Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1996-12-17
pubmed:abstractText
SJL mouse lymphomas (reticulum cell sarcomas, or RCSs) of germinal center B cell origin express an endogenous mouse mammary tumor virus (mtv-29) superantigen (vSAg) that stimulates Vbeta16+ T cells to produce cytokines essential for RCS growth. Normal or LPS-activated SJL/J B cells contain two to three larger mRNAs for mouse mammary tumor virus-long terminal repeat (LTR) but not the 1.8-kb mRNA, which is prominent in RCS cells and encodes the vSAg-29. mRNAs from RCS and normal lymphoid cells were characterized by Northern hybridization using DNA probes from various regions of mtv-29, as well as by reverse transcription PCR, RNase protection, and primer extension. The larger mtv-29 transcripts, coding for envelope protein, are initiated in the 5' LTR, as expected. Surprisingly, the 1.8-kb mRNA, encoding the open reading frame of the LTR, is initiated in the middle of the env region and spliced in the 3' env. This is the first report of an mtv-vSAg transcript that is not controlled by promoter(s) located in the 5' LTR. The env initiation site appears identical to that of the mouse mammary tumor virus env transcriptional activator-directed PMA-induced defective LTR transcript in the C57BL6 T cell lymphoma, EL-4. The stimulus independence, B lymphoma specificity, and absence of deletions within either the 5' or 3' LTR regions of mtv-29 in RCS distinguish the situation in RCS cells from that in EL-4. These findings suggest that the novel mtv-29-vSAg transcript reflects an RCS-cell-specific regulation of transcription.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3510-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8871650-Animals, pubmed-meshheading:8871650-Base Sequence, pubmed-meshheading:8871650-DNA, Complementary, pubmed-meshheading:8871650-DNA Primers, pubmed-meshheading:8871650-Female, pubmed-meshheading:8871650-Genes, env, pubmed-meshheading:8871650-Lymphoma, Large B-Cell, Diffuse, pubmed-meshheading:8871650-Mammary Tumor Virus, Mouse, pubmed-meshheading:8871650-Mice, pubmed-meshheading:8871650-Mice, Inbred AKR, pubmed-meshheading:8871650-Molecular Sequence Data, pubmed-meshheading:8871650-Polymerase Chain Reaction, pubmed-meshheading:8871650-Promoter Regions, Genetic, pubmed-meshheading:8871650-Proviruses, pubmed-meshheading:8871650-RNA, Messenger, pubmed-meshheading:8871650-RNA, Neoplasm, pubmed-meshheading:8871650-RNA, Viral, pubmed-meshheading:8871650-Repetitive Sequences, Nucleic Acid, pubmed-meshheading:8871650-Superantigens, pubmed-meshheading:8871650-Transcription, Genetic
pubmed:year
1996
pubmed:articleTitle
Control of endogenous mouse mammary tumor virus superantigen expression in SJL lymphomas by a promoter within the env region.
pubmed:affiliation
Department of Pathology and Kaplan Cancer Center, New York University School of Medicine, NY 10016, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.