Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.11.1 (protein kinase)
81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The DNA sequence (8.9 kb) covering about 70% of the short unique region (Us) and part of the short inverted repeat of the Marek's disease virus type 1 GA strain was determined. Computer analysis of the sequence showed the presence of nine potential open reading frames (ORFs), consisting of more than 300 nucleotides in the Us region. Of these ORFs, four were found to be homologous to US10 (minor virion protein), US3 (protein kinase), US2, and US6 (gD) in the Us region of alpha-herpesvirus herpes simplex virus type 1. The protein kinase homologue is especially well conserved in alpha-herpesviruses. No counterpart of the nine MDV1 ORFs was found in the beta-herpes virus human cytomegalovirus and gamma-herpesvirus Epstein-Barr virus, suggesting that MDV1 is more similar to the alpha-herpesviruses. The junction of the Us region and the short inverted repeat was also determined by comparison between the sequences of the DNA fragments, including the terminal and internal repeats. Northern blot analysis showed that the Us region within the 8.9 kb sequence was transcriptionally active in MDV1-infected cells.
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PMID:Sequence determination and genetic content of an 8.9-kb restriction fragment in the short unique region and the internal inverted repeat of Marek's disease virus type 1 DNA. 128 82

The deduced amino acid sequences of the open reading frames (ORFs) mapping in the short unique segment (US) of Marek's disease virus (MDV) reported in the accompanying paper have been analysed using computer programs to determine their relationships to herpesvirus proteins. Analysis of the catalytic domains of protein kinases showed that the MDV kinase (MDV PK) was closely related to the alphaherpesvirus protein kinase mapping in US. The results also showed that the MDV PK was more closely related to the cellular kinases that control cell division than to the proto-oncogenes c-src and c-mos and it was predicted that the MDV PK would phosphorylate serine/threonine. The MDV homologue of herpes simplex virus (HSV) glycoprotein D (gD) contained several residues that were conserved in mammalian herpesviruses. In particular, six cysteines were perfectly aligned in all the gDs and there were numerous conservative substitutions. Although only approximately 65% of the MDV homologue of glycoprotein I (gI) of HSV has been sequenced, it was clear that a significant number of amino acid residues including four cysteines were conserved in the gI homologues of MDV and mammalian herpesviruses. Further analysis suggested that MDV gD was more closely related to the gDs of pseudorabies virus (PRV) and equine herpesvirus 1 than to the gD of HSV-1 and HSV-2. It was noted that HSV-2 glycoprotein G (gG), PRV gX and MDV gD were related and that MDV ORF4 was related to MDV gD and probably to HSV-1 gG. The results have shown a clear relationship between the genes of MDV and their counterparts in mammalian alphaherpesviruses and are consistent with the idea that MDV glycoprotein genes in US might have arisen by a process of gene duplication and independent evolution.
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PMID:Properties and evolutionary relationships of the Marek's disease virus homologues of protein kinase, glycoprotein D and glycoprotein I of herpes simplex virus. 184 76

The DNA sequence of a 5.5 kbp EcoRI fragment located in the short unique region (US) of the 'highly oncogenic' strain RB1B of Marek's disease virus (MDV) was determined. The sequence contained six open reading frames (ORFs), four of which were homologous to proteins mapping in the US region of herpes simplex virus type 1 (HSV-1). These include the homologues of HSV-1 protein kinase, glycoprotein D (gD), glycoprotein I (gI) and US2 which is of unknown function. The MDV ORFs had a marked bias for A or T in the third codon position and analysis of the dinucleotide frequencies showed a marginal deficit in ApG/CpT but no overall deviation of CpG from random expectations. Comparison of genes in the US region of MDV to herpesvirus proteins confirmed and extended our previous observation that MDV is more closely related to alphaherpesviruses than to gamma-herpesviruses. We also showed that MDV possessed a homologue of HSV-1 gD which is lacking in varicella-zoster virus (VZV) but that MDV probably lacked homologues of US4 and US5 of HSV-1. These results show that in contrast to the genes in the long unique region which were grossly collinear in HSV, VZV and MDV, those mapping in US show greater diversity.
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PMID:DNA sequence and organization of genes in a 5.5 kbp EcoRI fragment mapping in the short unique segment of Marek's disease virus (strain RB1B). 184 77

