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)

Radiation leukemia virus (RadLV) causes thymic lymphoma in 90% of susceptible mice after a latent period of several months. The virally encoded polypeptides produced by RadLV-induced lymphoma cells were analyzed by immunoprecipitation and NaDodSO4/polyacrylamide gel electrophoresis. Along with the expected precursor and mature forms of gag and env gene products, a polypeptide of 36,000 molecular weight (p36) was precipitated by anti-gag antisera. It was not precipitable by normal sera or anti-env antibodies. Like the gag-associated fusion proteins of some acute leukemia viruses, p36 was found to be phosphorylated in vivo, although it lacked detectable ATP-specific protein kinase activity in vitro. By kinetics during pulse-chase labeling experiments and by comparison of two-dimensional tryptic peptide maps, this protein is not an intermediate in gag precursor processing. One lymphoma cell line is described that resembles a nonproducer RadLV-transformant, synthesizing relatively large amounts of p36 in the absence of Pr66gag or p30 production. Several RadLV-induced lymphoma cell lines also produce p36, while it was not detectable in the radiation-induced lines tested. In addition, p36 was not produced by mouse or mink fibroblasts or cultured thymocyte cell lines infected with virus passaged from the RadLV-induced lymphomas. We conclude that p36 may represent a previously unrecognized transformation-related protein induced directly or indirectly by infection with RadLV.
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PMID:Identification of a 36,000-molecular weight, gag-related phosphoprotein in lymphoma cells transformed by radiation leukemia virus. 633 Feb 69

Retroviruses carry cell-derived oncogenes (v-onc) that have the potential to transform cells in culture and induce tumours in vivo. One of the few carcinoma-inducing viruses is the acutely transforming retrovirus MH2, which carries the putative oncogene v-mil and the known oncogene v-myc. Recently, a high degree of homology was discovered between v-mil and v-raf, the transforming gene of the murine retrovirus 3611 murine sarcoma virus (MSV), whereas homology to v-src is low. Both viruses express their oncogenes as the gag-fusion polyproteins p100gag-mil and p75gag-raf (of respective relative molecular mass (Mr) 100,000 and 75,000), while the myc oncogene of MH2 is expressed by means of a subgenomic messenger RNA. We have recently demonstrated that p100gag-mil is not a nuclear protein. Here we report that purified p100gag-mil and p75gag-raf exhibit protein kinase activities in vitro which, in contrast to the src-related p130gag-fps of Fujinami sarcoma virus (FSV) and all other characterized oncogene-encoded protein kinases, phosphorylate serine and threonine but not tyrosine. Both types of protein kinases phosphorylate lipids in vitro.
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PMID:Serine- and threonine-specific protein kinase activities of purified gag-mil and gag-raf proteins. 643 34

From molecularly cloned DNAs of Fujinami sarcoma virus (FSV) and the Schmidt-Ruppin-A strain of Rous sarcoma virus (SRA), viral DNA was constructed in which fps-specific sequences encoded in FSV replaced the src gene of SRA. A 3' fragment of FSV DNA, from an ATG methionine coding sequence 148 base pairs downstream from the gag-fps junction through the long terminal repeat, was joined to cloned SRA DNA at the translation start site for the src gene. The resultant DNA clone contained the splice acceptor site for src mRNA processing in SRA, but contained no src coding sequences from SRA nor any gag sequences from FSV. All genes for the replication of SRA were retained. Transfection of this cloned viral DNA genome into chicken embryo fibroblasts induced morphological transformation of the cells in culture. However, the morphology of the transformed cells was distinct from that observed in cells infected with wild-type FSV. The transformed cells produced a nondefective transforming virus called F36 which contained a hybrid FSV-SRA long terminal repeat. F36-infected cells produced a protein with the expected molecular weight of 91,000, which had an associated protein kinase activity and was immunoprecipitated by antibodies raised against fps gene determinants but not by antibodies raised against gag or src proteins. Injection of F36 virus into 8-day-old chicks produced tumors at the site of inoculation, detectable within 7 days. These results demonstrated that the gag portion of the gag-fps fusion protein of FSV is not required for transformation or tumorigenesis.
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PMID:A fps gene without gag gene sequences transforms cells in culture and induces tumors in chickens. 660 29

