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PubMed1980

Sites of synthesis of viral proteins in avian sarcoma virus-infected chicken cells.

We determined the sites of synthesis of avian sarcoma virus-specific proteins in infected chicken cells by immunoprecipitation of the products synthesized in vitro by free and membrane-bound polyribosomes; 85% of Pr76, the precursor of the viral internal structural proteins (group-specific antigens), was synthesized on free polyribosomes, and 15% was synthesized on membrane-bound polyribosomes. Pr92, the lycosylated precursor of the viral glycoproteins (gp85 and gp35), was synthesized exclusively on membrane-bound polyribomes, which is consistent with its role as a membrane protein. When we investigated the site of synthesis of pp60src, the product of the avian sarcoma virus src gene, we found that 90% was synthesized on free polyribosomes, whereas 10% was detected on membrane-bound polyribosomes. The implications of these results with respect to the subcellular location of pp60src are discussed.

Alpharetrovirus↗
PubMed1981

Some biological properties of two new avian sarcoma viruses.

The new avian retroviruses UR1 and UR2 were isolated from spontaneous tumors of chickens by cocultivation of tumor material with susceptible chicken embryo fibroblasts. In vitro, UR1 induced formation of small foci of round and fusiform cells. On the other hand, cells infected by UR2 assumed an extremely elongated morphology. In vivo, both viruses induced fibrosarcomas and myxosarcomas with short latencies. Infectivity assays with and without mitomycin C showed that both viruses were defective for replication, but transformed nonproducing cell clones were obtained only with UR1. UR1-infected transformed nonproducing clones did not release particles detectable by reverse transcriptase assays, and fusion of transformed nonproducing cells with quail cells chronically infected with Rous sarcoma virus (a Bryan strain) failed to rescue infectious virus. This suggested that UR1 does not code for functional envelope glycoproteins. In this regard, UR1 appeared to be similar to Fujinami, PRCII, and Y73 viruses. The helper viruses of partially purified stocks of UR1 and UR2 appeared to belong to subgroup A, but these helper viruses were distinguishable from each other, as shown by host range experiments and neutralization tests. Hybridization studies with DNA complementary to the src gene of Rous sarcoma virus and RNAs extracted from both UR1 and UR2 showed no homology between the genomes of the new isolates and the transforming gene of Rous sarcoma virus.

Alpharetrovirus↗
PubMed1982

Isolation of a transformation-defective deletion mutant of Moloney murine sarcoma virus.

A transformation-defective (td) deletion mutant of Moloney murine sarcoma virus (td Mo-MSV) and a transforming component termed Mo-MSV 3 were cloned from a stock of clone 3 Mo-MSV. To define the defect of the transforming function, the RNA of td Mo-MSV was compared with those of Mo-MSV 3 and of another transforming variant termed Mo-MSV 124 and with helper Moloney murine leukemia virus (Mo-MuLV). The RNA monomers of td Mo-MSV and Mo-MSV 3 comigrated on polyacrylamide gels and were estimated to be 4.8 kilobases (kb) in length. In agreement with previous analyses, the RNA of Mo-MSV 124 measured 5.5 kb and that of Mo-MuLV measured 8.5 kb. The interrelationships among the viral RNAs were studied by fingerprinting and mapping of RNase T(1)-resistant oligonucleotides (T(1)-oligonucleotides) and by identification of T(1)-oligonucleotides present in hybrids formed by a given viral RNA with cDNA's made from another virus. The nontransforming td Mo-MSV RNA lacked most of the Mo-MSV-specific sequence, i.e., the four 3'-proximal T(1)-oligonucleotides of the six T(1)-oligonucleotides that are shared by the Mo-MSV-specific sequences of Mo-MSV 3 and Mo-MSV 124. The remaining two Mo-MSV-specific oligonucleotides identified td Mo-MSV as a deletion mutant of MSV rather than a deletion mutant of Mo-MuLV. td Mo-MSV and Mo-MSV 124 exhibited similar deletions of gag, pol, and env sequences which were less extensive than those of Mo-MSV 3. Hence, td Mo-MSV is not simply a deletion mutant of Mo-MSV 3. In addition to their MSV-specific sequences, all three MSV variants, including td Mo-MSV, shared the terminal sequences probably encoding the proviral long terminal repeat, which differed from their counterpart in Mo-MuLV. This may indirectly contribute to the oncogenic potential of MSV. A comparison of td Mo-MSV sequences with either Mo-MSV 124 or Mo-MSV 3 indicated directly, in a fashion similar to the deletion analyses which defined the src gene of avian sarcoma viruses, that Mo-MuLV-unrelated sequences of Mo-MSV are necessary for transformation. A definition of transformation-specific sequences of Mo-MSV by deletion analysis confirmed and extended previous analyses which have identified Mo-MuLV-unrelated sequences in Mo-MSV RNA and other studies which have described transformation of mouse 3T3 fibroblasts upon transfection with DNAs containing the Mo-MSV-specific sequence.