Infection of normocholesterolemic, specific-pathogen-free chickens with Marek's disease herpesvirus (MDV) has been shown histologically to lead to chronic atherosclerosis like that in humans. The development of herpesvirus-induced atherosclerosis in vivo and the presence of specific Marek's antigen within aortic cells suggested that MDV infection may modify lipid metabolism and lead to significant lipid accumulation. Experiments reported herein were designed to determine the types and quantity of lipid present in aortas from MDV-infected and uninfected chickens between 2 and 8 months of age following infection and assess one possible mechanism of lipid accumulation by evaluating the effect of MDV infection on aortic cholesterol and cholesteryl ester (CE) metabolism. Chromatographic-fluorometric analyses indicated that at 4 and 8 months of age after MDV inoculation, MDV-infected animals had a significant (P less than 0.05) two-fold to threefold increase in total aortic lipid accumulation characterized by significant increases in cholesterol, CE, triacylglycerol, and phospholipid as compared with aortas from uninfected animals. At 8 months of age, similar increases in aortic lipid accumulation were observed in MDV-infected animals as compared with those animals vaccinated with turkey herpesvirus and later challenged with MDV. CE synthetic activity was increased significantly by 50% at 4 months of age in the MDV-infected group as compared with the uninfected group, which could explain the initial increase in CE accumulation. By 8 months of age, the authors also observed a twofold increase in CE synthetic activity and a 30% and 80% reduction in lysosomal and cytoplasmic CE hydrolytic activities, respectively, in aortas of MDV-infected chickens as compared to controls. Moreover, infection with MDV blocked the activation of cytoplasmic CE hydrolytic activity by dibutyryl cyclic AMP or exogenous cyclic AMP-dependent protein kinase. Taken together, these results suggest that lipid accretion in aortas of MDV-infected chickens results, in part, from alterations in cholesterol/CE metabolism during early stages of the disease. These findings support the hypothesis that human atherosclerosis may result from specific herpesvirus infection which can alter lipid metabolism and lead to lipid accretion.
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PMID:Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation. 293 87

Herpesvirus infection has been shown to alter the cholesteryl ester cycle in avian arterial smooth muscle cells, resulting in cytoplasmic cholesteryl ester accumulation (Hajjar, D. P., Falcone, D. J., Fabricant, C. G., and Fabricant, J. (1985) J. Biol. Chem. 260, 6124-6128). In this study, we attempted to define some of the regulatory mechanisms associated with the control of cytoplasmic cholesteryl esterase in Marek's disease herpesvirus (MDV)-infected cells. We found that cholesteryl esterase activity in MDV-infected cells could not be activated by dibutyryl cyclic AMP, dibutyryl cyclic AMP added together with protein kinase, or agonists of adenylate cyclase. Activation of cytoplasmic cholesteryl esterase activity occurred in uninfected cells and in cells infected with a control virus, turkey herpesvirus. Furthermore, the rate of cholesterol efflux from arterial smooth muscle cells challenged with dibutyryl cyclic AMP was unchanged in MDV-infected cells as compared to uninfected or turkey herpesvirus-infected cells in which efflux was increased. We propose that the reduced cytoplasmic cholesteryl esterase activity in lipid-laden, herpesvirus-infected cells is due partly to its inability to be activated by the cyclic AMP-protein kinase mechanism. This may contribute to the pathologic changes seen in MDV-infected arterial cells, including accumulation of intracellular cholesteryl esters.
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PMID:Herpesvirus infection prevents activation of cytoplasmic cholesteryl esterase in arterial smooth muscle cells. 301 90

A fowlpox recombinant expressing the pp38 antigen of Marek's disease virus has been constructed. Production of pp38 in chick embryo fibroblasts (CEF) infected at a m.o.i. of 1 pfu/cell occurred over a period of 5 days and reached a peak at 72 h after infection. The pp38 antigen could be released from infected cells by freezing and thawing. Western blot analysis showed that denatured pp38 antigen reacted with antisera from chickens inoculated with serotype 1 MDV but failed to react with antisera from chickens inoculated with MDV serotype 2 or HVT. The results suggest that MDV pp38 contains a serotype 1-specific epitope which becomes available upon denaturation of the antigen and that this could be exploited to identify MDV-specific antibodies in epidemiological studies. The relationship between pp38 and the related polypeptides pp24 and pp41 in MDV-infected cells was also examined. The results suggest that pp24 and pp38 are synthesised independently and that MDV coded proteins (probably a protein kinase) might be required to convert pp38 to pp41.
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PMID:Use of recombinant pp38 antigen of Marek's disease virus to identify serotype 1-specific antibodies in chicken sera by western blotting. 771 41

The open reading frame (ORF) of 1206 bp within the short unique region (Us) of Marek's disease virus type 1 (MDV1) shows significant homology with the herpes simplex virus type 1 US3 gene encoding protein kinase (PK). The lacZ gene of Escherichia coli was inserted within the ORF, designated MDV1-US3, of MDV1 K544 strain DNA by homologous recombination. The plaque-purified recombinant MDV1 stably expressed the beta-galactosidase encoded by the inserted lacZ gene in infected cells and replicated well as the parental K544 strain. Antibodies against both MDV1 antigen and beta-galactosidase were detected in the sera of chickens immunized with recombinant MDV1. Chickens vaccinated with the recombinant MDV1 were protected from challenge with virulent MDV1. The MDV1 US3 gene expressed by a baculovirus vector encoded a 44-kDa protein. Mouse antisera against the 44-kDa protein reacted with two proteins of 44 and 45 kDa in extracts of cells infected with MDV1 but not with MDV types 2 or 3. The PK activity was detected in immune complexes of the anti-44-kDa sera with extracts of cells infected with MDV1 but not with the recombinant MDV1. Thus, PK encoded from the MDV1-US3 is not essential for virus replication in cell culture and vaccine-induced immunity.
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PMID:Marek's disease virus protein kinase gene identified within the short unique region of the viral genome is not essential for viral replication in cell culture and vaccine-induced immunity in chickens. 839 Nov 81

