Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A persistent infection with rabies virus (HEP-Flury) was established in the CNS-derived hybrid cell line 108CC15 which possesses specific membrane receptors for prostaglandins, catecholamines and acetylcholine. We report a differential virus influence on the specific receptor response to PGE, isoproterenol and acetycholine as indicated by typical changes of the intracellular cyclic AMP levels. As the adenylate cyclase activity was unchanged in infected cells in vitro, a selective virus influence on specific receptors themselves or their coupling to the cAMP synthesizing system must be considered.
J Gen Virol 1979 Mar
PMID:Rabies virus infection selectively impairs membrane receptor functions in neuronal model cells. 21 41

In order to elucidate the properties of an inhibitor of rabies virus haemagglutinin in normal animal sera, experiments were made with the HEP Flury strain and calf serum which contains the inhibitor. The results of physico-chemical treatment, gel-filtration and density analysis suggested lipoprotein involvement. When inhibitor and haemagglutinin were mixed, the separate activities could be recovered from the mixture by centrifuging on a sucrose density gradient. By contrast, neither haemagglutinin nor inhibitor could be recovered by this treamtnet when the inhibitor was added at the start of virus growth. The binding of inhibitor with rabies virus during virus growth seems irreversible and different from the binding of inhibitor with pre-formed rabies haemagglutinin.
J Gen Virol 1977 Jul
PMID:Interaction of non-specific inhibitor and rabies virus haemagglutinim. 56 Apr 27

The assimilation of sulphate in Saccharomyces cerevisiae, comprising the reduction of sulphate to sulphide and the incorporation of the sulphur atom into a four-carbon chain, requires the integrity of 13 different genes. To date, the functions of nine of these genes are still not clearly established. A set of strains, each bearing a mutation in one MET gene, was studied. Phenotypic studies and enzyme determinations showed that the products of at least five genes are needed for the synthesis of an enzymically active sulphite reductase. These genes are MET1, MET5, MET8, MET10 and MET20. Wild-type strains of S. cerevisiae can use organic metabolites such as homocysteine, cysteine, methionine and S-adenosylmethionine as sulphur sources. They are also able to use inorganic sulphur sources such as sulphate, sulphite, sulphide or thiosulphate. Here we show that both of the two sulphur atoms of thiosulphate are used by S. cerevisiae. Thiosulphate is cleaved into sulphite and sulphide prior to utilization by the sulphate assimilation pathway, as the metabolism of one sulphur atom from thiosulphate requires the presence of an active sulphite reductase.
J Gen Microbiol 1992 Oct
PMID:Physiological analysis of mutants of Saccharomyces cerevisiae impaired in sulphate assimilation. 147 40

A computer search revealed 10 proteins with homology to the sequence we originally identified in vimentin as the site of cleavage by human immunodeficiency virus type 1 (HIV-1) protease. Of these 10 proteins (actin, alpha-actinin, spectrin, tropomyosins, vinculin, dystrophin, MAP-2, villin, TRK-1 and Ig mu-chain), we show that 4 of the first 5 were cleaved in vitro by this protease, as are MAP-1 and -2 [(1990) J. Gen. Virol. 71, 1985-1991]. In these proteins, cleavage is not restricted to a single motif, but occurs at many sites. However, cleavage is not random, since 9 other proteins including the cytoskeletal proteins filamin and band 4.1 are not cleaved in the in vitro assay. Thus, the ability of HIV-1 protease to cleave specific components of the cytoskeleton may be an important, although as yet unevaluated aspect of the life cycle of this retrovirus and/or may directly contribute to the pathogenesis observed during infection.
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PMID:Non-viral cellular substrates for human immunodeficiency virus type 1 protease. 199 13

Oral inoculation of newborn mice with the MET strain of human rotavirus produced transient diarrhoeal disease. Light and scanning electron microscopy showed typical rotavirus-induced morphological lesions in the villous epithelium of the small intestine consisting of extensive cytoplasmic vacuolation, villous necrosis and atrophy. Virus recovered from intestinal suspensions of infected mice showed the typical electrophoretic profile of the genome of the inoculated strain. Rotavirus antibody appeared in infected mice 10 to 20 days after inoculation but not in controls or nursing dams. The availability of a small animal model for experimental infection with human rotaviruses should prove useful for virulence and protection studies.
J Gen Virol 1986 Mar
PMID:Diarrhoea in mice infected with a human rotavirus. 300 82

Seventeen Thy-1+ cell clones were induced in A/J mice immunized with the HEP-Flury strain of rabies virus after repeated stimulations with antigens in vitro. Ten clones with cell surface phenotypes Thy-1+, Lyt-1-,2+ were cytotoxic T lymphocytes (CTL) which lysed the virus-infected target cells under H-2 restriction. Target cells expressed the G and M2 structural proteins of rabies virus on their surface; however, target lysis by CTL clones was not blocked by anti-rabies antibody or by monoclonal antibodies to these proteins. All of the CTL clones efficiently and equally lysed target cells infected with three different strains of rabies virus and were cross-reactive for target cells infected with one (Duvenhage virus) of three different rabies serogroup viruses. Another five clones having phenotype Thy-1+, Lyt-1+,2- did not show any cytotoxic activity. The proliferation response of these clones to antigen stimulation was virus-specific and H-2-restricted. These clones were able to grow in culture medium without any or with the addition of low concentrations of T cell growth factor, in contrast to CTL clones, and were considered to be helper T lymphocytes (HTL). Both CTL and HTL clones produced gamma-interferon in response to antigen stimulation. The remaining two clones were Thy-1+, Lyt-1-,2-, asialo-GM1+, and were not cytotoxic to target cells even in the presence of anti-rabies antibody but were cytotoxic to YAC-1 cells. Further studies with these clones should allow us to investigate more closely the role of T cells in the pathogenesis of rabies.
J Gen Virol 1987 Apr
PMID:Murine T cell clones directed to rabies virus: isolation and some of their properties. 310 64

