| pubmed-article:1348148 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1348148 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:1348148 | lifeskim:mentions | umls-concept:C0034850 | lld:lifeskim |
| pubmed-article:1348148 | lifeskim:mentions | umls-concept:C0752348 | lld:lifeskim |
| pubmed-article:1348148 | lifeskim:mentions | umls-concept:C0332466 | lld:lifeskim |
| pubmed-article:1348148 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:1348148 | pubmed:issue | 5052 | lld:pubmed |
| pubmed-article:1348148 | pubmed:dateCreated | 1992-4-30 | lld:pubmed |
| pubmed-article:1348148 | pubmed:abstractText | Guanosine triphosphate (GTP)-binding proteins are required for intracellular vesicular transport. Mastoparan is a peptide component of wasp venom that increases nucleotide exchange in some classes of G alpha subunits of regulatory heterotrimeric GTP-binding proteins (G proteins). Mastoparan and other compounds that increase nucleotide exchange by G proteins inhibited endosome fusion in vitro and reversed the effects of guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S), a nonhydrolyzable GTP analog. Addition of beta gamma subunits of G proteins to the fusion assay antagonized the stimulatory effect of GTP-gamma-S, confirming the participation of G proteins. These results indicate that GTP-binding proteins are required for endosome fusion and in particular that a G protein is involved. Given the function of G proteins in signal transduction, these findings may provide insight into the mechanism by which endosomal vesicles become competent for fusion after their formation at the cell surface. | lld:pubmed |
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| pubmed-article:1348148 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:1348148 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1348148 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1348148 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:1348148 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:1348148 | pubmed:author | pubmed-author:StahlP DPD | lld:pubmed |
| pubmed-article:1348148 | pubmed:author | pubmed-author:CaseyP JPJ | lld:pubmed |
| pubmed-article:1348148 | pubmed:author | pubmed-author:MayorgaL SLS | lld:pubmed |
| pubmed-article:1348148 | pubmed:author | pubmed-author:ColomboM IMI | lld:pubmed |
| pubmed-article:1348148 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1348148 | pubmed:day | 27 | lld:pubmed |
| pubmed-article:1348148 | pubmed:volume | 255 | lld:pubmed |
| pubmed-article:1348148 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1348148 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1348148 | pubmed:pagination | 1695-7 | lld:pubmed |
| pubmed-article:1348148 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:1348148 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1348148 | pubmed:articleTitle | Evidence of a role for heterotrimeric GTP-binding proteins in endosome fusion. | lld:pubmed |
| pubmed-article:1348148 | pubmed:affiliation | Department of Cell Biology and Physiology, Washington University, School of Medicine, St. Louis, MO 63110. | lld:pubmed |
| pubmed-article:1348148 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1348148 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1348148 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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