Cell Transformation, Viral↗
PubMed1982

Genetic structure and transforming sequence of avian sarcoma virus UR2.

We have recently shown that a newly isolated avian sarcoma virus, UR2, is defective in replication and contains no sequences homologous to the src gene of Rous sarcoma virus. In this study, we analyzed the genetic structure and transforming sequence of UR2 by oligonucleotide fingerprinting. The sizes of the genomic RNAs of UR2 and its associated helper virus, UR2AV, were determined to be 24S and 35S, respectively, by sucrose gradient sedimentation. The molecular weight of the 24S UR2 genomic RNA was estimated to be 1.1 x 10(6), corresponding to 3,300 nucleotides, by gel electrophoresis under the native and denatured conditions. RNase T1 oligonucleotide mapping indicated that UR2 RNA contains seven unique oligonucleotides in the middle of the genome and shares eight 5'- and six 3'-terminal oligonucleotides with UR2AV RNA. From these data, we estimated that UR2 RNA contains a unique sequence of about 12 kilobases in the middle of the genome, and contains 1.4 and 0.7 kilobases of sequences shared with UR2AV RNA at the 5' and 3' ends, respectively. Partial sequence analysis of the UR2-specific oligonucleotides by RNase A digestion revealed that there are no homologous counterparts to these oligonucleotides in the RNAs of other avian sarcoma and acute leukemia viruses studied to date. UR2-transformed non-virus-producing cells contain a single 24S viral RNA which is most likely the message coding for the transforming protein of UR2. On the basis of the uniqueness of the transforming sequence, we concluded that UR2 is a new member of the defective avian sarcoma viruses.

Alpharetrovirus↗
PubMed1983

cis-Acting RNA packaging locus in the 115-nucleotide direct repeat of Rous sarcoma virus.

The v-src gene of Schmidt-Ruppin strain A of Rous sarcoma virus is flanked by a 115-nucleotide direct repeat. Mutants that lack either the upstream or downstream copy replicate normally. However, mutants that lack both copies do not replicate. Cloned viral DNA lacking both copies of the 115-nucleotide sequence is capable of directing the transcription of viral RNA posttransfection. This viral RNA is polyadenylated, spliced, exported from the nucleus, and translated into protein normally. However, virions isolated from the culture medium 48 h posttransfection lack viral RNA. When mutant DNA is contransfected with wild-type DNA, the virions produced 48 h later contain wild-type RNA but not mutant RNA, even though both RNAs are present in the cytoplasm. We propose that the 115-nucleotide element of Rous sarcoma-avian leukosis virus encodes a cis-acting sequence that is necessary for the proper incorporation of viral RNA into virions.

Animals↗
PubMed1984

Characterization of a Rous sarcoma virus mutant defective in packaging its own genomic RNA: biochemical properties of mutant TK15 and mutant-induced transformants.

