Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

f gr is a member of the protein kinase oncogene family and was found to have the highest homology to yes gene among the members of the family. Using a v-yes probe, a molecular clone of human c-f gr locus was isolated from a genomic library. Nucleotide sequence determination revealed that the actin gene-like sequence found in v-f gr gene was absent at the corresponding position of the c-f gr gene. Thus, the v-f gr gene product is considered to be a tri-chimeric gene product consisting of viral gag gene and two distinct cellular genes, actin gene and the proto-f gr gene.
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PMID:Human c-f gr gene does not contain coding sequence for actin-like protein. 392 31

The nucleotide sequence of a PstI fragment prepared from a cloned MH2 virus genome, pMH2-Hd, has been deduced using chemical and enzymatic methods. This fragment, 1862 nucleotides in length, starts with the gag gene, encodes the v-mil sequence and stops within the v-myc gene. This sequence shows that the v-mil gene is fused to the gag gene giving rise to a fused polyprotein of 98 000 daltons: 515 amino acids at the amino terminus would correspond to p10, p19, p27 and part of p12 determinants, 347 amino acids at the carboxy terminus correspond to the v-mil specific sequence. The mil protein shares homology with a number of onc proteins such as src, fes, fms, mos, yes, fps and erbB, as well as with the catalytic chain of the cAMP-dependent protein kinase. This PstI fragment also encodes the beginning of the myc gene which was integrated in MH2 along with the 3' end of the preceding intron placing an acceptor splice site in front of the used open reading frame. As deduced from the sequence, the MH2 myc protein is not identical to the MC29 myc protein. It differs at its amino terminus, which contains little or no gag determinants, depending on the ATG used to initiate translation.
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PMID:The second oncogene mil of avian retrovirus MH2 is related to the src gene family. 608 17

Expression of RSV-specific proteins was analysed in two virogenic and three helper-dependent RSV-transformed mammalian cell lines by the radioimmunoprecipitation technique. In all cell lines the only product of the gag gene was represented by the precursor Pr76gag without its further processing. The env gene was expressed in several lines in the form of 85K protein, but the product of this gene was absent in TWERC cells. The src gene product (pp60src) was identified by the protein kinase assay in all cells. In the kinase reaction in vitro, this protein can also phosphorylate some cellular proteins (130K, 34-36K and others) and the heavy chain of IgG.
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PMID:Expression of RSV-specific proteins in RSV-transformed mammalian cells. 609 Feb 35

Two replication-defective avian sarcoma viruses, S1 and S2, which were independently isolated from tumors of chickens inoculated with avian lymphatic leukosis virus (LLV) were characterized. The genomes of S1 and S2 contain src-related sequences and are, respectively, about 3.9 and 4.5 kilobases long. pp60src-related proteins with molecular weights of 62,000 (p62) were detected in cells infected with these viruses, and protein kinase activity was found to be associated with these proteins. No other viral proteins, such as gag, pol, and env gene products, were detected. These results suggested that the c-src sequence in normal chicken cells was incorporated into LLV genomes by recombination at the expense of most of the viral genes to generate highly defective new sarcoma viruses.
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PMID:Characterization of two strains of avian sarcoma virus isolated from avian lymphatic leukosis virus-induced sarcomas. 609 28

The gag-mos hybrid protein encoded by ts110 MoMuSV was shown to have an associated protein kinase activity which phosphorylated both P85gag-mos and P58gag when [gamma-32P]ATP and a manganese cofactor were added to an immune complex containing P85gag-mos. Immunoprecipitation and removal of P85gag-mos from the reaction mixture by either an anti-mos or anti-gag serum resulted in a subsequent elimination of in vitro P85gag-mos and P58gag phosphorylation. This kinase activity was shown to be either an intrinsic property of P85gag-mos or else a tightly bound cellular enzyme activity resistant to elution with 2.0 M NaCl, 0.5% deoxycholate, and 0.1% SDS. A correlation was made between the amount of kinase activity and the concentration of P85gag-mos. Viral gag antisera were also used to show immune complex phosphorylation of another gag-mos hybrid protein termed P100gag-mos, derived from a revertant of ts110. In vitro phosphorylation experiments derived from v-mos transformed MuSV 124 cells using viral gag antisera were completely negative which shows that the gag-mos kinase in 6m2 cells is not merely a gag-associated kinase that phosphorylates MuSV coded gag gene products. When shifting 6m2 cells from a permissive temperature to the nonpermissive temperature of 39 degrees for 2-4 hr, a noticeable change toward a more normal morphology occurs. NRK 54-5A4 cells infected with a revertant of ts110 with wild-type phenotype, showed little change in morphology between permissive and nonpermissive temperatures. In addition to the ts defect affecting P85gag-mos production previously reported, a second ts defect in ts110 is reported here which is functional in nature; it can be detected within 5 min after shift to 39 degrees by the heat lability of the P85-associated kinase activity. The P100gag-mos protein kinase from the wild-type revertant cells did not exhibit this heat sensitivity under similar conditions. The thermal inactivation of the P85 kinase was shown to precede events that occur as cells are shifted to the restricted temperature including morphological reversion to the normal phenotype, and the decrease in P85gag-mos concentration. Based on all of these observations, it is suggested that the P85-associated kinase activity is not merely an adherent cellular kinase, but actually a function of the gag-mos gene product.
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PMID:Further characterization of the P85gag-mos -associated protein kinase activity. 609 55