The protein kinase Akt, also known as Protein Kinase B, has been implicated in the survival of several cell types challenged with various apoptotic stimuli. In CCL39 lung fibroblasts, apoptosis is induced by anchorage and mitogen removal. Mitogen-induced activation of Akt is highly anchorage dependent in these cells and removal of adhesion is accompanied by a rapid loss in responsiveness to soluble agonists followed by a significant decrease in Akt abundance. Loss of the protein appears to be independent of kinase activation since the expression of a constitutively active form, gag-Akt, is also dependent upon cell adhesion. Although the disappearance of Akt is coincident with the induction of programmed cell death, it cannot be fully prevented by treatment of cells with the caspase inhibitor ZVAD or by sustained activation of the anti-apoptotic Raf/ERK pathway, in cells expressing an inducible DeltaRaf-1:ER construct. In addition, a previously unrecognized decrease in Akt mRNA levels following anchorage removal occurs suggesting that anchorage-dependent transcriptional and/or post-transcriptional mechanisms contribute to the adhesion-dependent regulation of Akt expression.
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PMID:Adhesion-dependent control of Akt/protein kinase B occurs at multiple levels. 1276 45

The host cell MAP kinase ERK-2 incorporated within human immunodeficiency virus type 1 particles plays a critical role in virus infectivity by phosphorylating viral proteins. Recently, a fraction of the virus incorporated late (L) domain-containing p6(gag) protein, which has an essential function in the release of viral particles from the cell surface, was reported to be phosphorylated by an unknown virus-associated cellular protein kinase (Muller, B., Patschinsky, T., and Krausslich, H. G. (2002) J. Virol. 76, 1015-1024). The present study demonstrates the contribution of the MAP kinase ERK-2 in p6(gag) phosphorylation. According to mutational analysis, a single ERK-2-phosphorylated threonine residue, belonging to a highly conserved phosphorylation MAP kinase consensus site, was identified at position 23 within p6(gag). Substitution by an alanine of the Thr(23) phosphorylable residue within the pNL4.3 molecular clone was found to decrease viral release from various cell types. As observed from electron microscopy experiments, most virions produced from this molecular clone remained incompletely separated from the host cell membrane with an immature morphology and displayed a reduced infectivity in single round infection experiments. Analysis of protein processing by Western blotting experiments revealed an incomplete Pr55(gag) maturation and a reduction in the virion-associated reverse transcriptase proteins was observed that was not related to differences in intracellular viral protein expression. Altogether, these data suggest that phosphorylation of p6(gag) protein by virus-associated ERK-2 is involved in the budding stage of HIV-1 life cycle.
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PMID:The host cell MAP kinase ERK-2 regulates viral assembly and release by phosphorylating the p6gag protein of HIV-1. 1515 23

The detailed properties of the enzyme from Pseudomonas aeruginosa, which catalyzes the N-acyl linkage between myristic acid and the N-terminal glycine residue of the octapeptide GNAAAARR-NH(2) (PKA) in aqueous solution without ATP and CoA, were studied. The substrate specificity for the acyl peptide in the synthetic reaction was examined, and it was found that at least eight amino acid residues are required for the reaction and that the N-terminal glycine residue is not absolutely essential for the reaction because the activity was detected using the octapeptide that has an N-terminal alanine. The activity was also strongly affected by the amino acid sequence because the activity was very weak in the reaction using GARASVLS-NH(2) (HIV-1p17(gag)). The substrate specificity for fatty acids was also examined. In the reactions using lauric acid and decanoic acid, only slight activities were detected; however, those activities were very small compared with the activity in the reaction using myristic acid. In addition, the degradation of myristoyl PKA by the enzyme was detected, although there are only a few reports on demyristoylation. The optimum pH and temperature of the degradation reaction were consistent with those of the synthetic reaction. The degradation reaction was inhibited by divalent cations.
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PMID:Synthesis and degradation of acyl peptide using enzyme from Pseudomonas aeruginosa. 1839 80

Ty3 elements of S. cerevisiae contain two overlapping coding regions, GAG3 and POL3, which are functional homologues of retroviral gag and pol genes, respectively. Pol3 is translated as a Gag3-Pol3 fusion protein dependent on a +1 programmed frameshift at a site with the overlap between the two genes. We show that the Ty3 frameshift frequency varies up to 10-fold in S. cerevisiae cells depending on carbon source. Frameshift efficiency is significantly lower in cells growing on glucose as carbon source than in cells growing on poor alternative carbon sources (glycerol/lactate or galactose). Our results indicate that Ty3 programmed ribosomal frameshift efficiency in response to glucose signalling requires two protein kinases: Snf1p and cAMP-dependent protein kinase A (PKA). Increased frameshifting on alternative carbon sources also appears to require cytoplasmic localization of Snf1p, mediated by the Sip2p protein. In addition to the two required protein kinases, our results implicate that Stm1p, a ribosome-associated protein involved in nutrient sensing, is essential for the carbon source-dependent regulation of Ty3 frameshifting. These data indicate that Ty3 programmed ribosomal frameshift is not a constitutive process but that it is regulated in response to the glucose-signalling pathway.
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PMID:Glucose signalling pathway controls the programmed ribosomal frameshift efficiency in retroviral-like element Ty3 in Saccharomyces cerevisiae. 2198 11


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