scholarly journals Kirsten murine sarcoma virus abolishes interferon gamma-induced class II but not class I major histocompatibility antigen expression in a murine fibroblast line.

1988 ◽  
Vol 167 (2) ◽  
pp. 706-711 ◽  
Author(s):  
D J Maudsley ◽  
A G Morris
Keyword(s):  
Leukemia Virus ◽  
Constitutive Expression ◽  
Antigen Expression ◽  
Class Ii ◽  
Class I ◽  
Ras Gene ◽  
Ifn Gamma ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Murine Sarcoma

The effect of infecting fibroblasts with Kirsten murine sarcoma virus/murine leukemia virus (Ki-MSV/MLV) on constitutive and IFN-gamma-induced H-2 antigen expression was investigated. The fibroblasts used were two established cell lines (C3H10T1/2 and BALB/c3T3) and fresh embryo fibroblasts from C3H mice. Class I antigens were expressed constitutively by BALB/c3T3; infection with MLV, MSV or the two together had little effect on this constitutive expression. Class I antigens (H-2K, H-2D) were strongly induced on all three types of fibroblast by rIFN-gamma, and infection had little effect on this. None of the fibroblasts expressed constitutively detectable levels of class II antigen; however, C3H10T1/2 fibroblasts could be induced for both H-2A and H-2E by IFN-gamma. Infection of C3H10T1/2 with helper-free Ki-MSV, or MSV together with MLV, completely abolished this induction of class II antigens, while infection with MLV alone had little effect, implying that the abolition of class II induction was due to genomic regions of Ki-MSV not shared with Ki-MLV, probably the v-Ki-ras gene.

scholarly journals Nucleotide sequence of the two rat cellular rasH genes.

1986 ◽  
Vol 6 (5) ◽  
pp. 1706-1710 ◽  
Author(s):  
M Ruta ◽  
R Wolford ◽  
R Dhar ◽  
D Defeo-Jones ◽  
R W Ellis ◽  
...  
Keyword(s):  
Amino Acids ◽  
Nucleotide Sequence ◽  
Coding Region ◽  
3T3 Cells ◽  
Ras Gene ◽  
P21 Protein ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Nih 3T3 ◽  
Murine Sarcoma

We present the nucleotide sequence of the coding region of the rat c-rasH-1 gene and a partial sequence analysis of the rat c-rasH-2 gene. By comparing these sequences with the Harvey murine sarcoma virus ras gene, we predict that the p21 protein encoded by the Harvey virus differs from the cellular c-rasH-1-encoded p21 at only two amino acids; those at positions 12 and 59. Alterations at each of these positions may play a role in activating the viral p21 protein. The c-rasH-2 gene is likely to be a nonfunctional pseudogene because it lacks introns, cannot be activated to transform NIH 3T3 cells, and differs in sequence from both c-rasH-1 and v-rasH at several base pair positions.

Mouse cells contain two distinct ras gene mRNA species that can be translated into a p21 onc protein

1982 ◽  
Vol 2 (11) ◽  
pp. 1339-1345
Author(s):  
R W Ellis ◽  
D DeFeo ◽  
M E Furth ◽  
E M Scolnick
Keyword(s):  
Normal Mouse ◽  
Velocity Sedimentation ◽  
Ras Gene ◽  
Mrna Species ◽  
P21 Ras ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Mouse Cells ◽  
Murine Sarcoma

The Kirsten (Ki) and Harvey (Ha) strains of murine sarcoma virus encode a 21,000-dalton protein (p21 ras) which is the product of the transforming gene of these viruses. Normal cells express low levels of p21 ras encoded by cellular genes (Ki-ras and Ha-ras) homologous to the Ki and Ha murine sarcoma virus transformation genes. A bone marrow-derived mouse cell line, 416B, has been shown to express unusually high levels of p21 ras. In this manuscript, we investigated the molecular biology of p21 ras gene expression in 416B and other normal mouse cells. We identified four distinct polyadenylated and polysome-associated RNAs, two related to Ki-ras and two to Ha-ras. The levels in 416B cells of the two Ki-ras RNAs, sized 5.2 and 2.0 kilobases, were both elevated approximately 25-fold over levels found in normal mouse cells; there was no corresponding change in 416B cells in the levels of the two Ha-ras RNAs. We partially purified the two Ki-ras mRNAs and separated them by velocity sedimentation in sucrose density gradients. Both the 5.2- and 2.0-kilobase mRNAs could be translated in vitro into p21 ras. These results show that a cellular onc protein can be translated from two distinct cellular mRNA species.