We cloned the MET 17 gene of Saccharomyces cerevisiae by functional complementation after transformation of a yeast met 17 mutant. Restriction mapping and nucleotide sequencing of the MET 17 clones revealed that these were from the same genomic region as clones isolated previously and shown to contain the MET 25 gene encoding the enzyme O-acetylhomoserine, O-acetylserine sulphydrylase (OAH-OAS sulphydrylase). Transformation studies with MET 25 clones showed that the MET 17 and MET 25 functions were both endoced in a single transcription unit. We conclude that met 17 and met 25 are both mutations in the structural gene for the OAH-OAS sulphydrylase subunit and that each affects a different functional domain of the enzyme allowing subunit complementation in the met 17 X met 25 diploid. Enzyme assays indicated that the diploid, although not requiring methionine, had a low OAH-OAS sulphydrylase activity (10% of wild type). This is consistent with MET 17 and MET 25 being the same gene. We found that both met 17 and met 25 mutants were devoid of 3' phospho-adenosine 5' phospho-sulphite (PAPS) reductase activity and that this activity was fully restored in the met 17 X met 25 diploid. The possible interactions between OAH-OAS sulphydrylase and PAPS reductase are discussed.
Mol Gen Genet 1987 Apr
PMID:Molecular genetics of met 17 and met 25 mutants of Saccharomyces cerevisiae: intragenic complementation between mutations of a single structural gene. 329 1

Ultraviolet light (UV) inhibits DNA replication in Eschericia coli and induces the SOS response, a set of survival-enhancing phenotypes due to derepression of DNA damage-inducible genes, including recA and umuDC. Recovery of DNA synthesis after UV irradiation ("induced replisome reactivation," or IRR) is an SOS function requiring RecA protein and postirradiation synthesis of additional protein(s), but this recovery does not require UmuDC protein [Khidhir, M. A., Casaregola, S. & Holland, I. B. (1985) Mol. Gen. Genet. 199, 133-140]. IRR occurs in strains carrying either recA718 (which does not reduce recombination, SOS inducibility, or UV mutagenesis) or umuC36 (which eliminates UV mutability), but not in recA718 umuC36 double mutants. In recA430 mutant strains, IRR does not occur whether or not functional UmuDC protein is present. IRR occurs in lexA-(Ind-) (SOS noninducible) strains if they carry an operator-constitutive recA allele and are allowed to synthesize proteins after irradiation. We conclude the following: (i) that UmuDC protein corrects or complements a defect in the ability of RecA718 protein (but not of RecA430 protein) to promote IRR and (ii) that in lexA(Ind-) mutant strains, IRR requires amplification of RecA+ protein (but not of any other LexA-repressed protein) plus post-UV synthesis of at least one other protein not controlled by LexA protein. We discuss the results in relation to the essential, but unidentified, roles of RecA and UmuDC proteins in UV mutagenesis.
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PMID:Recovery from ultraviolet light-induced inhibition of DNA synthesis requires umuDC gene products in recA718 mutant strains but not in recA+ strains of Escherichia coli. 330 46

Apparent interferon-mediated persistent infection of rabies virus (HEP-Flury strain) was established in a human neuroblastoma SYM-I (clone K-104) cell line, which had the ability to produce interferon. This infection produced variable but small amounts of progeny virus and interferon (up to 100 IU/ml), and resisted superinfection with vesicular stomatitis virus (VSV) and Sindbis virus as well as homologous rabies virus. The treatment of this infection with anti-interferon antibody stimulated virus replication and extensive c.p.e. However, some cells survived and grew rapidly without any sign of c.p.e. These produced increased amounts (100 to 1000 times) of infectious and DI particles in the presence of anti-interferon antibody, becoming susceptible to superinfection with VSV but remaining resistant to the original rabies virus. Small plaque mutants appeared and replaced the original virus during the long-term cultivation of the persistent infection. Several mutants tested were all identified as Sdi (DI-resistant) mutants, suggesting that the persisting viruses were endowed by the Sdi mutation with a selective advantage over the original virus even in interferon-mediated persistent infections.
J Gen Virol 1985 May
PMID:Persistent infection of rabies virus (HEP-Flury strain) in human neuroblastoma cells capable of producing interferon. 399 11

Twenty-one hybridoma cultures, obtained through the fusion of mouse myeloma cells with splenocytes of BALB/c mice immunized with either rabies virus or Mokola virus, secreted monoclonal antibodies specific for the nucleocapsid of the inducer virus. They displayed different specificities for the nucleocapsids of rabies and rabies-related viruses and could be classified into eight groups which are likely to correspond to different antigenic determinants on the nucleocapsid. Four strains of fixed rabies virus (CVS, ERA, Flury-LEP and Kelev) could not be differentiated by the nucleocapsid-specific hybridoma antibody. The Flury-HEP virus (derived from Flury-LEP) as well as the rabies-related viruses Mokola, Lagos bat and Duvenhage, showed marked differences in their reactivities with hybridoma antibodies to nucleocapsid. A selected panel of three of these hybridomas may be used for a rapid differential diagnosis among all members of the Lyssavirus group.
J Gen Virol 1980 May
PMID:Use of hybridoma monoclonal antibodies in the detection of antigenic differences between rabies and rabies-related virus proteins. I. The nucleocapsid protein. 615 36


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