Linked Life Data

1374455

Source:http://linkedlifedata.com/resource/pubmed/id/1374455

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-6-10
pubmed:abstractText
Resistance to interferon-alpha (IFN-alpha) in the 38C13 B-lymphoma cell line results in the loss of antiviral, antiproliferative, and immune regulatory functions of IFN-alpha. Mutagenesis with ethylmethylsulfonic acid (EMS), which can induce point mutations in DNA, increases the frequency of resistance to IFN-alpha 20 to 40-fold. In contrast, treatment with 5-azacytidine, which causes hypomethylation of DNA, reduces the frequency of resistance to 5-10% of control. Furthermore, 5-azacytidine treatment reverts IFN-alpha-resistant cells to the IFN-alpha-sensitive state. Resistance to IFN-alpha occurs spontaneously at a rate of approximately 3 x 10(-6) variants/cell.generation, and is stable for more than 30 passages without selection in IFN-alpha. There is no evidence that gene amplification contributes to the high rate of resistance to IFN-alpha in these cells. These results indicate that DNA mutation and methylation are important in the development of IFN-alpha resistance in these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0197-8357
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
131-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Resistance to interferon-alpha in a mouse B-cell lymphoma involves DNA methylation.
pubmed:affiliation
Department of Medicine, Stanford University School of Medicine, CA 94305.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't