The accompanying paper (S. Kawai and T. Koyama , J. Virol. 51:147-153, 1984) describes the isolation and biological properties of a mutant, TK15 , derived from a Rous sarcoma virus mutant, tsNY68 . The cis-acting defect of the mutant is analyzed biochemically in this paper. TK15 virions released from virus-producing 15c (+) cells were deficient in viral genomic 39S RNA, although comparable amounts of viral RNAs were transcribed in 15c (+) and tsNY68 -infected cells. Analysis of provirus DNA occurring in 15c (+) cells suggested that the mutant genome had a deletion of ca. 250 bases near the 5' end of the genome somewhere between the primer binding site and the 5' end of the gag-coding region. These findings indicate that at least part of the sequence lost in the TK15 genome is indispensable for packaging viral genomic RNA into virions. TK15 induces nonvirus -producing 15c (-) transformants at high frequency. Southern blot analysis of DNAs from those 15c (-) clone cells revealed that TK15 -derived proviruses contained various extents of internal deletions. Many 15c (-) clones had a provirus carrying only the src gene with long terminal repeat sequences at both ends. The mechanism for the segregation of 15c (-) cells is discussed.

Avian Sarcoma Viruses↗
PubMed1996

Avian retroviral RNA element promotes unspliced RNA accumulation in the cytoplasm.

All retroviruses need mechanisms for nucleocytoplasmic export of their unspliced RNA and for maintenance of this RNA in the cytoplasm, where it is either translated to produce Gag and Pol proteins or packaged into viral particles. The complex retroviruses encode Rev or Rex regulatory proteins, which interact with cis-acting viral sequences to promote cytoplasmic expression of incompletely spliced viral RNAs. Since the simple retroviruses do not encode regulatory proteins, we proposed that they might contain cis-acting sequences that could interact with cellular Rev-like proteins. To test this possibility, we initially looked for a cis-acting sequence in avian retroviruses that could substitute for Rev and the Rev response element in human immunodeficiency virus type 1 expression constructs. A cis-acting element in the 3' untranslated region of Rous sarcoma virus (RSV) RNA was found to promote Rev-independent expression of human immunodeficiency virus type 1 Gag proteins. This element was mapped between RSV nucleotides 8770 and 8925 and includes one copy of the direct repeat (DR) sequences flanking the RSV src gene; similar activity was observed for the upstream DR. To address the function of this element in RSV, both copies of the DR sequence were deleted. Subsequently, each DR sequence was inserted separately back into this deleted construct. While the viral construct lacking both DR sequences failed to replicate, constructs containing either the upstream or downstream DR replicated well. In the absence of both DRs, Gag protein levels were severely diminished and cytoplasmic levels of unspliced viral RNA were significantly reduced; replacement of either DR sequence led to normal levels of Gag protein and cytoplasmic unspliced RNA.

Animals↗
PubMed2000

Rous sarcoma virus DR posttranscriptional elements use a novel RNA export pathway.

Rous sarcoma virus (RSV), a simple retrovirus, needs to export unspliced viral RNA from the nucleus to the cytoplasm, circumventing the host cell restriction on cytoplasmic expression of intron-containing RNA. The cytoplasmic accumulation of full-length viral RNA is promoted by two cis-acting direct repeat (DR) elements that flank the src gene; at least one copy of the DR sequence is necessary for viral replication. We show here that the DR mediates export of a reporter construct from the nucleus, suggesting it is a constitutive transport element (CTE). In contrast, human immunodeficiency virus type 1 (HIV-1) and other complex retroviruses encode accessory proteins, Rev or Rex, which promote export of incompletely spliced viral transcripts. This RNA export pathway is CRM1 dependent and can be blocked by the cytotoxic agent leptomycin B. We show here that DR-mediated export is CRM1 independent, suggesting that RSV uses a different export pathway from that of HIV-1 and other complex retroviruses. The simian retroviruses have a CTE which interacts with the cellular Tap export protein. However, we were unable to detect binding of the RSV DR RNA to Tap, suggesting it may use a different export pathway from that of the simian retroviruses. These data suggest that the RSV DR element uses a novel nucleocytoplasmic export pathway.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1981

Markedly elevated levels of an endogenous sarc protein in a hemopoietic precursor cell line.

