Source:http://linkedlifedata.com/resource/pubmed/id/14648099
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2004-3-4
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pubmed:abstractText |
We used the Aplysia californica intestinal epithelium to investigate the effect of alanine-stimulated Na+ absorption on apical membrane exocytosis and whether stimulated exocytosis requires intact actin filaments. The fluid-phase marker fluorescein dextran was used to determine rates of apical membrane exocytosis. L-alanine significantly increased apical exocytosis by approximately 30% compared to controls, and there is a modest, positive correlation between alanine-stimulated exocytosis and short-circuit current (ISC). Thus, apical exocytosis is modulated to some extent by the magnitude of Na+ and alanine entry across the apical membrane. Apical exocytosis is also responsive to virtually any increase in Na+ and alanine entry because increments in alanine-stimulated ISC as small as 1 microA/cm2 stimulated exocytosis. We used D-alanine to determine which parameter (sensitivity to transport vs. magnitude of transport) was most important in activation of apical exocytosis. D-alanine-stimulated ISC was one-sixth that of L-alanine, but stimulated exocytosis was only 29% less than that of L-alanine. Therefore, the apical exocytic system is more responsive to small increases in transport than to the magnitude of transport. Latrunculin A (Lat-A) disrupts the actin cytoskeleton and reduced constitutive apical exocytosis by approximately 65% and completely abolished alanine-stimulated exocytosis. Hence, constitutive exocytosis and alanine-stimulated exocytosis require actin filaments for recruitment of vesicles to the apical membrane. During nutrient absorption, actin filament-regulated apical exocytosis may represent a negative feedback system that modulates apical membrane tension.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Alanine,
http://linkedlifedata.com/resource/pubmed/chemical/Dextrans,
http://linkedlifedata.com/resource/pubmed/chemical/Fluoresceins,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/fluorescein-dextran
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0174-1578
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
129-38
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pubmed:dateRevised |
2009-6-8
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pubmed:meshHeading |
pubmed-meshheading:14648099-Actins,
pubmed-meshheading:14648099-Alanine,
pubmed-meshheading:14648099-Animals,
pubmed-meshheading:14648099-Aplysia,
pubmed-meshheading:14648099-Dextrans,
pubmed-meshheading:14648099-Enterocytes,
pubmed-meshheading:14648099-Exocytosis,
pubmed-meshheading:14648099-Fluoresceins,
pubmed-meshheading:14648099-Fluorescent Dyes,
pubmed-meshheading:14648099-Ion Transport,
pubmed-meshheading:14648099-Sodium
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pubmed:year |
2004
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pubmed:articleTitle |
Alanine-stimulated exocytosis in Aplysia enterocytes: effect of Na+ transport and requirement for actin filaments.
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pubmed:affiliation |
Department of Biology, University of Central Arkansas, Conway, AR 72035-5003, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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