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101.
Paul C. Letourneau Florence K. Roche Terri A. Shattuck Vance Lemmon Masatoshi Takeichi 《Developmental neurobiology》1991,22(7):707-720
During embryogenesis, Schwann cells interact with axons and other Schwann cells, as they migrate, ensheath axons, and participate in organizing peripheral nervous tissues. The experiments reported here indicate that the calcium-dependent molecule, N-cadherin, mediates adhesion of Schwann cells to neurites and to other Schwann cells. Cell cultures from chick dorsal root ganglia and sciatic nerves were maintained in media containing either 2mM Ca++ or 0.2 mM Ca++, a concentration that inactivates calcium-dependent cadherins. When the leading lamellae of Schwann cells encountered migrating growth cones in medium with 2 mM Ca++, they usually remained extended, and the growth cones often advanced onto the Schwann cell upper surface. In the low Ca++ medium, the frequency of withdrawal of the Schwann cell lamella after contact with a growth cone was much greater, and withdrawal was the most common reaction to growth cone contact in medium with 2 mM Ca++ and anti-N-cadherin. Similarly, when motile leading margins of two Schwann cells touched in normal Ca++ medium, they often formed stable areas of contact. N-cadherin and vinculin were co-concentrated at these contact sites between Schwann cells. However, in low Ca++ medium or in the presence of anti-N-cadherin, interacting Schwann cells usually pulled away from each other in a behavior reminiscent of contact inhibition between fibroblasts. In cultures of dissociated cells in normal media, Schwann cells frequently were aligned along neurites, and ultrastructural examination showed extensive close apposition between plasma membranes of neurites and Schwann cells. When dorsal root ganglia explants were cultured with normal Ca++, Schwann cells migrated away from the explants in close association with extending neurites. All these interactions were disrupted in media with 0.2 mM Ca++. Alignment of Schwann cells along neurites was infrequent, as were extended close apposition between axonal and Schwann cell plasma membranes. Finally, migration of Schwann cells from ganglionic explants was reduced by disruption of adhesive contact with neurites. The addition of antibodies against N-cadherin to medium with normal Ca++ levels had similar effects as lowering the Ca++ concentration, but antibodies against the neuronal adhesive molecule, L1, had no effects on interactions between Schwann cells and neurites. 相似文献
102.
Neural cell recognition molecule F11: homology with fibronectin type III and immunoglobulin type C domains 总被引:27,自引:0,他引:27
We report here the complete cDNA sequence of F11 130 kd polypeptide, a chick neural cell surface-associated glycoprotein implicated in neurite fasciculation and elongation. The predicted protein sequence of 1010 amino acids includes an amino-terminal signal peptide and a carboxy-terminal hydrophobic stretch, which is compatible with the consensus motif for covalent attachment of glycosyl-phosphatidylinositol. Accordingly, F11 lacks an intracellular domain, which is consistent with evidence obtained from protease protection experiments on isolated microsomes. In addition, the molecule comprises six domains related to the immunoglobulin domain type C and four resembling fibronectin repeat type III. Both types of repeats resemble those present in neural cell adhesion molecules L1 and N-CAM. The possible identity of F11 with the chick neural glycoprotein contactin is discussed. 相似文献
103.
S K Juhn L Orning S Hammarstr?m P Hedqvist J Wers?ll 《Prostaglandins, leukotrienes, and essential fatty acids》1989,36(3):135-141
Following cisternal injection of [3H8]LTC4 into guinea pigs, leukotriene metabolites were identified in the brain, cerebellum, perilymph, blood, liver and kidneys. LTC4 was metabolized into LTD4 and LTE4 in the cerebrospinal fluid and LTE4 was transported into the blood for general circulation and uptake into the liver and kidneys. The excretion of LTE4 from CNS to blood seemed to be the rate-limiting step in the elimination of leukotrienes from the body. Leukotrienes were also transported into the perilymph. The conversion of LTC4 into LTD4 and LTE4 was lower in perilymph as compared to the cerebrospinal fluid, suggesting a rate limiting function of the cochlear aqueduct that can be defined as a cerebrospinal fluid-labyrinth barrier. 相似文献
104.