The src gene product of Harvey murine sarcoma virus is a 21,000-dalton guanine nucleotide-binding protein. We have recently shown that a wide variety of vertebrate cell strains and cell lines express much lower levels of an endogenous p21 immunologically related to the Harvey murine sarcoma virus-coded p21. In this report, we have examined the levels of endogenous p21 in a unique hemopoietic precursor cell line, 416B, which was originally described as a continuous cell line of a hemopoietic stem cell, CFU-S. The currently available 416B cells express markedly elevated levels of endogenous p21. The level of endogenous p21 in the 416B cells is 5- to 10-fold higher than the level of p21 in Harvey murine sarcoma virus-infected cells and more than 100 times higher than the level of endogenous p21 that we have observed in a variety of other fresh or cultured cells. The results indicate that marked regulation of the levels of an endogenous sarc gene product can occur, and speculation about a possible role for endogenous p21 in normal hemopoietic stem cells is discussed.

Animals↗
PubMed2000

Influence of cell cycle and oncogene activity upon topoisomerase IIalpha expression and drug toxicity.

The cell cycle, oncogenic signaling, and topoisomerase (topo) IIalpha levels all influence sensitivity to anti-topo II drugs. Because the cell cycle and oncogenic signaling influence each other as well as topo IIalpha levels, it is difficult to assess the importance of any one of these factors independently of the others during drug treatment. Such information, however, is vital to an understanding of the cellular basis of drug toxicity. We, therefore, developed a series of analytical procedures to individually assess the role of each of these factors during treatment with the anti-topo II drug etoposide. All studies were performed with asynchronously proliferating cultures by the use of time-lapse and quantitative fluorescence staining procedures. To our surprise, we found that neither oncogene action nor the cell cycle altered topo IIalpha protein levels in actively cycling cells. Only a minor population of slowly cycling cells within these cultures responded to constitutively active oncogenes by elevating topo IIalpha production. Thus, it was possible to study the effects of the cell cycle and oncogene action on drug-treated cells while topo IIalpha levels remained constant. Toxicity analyses were performed with two consecutive time-lapse observations separated by a brief drug treatment. The cell cycle phase was determined from the first observation, and cell fate was determined from the second. Cells were most sensitive to drug treatment from mid-S phase through G(2) phase, with G(1) phase cells nearly threefold less sensitive. In addition, the presence of an oncogenic src gene or microinjected Ras protein increased drug toxicity by approximately threefold in actively cycling cells and by at least this level in the small population of slowly cycling cells. We conclude that both cell cycle phase and oncogenic signaling influence drug toxicity independently of alterations in topo IIalpha levels.

3T3 Cells↗
PubMed1986

Antipeptide antiserum identifies a widely distributed cellular tyrosine kinase related to but distinct from the c-fps/fes-encoded protein.

We raised antibodies directed against a synthetic peptide representing an amino acid sequence of the conserved kinase domain of the transforming protein of Fujinami sarcoma virus (FSV) (P140). The antiserum obtained specifically recognized FSV-P140 and its cellular homolog and in addition, it recognized a new cellular protein of 94,000 daltons (NCP94) in avian and mammalian cells. NCP94 was found to be associated with a cyclic nucleotide-independent protein kinase activity that was specific for tyrosine residues. Although NCP94 and FSV-P140 share antigenic determinants, NCP94 is not a cellular homolog of FSV-P140: NCP94 and the previously identified c-fps/fes product were different in their tryptic fingerprints and in their tissue specificities. Thus, the function of NCP94 in normal cells is probably different than that of the c-fps/fes product. NCP94 was expressed in every tissue and cell line that was examined. In chickens, NCP94 levels were highest during embryonic development and NCP94 expression was high in gizzard, brain, and spleen throughout embryonic and adult life. The universal expression of NCP94 suggests that this protein may be involved in an essential function of normal cells. NCP94 may be a new cellular tyrosine kinase of the src gene family.

