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Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells
In the search for the biochemical basis of the control of glycosylation of cell surface carbohydrates, revertant clones were isolated from previously characterized wheat germ agglutinin-resistant clones of B16 mouse melanoma cells by selection for resistance to Lotus tetragonolobus lectin or to rici...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1982
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2112079/ https://www.ncbi.nlm.nih.gov/pubmed/6895897 |
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collection | PubMed |
description | In the search for the biochemical basis of the control of glycosylation of cell surface carbohydrates, revertant clones were isolated from previously characterized wheat germ agglutinin-resistant clones of B16 mouse melanoma cells by selection for resistance to Lotus tetragonolobus lectin or to ricin. Comparison of the wheat germ agglutinin-resistant clones with the parent and revertant clones indicated that this phenotype was correlated with an increased sensitivity to the Lotus lectin, a 60- to 70-fold increase in alpha 1 leads to 3 fucosyltransferase activity and a decreased sialic acid content of the N-glycosidic chains of glycoproteins. The results suggest a novel type of control mechanism for lectin resistance, an increase in a glycosyltransferase activity. The presence of alpha 1 leads to 3 bound fucose on N-acetylglucosamine residues would interfere with the addition of sialic acid by alpha 2 leads to 3 linkages to galactose residues in the carbohydrate units, and this change could explain the resistance to wheat germ agglutinin and the increased sensitivity to the Lotus lectin. A change in a regulatory gene for the fucosyltransferase as a possible primary cause for the changed phenotype is discussed. |
format | Text |
id | pubmed-2112079 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1982 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21120792008-05-01 Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells J Cell Biol Articles In the search for the biochemical basis of the control of glycosylation of cell surface carbohydrates, revertant clones were isolated from previously characterized wheat germ agglutinin-resistant clones of B16 mouse melanoma cells by selection for resistance to Lotus tetragonolobus lectin or to ricin. Comparison of the wheat germ agglutinin-resistant clones with the parent and revertant clones indicated that this phenotype was correlated with an increased sensitivity to the Lotus lectin, a 60- to 70-fold increase in alpha 1 leads to 3 fucosyltransferase activity and a decreased sialic acid content of the N-glycosidic chains of glycoproteins. The results suggest a novel type of control mechanism for lectin resistance, an increase in a glycosyltransferase activity. The presence of alpha 1 leads to 3 bound fucose on N-acetylglucosamine residues would interfere with the addition of sialic acid by alpha 2 leads to 3 linkages to galactose residues in the carbohydrate units, and this change could explain the resistance to wheat germ agglutinin and the increased sensitivity to the Lotus lectin. A change in a regulatory gene for the fucosyltransferase as a possible primary cause for the changed phenotype is discussed. The Rockefeller University Press 1982-02-01 /pmc/articles/PMC2112079/ /pubmed/6895897 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title | Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title_full | Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title_fullStr | Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title_full_unstemmed | Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title_short | Enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
title_sort | enzymatic basis for a lectin-resistant phenotype: increase in a fucosyltransferase in mouse melanoma cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2112079/ https://www.ncbi.nlm.nih.gov/pubmed/6895897 |