A NRK cell clone (6m2 cells) infected with ts110 Moloney murine sarcoma virus (MuSV) produce a gag-mos protein, P85gag-mos, and a truncated gag protein of Mr 58,000d termed P58gag. The gag-mos protein is produced from a 3.5-kb mRNA whereas the gag protein is made from a 4.0-kb mRNA. It has been proposed that the 3.5-kb RNA is produced from the 4.0-kb RNA by a splicing mechanism (R. P. Junghans, E. C. Murphy, Jr., and R. B. Arlinghaus (1982) J. Mol. Biol. 161, 229-255). The results presented here provide further support for this model. The expression of the 3.5-kb RNA and the gag-mos protein increased as the temperature at which 6m2 cells were maintained was lowered from 39 to 28 degrees. This increase coincided with a decrease in both the 4.0-kb RNA and its product P58gag. The optimum temperature for syntheses of both the gag-mos mRNA and its protein was found to be 28 degrees. Consistent with the increase in the level of the gag-mos protein is the increase in the protein kinase activity associated with P85gag-mos and the degree of morphological transformation of 6m2 cells. Thus, the level of P85gag-mos within 6m2 cells is directly proportional to the degree of cell transformation and the amount of the kinase activity associated with the gag-mos protein, providing convincing evidence that P85gag-mos plays a direct role in the neoplastic transformation of these cells.
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PMID:The gag-mos hybrid protein of ts110 Moloney murine sarcoma virus: variation of gene expression with temperature. 609 31

Gallo and his coworkers isolated a retrovirus (HTLV) from human cells derived from T-cell leukemia and lymphoma. Hinuma and his coworkers isolated independently a similar virus from a cell line derived from adult T-cell leukemia (ATL) patient. The occurrence of ATL correlates with the formation of antibody to ATL associated antigens or ATLA. To understand the etiological relationship between ATL and HTLV, we analyzed the antigens termed ATLA and found that they are polypeptides encoded by HTLV genome. We further studied the genome of HTLV and its gene expression in cells as well as in a cell-free translation system. We focused on a defective type HTLV produced from a cell line MT-2 that transforms normal lymphocytes most efficiently. The 24S defective gene of HTLV consists of a fused gene of gag-pXs and is amplified at the proviral state. The in vitro translation experiments revealed that the 24S defective gene of HTLV directs the synthesis of p28 of ATLA. By the sequence analysis of the amplified gag-pXs fused genes, we found that a carboxy terminal portion of p28 is translated from a pX-0 region. We further investigated a function of the gag-pX-0 fusion protein, p28. The p28 has an associated protein kinase activity that requires manganese instead of magnesium and phosphorylates the serine residue specifically. Another defective HTLV with a genomic 32S RNA was analyzed. The 32S defective genomic RNA forms a subgenomic 20S RNA in cells. The 20S mRNA is a transcript of an env-pXs fused genome and directs the synthesis of a fused glycoprotein, gp68 of ATLA. The sequence analysis of a cloned cDNA derived from the subgenomic 20S mRNA revealed that a coding frame of the entire pX-IV region is translated. In fact, an antibody against synthetic polypeptides of the pX-IV, immunoprecipitated the gp68. These results demonstrate at the first time that the pX-0 and pX-IV of HTLV genome are expressed in human cells. The biological activities of the fused pXs proteins are also discussed. Human T-cell leukemia virus type I (HTLV-I), a family of human retrovirus and the predicted causative agent of human adult T-cell leukemia/lymphoma (ATL) consists of the gag, pol, env, and pX regions (1).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The pX region of HTLV-I. 610 Jun 40