Amino Acid Sequence↗
PubMed1980

Aggregation properties of chondrocytes infected with a temperature-sensitive mutant of Rous sarcoma virus.

Aggregation capacity of chicken embryo chondrocytes decreases when transformed by Rous sarcoma viruses. Cell-to-cell aggregation capacity of chondrocytes infected with a T class temperature-sensitive mutant (tsNY68) (with the temperature-sensitive lesion at the src gene) of Rous sarcoma virus is dependent upon the temperature at which these cells are grown. When grown at the permissive temperature (36 degrees C), where the transforming gene is expressed, aggregation capacity was lower than normal while infected cells grown at the non-permissive temperature (41.5 degrees C) had similar capacity to aggregate to that of normal chondrocytes. However, after a prolonged period of culture (10 days), chondrocytes transformed by wild type SR-RSV regained the normal level of aggregation capacity. Cells transformed by tsNY68 and incubated at the permissive temperature for 10 days also regained the normal level of aggregation capacity. It appears therefore that RSV-transformed chondrocytes first become less adhesive but during long-term cultivation they regain their property to aggregate. The decrease of aggregation capacity due to T class mutants of RSV at 36 degrees C is dependent on constant maintenance of protein synthesis because addition of cycloheximide restored the aggregation capacity even at the permissive temperature.

Animals↗
PubMed1992

Rat mammary myoepithelial-like cells in culture possess kinetically distinct low-affinity receptors for fibroblast growth factor that modulate growth stimulatory responses.

The rat mammary myoepithelial-like cell line Rama 401 possesses 46,000 high-affinity receptors (Kd 52 pM) and 2.8 x 10(6) low-affinity receptors (Kd 24 nM) for basic fibroblast growth factor (bFGF) per cell. Heparin or heparinase pretreatment of the cells inhibits the specific binding of [125I]-bFGF by over 70%, and abolishes binding to the low-affinity sites. Dissociation experiments suggest that there are three kinetically distinct low-affinity receptors, with dissociation rate constants of 3.8 s-1, 0.067 s-1 and 0.0018 s-1. Consistent with the presence of low-affinity receptors possessing a slow dissociation rate constant, exogenously added bFGF bound to the low-affinity receptor can stimulate DNA synthesis in Rama 401 cells without being released into the bulk of the culture medium. These results suggest that the low-affinity receptors on Rama 401 cells are heparan sulfate glycosaminoglycans (HSGAGs) and that their ability to modulate the action of bFGF may result from their diverse range of dissociation rate constants. A cell line, Rama 401ts, derived from Rama 401 by transformation with a temperature sensitive src gene, deposits less extracellular matrix at the permissive temperature of 34 degrees C than at the non-permissive temperature of 41 degrees C. Whilst the binding of [125I]-bFGF to Rama 401ts cells at 41 degrees C is identical to that observed with the parental Rama 401 cells, at 34 degrees C there are fewer low-affinity receptors. These results suggest the (HSGAGs) low-affinity receptors on Rama 401 cells are associated at least in part with the extracellular matrix.

Animals↗
PubMed2002

[Transplantation of mesenchymal derived stem cells followed by G-CSF injection can reconstitute hematopoiesis of lethally irradiated BALB/c mice].

