial cells (transcellular) appear to be distinct processes. During paracellular migration, membrane from a parajunctional reticulum of interconnected vesicles, the endothelial lateral border recycling compartment (LBRC), moves to surround the leukocyte in a kinesin-mediated, microtubule-dependent manner. We show that transcellular migration likewise requires targeted trafficking of LBRC membrane. We show that in addition to platelet/endothelial cell adhesion molecule (PECAM; CD31), CD99 and junctional adhesion molecule A (JAM-A), but apparently not vascular endothelial cell-specific cadherin (cadherin 5, CD144), are components of the LBRC. During transcellular migration, LBRC membrane invests the transmigrating leukocyte. Intracellular adhesion molecule 1 (ICAM-1) on the apical endothelial surface is enriched around adherent leukocytes. Depolymerization of microtubules has no effect on ICAM-1 enrichment but blocks targeted trafficking of LBRC membrane and transcellular migration by >90%. Similar to their effects on paracellular transmigration, antibodies against PECAM or CD99, but not JAM-A, block transcellular migration. We conclude that similar molecular mechanisms promote both para- and transcellular migration.
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PMID:Transcellular migration of leukocytes is mediated by the endothelial lateral border recycling compartment. 1988 95