The transformation-specific polyproteins of avian sarcoma viruses PRCII, PRCII-p, Fujinami sarcoma virus (FSV), and Esh sarcoma virus (ESV) consist of two domains, one derived from a partial viral gag gene and the other representing an apparently cell-derived insert in the defective viral genome. These gag-linked proteins were cleaved with retrovirion protease p15. Cleavage of PRCII-p polyprotein P170, P105 of PRCII, and P140 of FSV occurred within the gag domain and generated fragments of Mr 130,000, 70,000, and 115,000, respectively, containing all of the transformation-specific sequences linked to a remnant of the original gag sequences. ESV P80 was cleaved inside the transformation-specific domain, yielding a Mr 35,000--38,000 fragment from the NH2-terminal half of the molecule consisting of the entire gag portion and some no-gag sequences and a Mr 48,000 fragment containing most of the transformation-specific sequences. The tyrosine phosphorylation sites of the polyproteins were found in every case in the transformation-specific fragments. The major serine phosphorylation site of ESV P80 was found to reside in the Mr 35,000--38,000 gag-containing fragment, probably within the transformation-specific sequences of that cleavage product. Removal of all of the gag domain of ESV P80 or most of the gag domain in PRCII-p P170, PRCII P105, and FSV P140 does not affect their ability to be phosphorylated by the polyprotein-associated tyrosine-specific protein kinase activities. This observation suggests that the gag sequences of the polyproteins of classes II (PRCII-p, PRCII, and FSV) and III (ESV) avian sarcoma viruses may not be required for this enzymatic function, which appears to be of importance in transformation.
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PMID:Cleavage of four avian sarcoma virus polyproteins with virion protease p15 removes gag sequences and yields large fragments that function as tyrosine phosphoacceptors in vitro. 617 Sep 87

UR2 is a newly characterized avian sarcoma virus whose genome contains a unique sequence that is not related to the sequences of other avian sarcoma virus transforming genes thus far identified. This unique sequence, termed ros, is fused to part of the viral gag gene. The product of the fused gag-ros gene of UR2 is a protein of 68,000 daltons (P68) immunoprecipitable by antiserum against viral gag proteins. In vitro translation of viral RNA and in vivo pulse-chase experiments showed that P68 is not synthesized as a large precursor and that it is the only protein product encoded in the UR2 genome, suggesting that it is involved in cell transformation by UR2. In vivo, P68 was phosphorylated at both serine and tyrosine residues. Immunoprecipitates of P68 with anti-gag antisera had a cyclic nucleotide-independent protein kinase activity that phosphorylated P68, rabbit immunoglobulin G in the immune complex, and alpha-casein. The phosphorylation by P68 was specific to tyrosine of the substrate proteins. P68 was phosphorylated in vitro at only one tyrosine site, and the tryptic phosphopeptide of in vitro-labeled P68 was different from those of Fujinami sarcoma virus P140 and avian sarcoma virus Y73-P90. A comparison of the protein kinases encoded by UR2, Rous sarcoma virus, Fujinami sarcoma virus, and avian sarcoma virus Y73 revealed that UR2-P68 protein kinase is distinct from the protein kinases encoded by those viruses by several criteria. Our results suggest that several different protein kinases encoded by viral transforming genes have the same functional specificity and cause essentially the same cellular alterations.
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PMID:Avian sarcoma virus UR2 encodes a transforming protein which is associated with a unique protein kinase activity. 617 70

Hybridomas secreting monoclonal antibodies directed against polyprotein gene products of the Gardner, Snyder-Theilen, and McDonough strain of feline sarcoma virus have been isolated. Antibody produced by one hybridoma recognizes immunological determinants localized within a feline leukemia virus gag gene structural component (p15) common to polyproteins encoded by each feline sarcoma virus isolate while antibody produced by a second is specific for p30 determinants unique to P170gag-fms. Additional hybridomas secrete antibody directed against v-fes specific determinants common to the Gardner and Snyder-Theilen feline sarcoma virus-encoded polyproteins and to v-fms determinants unique to P170gas-fms polyprotein. GA P110gas-fes and ST P85gas-fes immunoprecipitated by antibody directed against p15 exhibit readily detectable levels of protein kinase activity but lack such activity when precipitated by antibody specific for their acquired sequence (v-fes) components. P170gas-fms immunoprecipitated by monoclonal antibody to either p15 or p30 lacks detectable levels of autophosphorylation but represents a substrate for the GA P110gag-fes and ST P85gag-fes enzymatic activities. These findings argue that the v-fes-associated protein kinase represents an intrinsic property of the v-fes gene product and recognizes tyrosine acceptor sites within polyprotein gene products of all three strains of feline sarcoma virus.
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PMID:Monoclonal antibodies specific to transforming polyproteins encoded by independent isolates of feline sarcoma virus. 618 42


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