OBJECTIVE: To explore the hematopoietic reconstitution potential of mesenchymal derived stem like cells. METHODS: We transplanted bone marrow mesenchymal derived stem like cells into lethally irradiated BALB/c mice. Hematopoietic cells were derived from the non-adherent bone marrow cells 24 hours after initial culture while murine mesenchymal derived stem like cells from bone marrow of donor mice were cultured for 10 days before the transplantation. RESULTS: All mice of group 1 and 3 died in 7-8 days post irradiation following transplantation, while all the mice from group 2 and 4 survived. The time course of hematopoietic reconstitution was then observed. The peripheral blood and bone marrow cell count recovered in the MSC + G-CSF transplanted group and the BM transplanted group after 3 weeks. Interestingly, CFU-GM number in the MSC + G-CSF transplanted group increased significantly after 2 weeks and even more than that in the BM transplanted group after 3 weeks while as CFU-GM colony dropped 2 weeks after in the BM transplanted group. Spleen colony (CFU-S) number and size of the MSC + G-CSF transplanted group was significantly greater than the BM transplanted group. Furthermore, PCR analysis was performed using peripheral blood cells to determine if any male-derived cells were present. No male-derived cells were found in any of the mice from group 1 and 3. Y-chromosome-specific src gene was found to be dominant in the MSC + G-CSF transplanted group and the BM transplanted group by week 4 post transplantation. In addition, we demonstrated that induction with G-CSF lead to CFU-GM colony formation from MSC compartment in vitro. CONCLUSION: These results indicate that under stimulation of G-CSF, mesenchymal derived stem like cells might differentiate into hematopoietic primitive stem cells in vivo and have the capacity to re-establish hematopoiesis in lethally irradiated mice. This study should provide an alternative transplantation treatment for malignancy.

Animals↗
PubMed1991

Malignant transformation of mouse BALB/3T3 cells by polyoma middle T antigen requires epidermal growth factor receptor expression.

The mouse cell line MO-5, which is defective in receptor-binding activity of epidermal growth factor (EGF), is very poorly transformed by polyoma middle T antigen or v-src gene, but activated c-H-ras and v-mos gene can induce the transformation (M. Ono, M. Yakushinji, K. Segawa, and M. Kuwano, Mol. Cell. Biol., 8: 4190-4196, 1988). We established clones of MO-5 expressing a functional EGF receptor (EGF-R) after introduction of the human EGF-R complementary DNA into MO-5 (MNER23 and MNER31), and we also established a clone (BNER4) expressing human EGF-R from the parental cell line, BALB/3T3. MNER23, MNER31, and BNER4 expressed EGF-R activity at about 2- to 6-fold higher levels than did control BALB/3T3 cells. A marked increase in DNA synthesis in response to EGF was observed in these BNER4, MNER23, and MNER31 cell lines compared to BALB/3T3 cells; however, there was little if any increase in DNA synthesis of MO-5 in the presence of EGF. Introduction of the polyoma middle T antigen gene into BALB/3T3, BNER4, MNER23, and MNER31 resulted in the appearance of transformation foci, but MO-5 again showed little response. We purified clones B4-mT-2, M23-mT-1, M23-mT-2, M23-mT-3, and M31-mT-13 from transformation foci of BNER4, MNER23, and MNER31 cells, which were respectively transfected with the middle T antigen. All of the middle T antigen-positive transfectants demonstrated abilities to form both colonies in soft agar and tumors in nude mice. The presence of EGF-R appears to be indispensable for malignant transformation by polyoma middle T antigen.

Animals↗
PubMed1991

[Tyrosine protein kinase from cattle cerebral cortex: purification, characteristics, protein substrates for phosphorylation and inhibitors of activity].

