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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-2-18
pubmed:abstractText
A mouse mammary carcinoma mutant cell line showing a characteristic alteration of glycosphingolipid (GSL) composition, but with unchanged protein glycosylation pattern, was isolated. Parent cell line FM3A/F28-7 is characterized by the predominance of lactosylceramide (LacCer) and virtual absence of more complex GSLs. Mutant cell line FUA169 was isolated after treatment of F28-7 cells with the mutagen N-methyl-N'-nitro-N-nitrosoguanidine and incubation with anti-LacCer monoclonal antibody T5A7 and complement. FUA169 cells were characterized by a dramatic reduction in LacCer and by the presence of a major ganglioside identified as GM3. They also showed high activity of CMP-sialic acid:LacCer 2,3-sialosyltransferase, whereas F28-7 cells had no detectable activity of this enzyme. In contrast to the difference in GSL pattern, F28-7 and FUA169 showed identical protein glycosylation patterns, as evidenced by "Western blotting" with various lectins and surface labeling with galactose oxidase/NaB3H4 and periodate/NaB3H4. Thus, FUA169 is identified as a glycosylation mutant with regard to GM3 expression and will be useful for studies of the functional role of GM3. Growth of FUA169 cells, relative to F28-7 cells, showed greater temperature sensitivity and greater inhibitability based on restriction of growth factors, particularly insulin.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2211-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Selection of a mutant cell line based on differential expression of glycosphingolipid, utilizing anti-lactosylceramide antibody and complement.
pubmed:affiliation
Department of Biochemical Oncology/Membrane Research, Fred Hutchinson Cancer Research Center, Seattle, Washington.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.