The DNA sequence of the whole of the short unique region (U(s)) and that of part of the short terminal repeat (TRs) of herpesvirus of turkeys (HVT) were determined. HVT U(s) is 8.6 kbp long and contains eight potential open reading frames (ORFs). Seven of these have counterparts in the U(s) of herpes simplex virus type 1 (HSV-1). The homologous proteins include US1, US2, US10, protein kinase (US3) and the glycoproteins gD, gI and gE. In addition, HVT contains one ORF which has a counterpart in the U(s) of Marek's disease virus (MDV) but is not homologous to any other known herpesvirus gene. Although HVT and MDV proteins encoded by U(s) genes have evident similarities with proteins encoded by alphaherpesviruses, multiple alignment analysis of predicted amino acid sequences show that HVT proteins are more closely related to MDV proteins than to homologous proteins of mammalian alphaherpesviruses. The percentage amino acid identity between HVT and MDV U(s)-encoded proteins ranges from 35 to 65, the most conserved protein being encoded by the homologues of the HSV-1 US2 gene. Most of the genes are colinear with those of HSV-1 except US10 which is transposed in HVT and MDV. A characteristic feature of HVT is the fact that approximately two-thirds of the gE gene is located in the inverted repeats flanking U(s).
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PMID:The complete sequence and gene organization of the short unique region of herpesvirus of turkeys. 840 40

The gene of Marek's disease virus (MDV) serotype 2 (MDV2) homologous to glycoprotein D (gD) of herpes simplex virus (HSV) was identified and characterized by its nucleotide and predicted amino acid sequences. The MDV2 gD homologous gene contains an open reading frame capable of specifying a polypeptide of 385 amino acids, which include N- and C-terminal hydrophobic domains consistent with signal and anchor regions, respectively, and two potential N-linked glycosylation sites, one of which was located in a highly conserved region when compared to MDV serotype 1 (MDV1) and herpesvirus of turkeys (HVT). By northern blot analysis using a MDV2 gD-specific DNA probe, two highly abundant polycistronic 6.0 and 4.2 kb transcripts were detected in MDV2-infected cells. The genes encoding MDV2 protein kinase (PK), gD, and glycoprotein I (gI) homologues are transcribed to form 3' coterminal mRNAs of 6.0 kb (encoding PK, gD and gI) and 4.2 kb (encoding gD and gI), respectively. By using rapid amplification cDNA end (RACE) method, several RNA start sites, to be thought those of the 4.2 kb mRNA, were detected in the upstream of MDV2 gD homologue.
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PMID:Identification of a potential Marek's disease virus serotype 2 glycoprotein D gene with homology to herpes simplex virus glycoprotein D. 897 34

Studies on the Marek's disease virus (MDV) serotype 2 (MDV2) genome may be important for understanding the naturally nononcogenic nature of the virus. To determine the complete DNA sequence of MDV2 unique short (Us) region, genomic BamHI fragments F, M1 and R were sequenced. The MDV2 Us region is 12109 bp long and contains 12 potential open reading frames (ORFs) likely to encode for proteins. Seven of them exhibit homologies to herpes simplex virus type 1 (HSV-1) US1 (ICP22), US2, US3 (protein kinase), US6 (gD), US7 (gI), US8 (gE) and US10 genes. These ORFs are conserved in a similar arrangement with those of HSV-1, except for US10 which is transposed in the Us regions of all three MDV serotypes. The predicted amino acid sequence of MDV2 ORF6 is homologous to SORF3 of the other serotypes of MDV serotype 1 (MDV1) and herpesvirus of turkeys (HVT) and to infectious laryngotracheitis virus SR1. In addition, four ORFs, which have been identified around the Us and inverted repeat junction regions, have no apparent relation to any other known herpesvirus genes. The identified ORFs in the MDV2 Us region were more colinear with their previously reported locations of MDV1 than with those of HVT and other alphaherpesviruses. Ten of the 12 ORFs in the MDV2 Us region were expressed and transcribed with 3'-coterminal transcripts and/or a unique transcript in the virus-infected cells. Compared to other MDV serotypes, the MDV2 Us-encoded proteins showed 46-70% and 33-59% identities with equivalent of MDV1 and HVT at the amino acid level, respectively. Our present data will be useful to understand the different pathogenicity among serotypes of MDV and to allow precise manipulation of the genes for a possible use in genetically engineered vaccines.
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PMID:The genetic organization and transcriptional analysis of the short unique region in the genome of nononcogenic Marek's disease virus serotype 2. 987 70


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