Tyrosine protein kinase present in the membrane fraction of bovine cerebral cortex were extracted and chromatographically fractionated. The activity associated with tyrosine protein kinases was fully extracted from the membranes by 1% sodium cholate and eluted in two peaks (I and II) during chromatography of protein extracts on DEAE-Toyopearl in the presence of sodium cholate. The predominant in cerebral cortex membrane tyrosine protein kinase of peak I (about 75% of the total activity) was purified 1930-fold by gel filtration on Sephacryl S-300, chromatography on hexyl- and phenyl-Sepharose and by rechromatography on DEAE-Toyopearl. The amount of the enzyme prepared from 250 g of bovine brain was 20 micrograms, the enzyme yield and specific activity being 3.8% and 3.9 nmol/mg protein/min, respectively. The purified protein kinase of peak I represents a protein with Mr of 62-63,000 (p62) capable of being autophosphorylated in the presence of [gamma-32P]. Protein kinase p62 phosphorylates enolase, tubulin and calpactin I as well as model substrates in the series: histone H5 greater than poly(G, T)n greater than or equal to histone H2A greater than poly(G, A, T)n, histone H4 greater than caseins, histones H1 and H2B, poly(G, A, L, T)n. The enzyme is specific for Mn2+ at the optimal concentration about 1 mM. The KmMn-ATP is 0.3 microM; Km for histone H5 and poly(G, T)n are 0.45 mg/ml and 0.06 mg/ml, respectively. The protein kinase p62 activity is inhibited by NaCl (IC50 approximately 75-100 mM) as well as by quercetin, adriamycin and lasalocid (IC50 approximately 14-34, 23 and 90 microM, respectively). It is concluded that protein kinase p62 is analogous to the c-src gene protein kinase.

Animals↗
PubMed1985

Pseudouridine excretion and transfer RNA primers for reverse transcriptase in tumors of retroviral origin.

To evaluate the relationship between pseudouridine increase in biological fluids and retroviral cell transformation, we have studied the effect of retrovirus infection and/or transformation on the rate of pseudouridine excretion by chick embryo fibroblasts. The results show that: pseudouridine excretion by chick embryo fibroblasts transformed by Rous sarcoma virus is several times higher than that of normal cells; this increased excretion precedes by many hours the appearance of the morphological signs of transformation and it is always present when neosynthesized infectious viral particles are released into the culture medium; and pseudouridine excretion was also increased in cells infected by a mutant of Rous sarcoma virus (RAV-1) which, lacking the src gene, does not transform the cells but replicates normally. To investigate if pseudouridine overproduction is related to an altered turnover rate of specific transfer RNA (tRNA) species which functions as primer of retrovirus reverse transcriptase, the concentration of non-acylated proline-accepting tRNA and non-acylated tryptophan-accepting tRNA, primers of reverse transcriptase of murine leukemia virus and of Rous sarcoma virus, respectively, has been measured, the former in normal and transformed AKR thymus and the latter in normal fibroblasts and in fibroblasts infected by Rous sarcoma virus or by its nontransforming mutant. The results show that in both systems a significant increase of the primer tRNA species occurs in the infected or transformed cells.

Animals↗
PubMed1987

[Expression of a cross-reactive antigen on the surface of human epidermoid carcinomas overproducing EGF-receptor shared with RSV-induced tumors].

Analysis based on the complement-dependent cytotoxicity (CDC) assays using syngeneic antiserum against a Rous sarcoma virus(RSV)-induced mouse tumor(CSA1M) showed that a cross-reactive antigen with a common tumor-associated cell surface antigen(TASA) of RSV-induced mouse tumors was shared with two human tumors A431 and MDA-468 overexpressing epidermal growth factor receptor(EGFR). The TASA, however, was not expressed on four human choriocarcinomas, a human lung cancer A2182, and human embryo fibroblasts HFF. Immunofluorescent studies demonstrated that A431 does not express a src gene product detected by anti-pp60src monoclonal antibody(MoAb). Two variant clones derived from A431 reducing number of ERFR (cl-15 and cl-16) have almost same growth rate and expression of transferrin receptor(Tf-R) in comparison with parental A431 cells. These clones, however, decreased the expression of TASA. Furthermore, CDC assays and enzyme-linked immunosorbent assay(ELISA) revealed that A431 reduced the expression of the TASA by pretreatment of EGF, but not with insulin. All these findings indicate a close association between a cross reactive antigen with the TASA of RSV-induced tumors and EGFR.

Animals↗