scholarly journals ANTIGENIC PROPERTIES OF MURINE SARCOMA VIRUS-TRANSFORMED BALB/3T3 NONPRODUCER CELLS

1972 ◽  
Vol 135 (3) ◽  
pp. 503-515 ◽  
Author(s):  
John R. Stephenson ◽  
Stuart A. Aaronson
Keyword(s):  
Cell Line ◽  
Leukemia Virus ◽  
Target Cells ◽  
Subsequent Challenge ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Rauscher Leukemia ◽  
Transplantation Antigens ◽  
Murine Sarcoma ◽  
Rauscher Leukemia Virus

The isolation of clonal lines of murine sarcoma virus-transformed, non-producer BALB/3T3 cells has provided a model system for determining whether RNA tumor virus-transformed cells possess virus-specific transplantation antigens. MSV nonproducer cells (K-234) were clonally derived from an inbred mouse cell line, BALB/3T3. A parallel virus-producing cell line was obtained by infection of the MSV nonproducer cells with Rauscher leukemia virus. K-234 was much more tumorigenic than K-234(R). Preimmunization of syngeneic mice with either K-234(R) or with UV-inactivated Rauscher leukemia virus induced transplantation resistance to subsequent challenge with K-234(R), but not with K-234. In contrast, mice preimmunized with nonproducer cells were not made resistant to subsequent challenge with the homologous cells. Antisera prepared from mice immunized with K-234(R) were specifically cytotoxic and positive by fluorescent antibody staining for K-234(R) target cells, but not to either BALB/3T3 or K-234. The results show that MSV nonproducer cells lack detectable transplantation antigens and suggest that the transplantation resistance to the producing cells is attributable to maturing virus at the cell surface.

scholarly journals Widespread and selective induction of major histocompatibility complex-determined antigens in vivo by gamma interferon.

1985 ◽  
Vol 162 (5) ◽  
pp. 1645-1664 ◽  
Author(s):  
M J Skoskiewicz ◽  
R B Colvin ◽  
E E Schneeberger ◽  
P S Russell
Keyword(s):  
Dendritic Cells ◽  
Small Intestine ◽  
Antigen Expression ◽  
Class Ii ◽  
Gamma Interferon ◽  
The Body ◽  
Class I ◽  
Ifn Gamma ◽  
Histocompatibility Complex

gamma Interferon (IFN-gamma) caused remarkable increases in class I (H-2Kk) and class II (I-Ak) antigens throughout the body by 6-9 d. Heart, kidney, and adrenals showed increases of 4-8 times their previous levels of class I antigen content, while the pancreas and small intestine increased 13-17-fold. Lesser increases were found in spleen, liver, and lung, which showed higher resting antigenic potency. Increases of class II antigenicity of 6-10-fold were found in heart, kidney, pancreas, lung, liver, adrenal, and small intestine, with lesser increases in thymus and spleen, and none in lymph node. Topographical analysis revealed that IFN-gamma induced class I and II antigens on most tissues in a highly selective fashion. For example, the renal proximal tubules expressed large amounts of both class I and II antigens, whereas the distal tubules and collecting ducts did not. In some epithelial cells class I and II determinants were induced only on the basal aspects of the cell membrane. IFN-gamma caused a remarkable increase in class II-positive dendritic cells in the liver, pancreas, salivary glands, and thyroid. Whether these cells were of local or systemic origin is uncertain, but the finding of a simultaneous depletion of dendritic cells from lymph nodes and spleen raises the possibility that they may have been derived, at least in part, from these sites. The dynamic and selective induction of class I and II antigen expression by IFN-gamma is likely to be important in regulation of the immune response in tissues.

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