PMID- 1318934
OWN - NLM
STAT- MEDLINE
DCOM- 19920721
LR  - 20191028
IS  - 0883-0185 (Print)
IS  - 0883-0185 (Linking)
VI  - 8
IP  - 4
DP  - 1992
TI  - Molecular characterization of Mls-1.
PG  - 279-88
AB  - Recently a series of endogenous and exogenous superantigens have been described 
      which have one common feature, namely, they lead to in vivo deletion and in vitro 
      stimulation of T cells expressing particular T cell receptor V beta genes. The 
      Mls antigens represent the prototypes of these molecules. We have mapped Mls-1 to 
      the endogenous mammary tumor virus (MMTV) Mtv-7, while other SAG have also been 
      associated with various MMTV. The open reading frame gene of the MMTV encodes the 
      SAG. Thus, the new terminology MMTV sag has been proposed for this gene. 
      Transfection experiments suggest that the expression of MMTV sag is tightly 
      controlled, probably by a negative acting factor encoded within the open reading 
      frame. Furthermore, a pronounced IL-4 effect is seen in the functional detection 
      of the transfected Mtv-7 sag. Since this lymphokine does not influence the mRNA 
      level of the endogenous or transfected MMTV genes, it is likely that it exerts 
      its effect by increasing transcription of MHC class II genes, whose products are 
      required for functional detection of Mls. We have identified one mouse strain, 
      MA/MyJ, which has an Mls-1 phenotype but does not contain Mtv-7. The SAG activity 
      of this strain was mapped to a new mammary tumor provirus, Mtv-43, not seen in 
      other inbred strains. Sequence analyses revealed that the predicted amino acid 
      sequences of the Mtv-7 and the Mtv-43 sag genes are very similar. This is 
      particularly striking in the C-terminus, where all other MMTV sag sequences 
      differ 100%. Thus, this region of the molecule seems to control the V beta 
      specificity of SAG molecules. It is likely that the SAG expression provides an 
      advantage for the infectious MMTV, probably by facilitating its transmission by T 
      cells from the site of primary residence in the gut to its final destination, the 
      mammary glands.
FAU - Beutner, U
AU  - Beutner U
AD  - Department of Pathology, Tufts University School of Medicine, Boston, MA 02111.
FAU - Rudy, C
AU  - Rudy C
FAU - Huber, B T
AU  - Huber BT
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Review
PL  - England
TA  - Int Rev Immunol
JT  - International reviews of immunology
JID - 8712260
RN  - 0 (Minor Lymphocyte Stimulatory Antigens)
RN  - 0 (Receptors, Antigen, T-Cell, alpha-beta)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Gene Expression Regulation, Viral/genetics
MH  - Genotype
MH  - Immunophenotyping
MH  - Interleukin-4/immunology
MH  - Lymphocyte Activation/immunology
MH  - Mammary Tumor Virus, Mouse/genetics/immunology
MH  - Minor Lymphocyte Stimulatory Antigens/*genetics/immunology
MH  - Molecular Sequence Data
MH  - Receptors, Antigen, T-Cell, alpha-beta/genetics/immunology
MH  - T-Lymphocytes/immunology
MH  - Transfection/genetics
RF  - 53
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
AID - 10.3109/08830189209053513 [doi]
PST - ppublish
SO  - Int Rev Immunol. 1992;8(4):279-88. doi: 10.3109/08830189209053513.