Surface distribution of the mannose 6-phosphate receptors in epithelial Madin-Darby canine kidney cells 总被引:8,自引:0,他引:8
We have analyzed the surface polarity of both the cation-independent (CI-MPR) and the cation-dependent (CD-MPR) mannose 6-phosphate receptors in the epithelial Madin-Darby canine kidney (MDCK) cell line grown on polycarbonate filters. The surface localization was studied by plasma membrane domain-specific surface labeling methods and by confocal microscopy using MPR-specific antibodies. The CI-MPR was shown to be exclusively present on the basolateral cell surface. In contrast, the CD-MPR was expressed neither apically nor basolaterally. However, an intracellular pool of CD-MPR could be detected. In MDCKII-RCAr cells, cell surface CI-MPR was shown to recycle between the basolateral plasma membrane and the trans-Golgi network. After exogalactosylation, cell surface CI-MPR acquired sialic acid residues in a time-dependent manner. Furthermore, the basolateral CI-MPR was shown to be functional. Lysosomal enzymes, bearing the mannose 6-phosphate recognition marker, were taken up from the basolateral medium and endocytosed into the cells. Uptake of lysosomal enzymes from the apical side was insignificant and not MPR mediated. These results extend previous immunoelectron microscopic studies on the intracellular polarity of the CI-MPR (Parton, R. G., Prydz, K., Bomsel, M., Simons, K., and Griffiths, G. (1989) J. Cell Biol. 109, 3259-3272) which showed that the CI-MPR was present in basolateral early endosomes and in late endosomes but absent from apical early endosomes. 相似文献
105.
106.
Multiple mutations of the first gene of a dimeric tRNA gene abolish in vitro tRNA gene transcription 总被引:3,自引:0,他引:3
M Nichols J Bell M S Klekamp P A Weil D S?ll 《The Journal of biological chemistry》1989,264(29):17084-17090
107.
108.
Book reviews
Improving vegetatively propagated cropsA.J. Abbott and R.K. Atkin (Eds.), London: Academic Press, 1987. xvii + 416 pages. £37.00. 0-12-041410-4 相似文献109.
The overlapping distribution of opioid and cholecystokinin (CCK) peptides and their receptors (μ and δ opioid receptors; CCK-A
and CCK-B receptors) in the central nervous system have led to a large number of studies aimed at clarifying the functional
relationships between these two neuropeptides. Most of the pharmacological studies devoted to the role of CCK and enkephalins
have been focused on the control of pain. Recently the existence of regulatory mechanisms between both systems have been proposed,
and the physiological antagonism between CCK and endogenous opioid systems has been definitely demonstrated by coadministration
of CCK-B selective antagonists with RB 101, a systemically active inhibitor, which fully protects enkephalins from their degradation.
Several studies have also been done to investigate the functional relationships between both systems in development of opioid
side-effects and in behavioral responses. This article will review the experimental pharmacology of association of enkephalin-degrading
enzyme inhibitors and CCK-B antagonists to demonstrate the interest of these molecules in the management of both pain and
opioid addiction.
Special issue dedicated to Dr. Eric J. Simon. 相似文献
110.
The mechanism(s) by which zinc is transported into cells has not been identified. Since zinc uptake is inhibited by reducing
the temperature, zinc uptake may depend on the movement of plasma membrane micoenvironments, such as endocytosis or potocytosis.
We investigated the potential role of potocytosis in cellular zinc uptake by incubating normal and acrodermatitis enteropathica
fibroblasts with nystatin, a sterol-binding drug previously shown to inhibit potocytosis. Zinc uptake was determined during
initial rates of uptake (10 min) following incubation of the fibroblasts in 50 μg nystatin/mL or 0.1% dimethyl-sulfoxide for
10 min at 37°C. The cells were then incubated with 1 to 30 μM
65zinc. Michaelis-Menten kinetics were observed for zinc uptake. Nystatin inhibited zinc uptake in both the normal and AE fibroblasts.
Reduced cellular uptake of zinc was associated with its internalization, not its external binding. In normal fibroblasts,
nystatin significantly reduced theK
m 56% and theV
max 69%. In the AE fibroblasts, nystatin treatment significantly reduced theV
max 59%, but did not significantly affect theK
m. The AE mutation alone affected theV
max for cellular zinc uptake. The control AE fibroblasts exhibited a 40% reduction inV
max compared to control normal fibroblasts. We conclude that nystatin exerts its effect on zinc uptake by reducing the velocity
at which zinc traverses the cell membrane, possibly through potocytosis. Furthermore, the AE mutation also effects zinc transport
by reducing zinc transport. 相似文献