Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparison was made of the calculated mol. wt. of RNA fragments from foot-and-mouth disease virus (FMDV) types A12 strain 119, C3 Resende and O1 Brugge. The mol. wt. were calculated by two methods: from the measurements of strand lengths in the electron micrographs and from the observed sedimentation rates (s-rates). RNA extracted from virus by dialysis against water usually had three to four prominent strands of different lengths. Mol. wt. calculated from s-rates (and converted to strand lengths) generally agreed with those measured on electron micrographs. Differences which occurred appeared to be attributable to further breakage during processing for electron microscopy. Major fragment strand lengths range from 0-65 to 2-45 mum. The modal lengths of RNA fragments were preparation-dependent, ranging from 1-25 to 1-95 mum for A12 119, 1-05 to 1-75 mum for C3 Resende, and 1-65 to 2-45 mum for O1 Brugge. There was one fragment length 1-95 mum common to all three types of FMDV RNA and several others which appear in at least two types. Calculations using the molar ratios of nucleotide residues in FMDV RNA, a mol. wt. of FMDV RNA of 2-65 X 10(6) and an internucleotide spacing of 3-17 A indicate that intact FMDV RNA should be 2-62 mum long and therefore would contain approx. 8270 nucleotides. The derived mathematical expression for the relationship between mol. wt. (M) and s-rate (S) giving the best fit for all data was M = 1725 S2-07, a result close to that derived by Spirin (1963) for other single-stranded RNAs.
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PMID:A comparison of molecular weights of foot-and-mouth disease virus RNA fragments determined from lengths and s-rates. 17 21

We have carried out a phylogenetic study of the evolution of the VP1 gene sequence from different serological types and subtypes of foot-and-mouth disease virus (FMDV). The maximum-likelihood method developed by Hasegawa and co-workers (Hasegawa et al. 1985) for the estimation of evolutionary parameters and branching dates has been used to decide between alternative models of evolution: constant versus variable rates. The results obtained indicate that a constant rate model, i.e., a molecular clock, seems to be the most plausible one. However, additional information suggests the possibility that the appearance of serotype CS has been accompanied by an episode of rapid evolution (Villaverde et al. 1991). We discuss the possibility that this evolution of RNA viruses was due to episodic positive Darwinian selection, which would have helped the new variant to escape the immunogenic pressure from the hosts.
J Mol Evol 1992 Sep
PMID:Does the VP1 gene of foot-and-mouth disease virus behave as a molecular clock? 132 67

The number of nucleotide (nt) substitutions found in the VP1 gene (encoding viral capsid protein) between any two of 16 closely related isolates of foot-and-mouth disease virus (FMDV) has been quantified as a function of the time interval between isolations [Villaverde et al., J. Mol. Biol. 204 (1988) 771-776]. One of them (isolate C-S12) includes some replacements found in isolates that preceded it and other replacements found in later isolates. The study has revealed alternating periods of rapid evolution and of relative genetic stability of VP1. During a defined period of acute disease, the rate of fixation of replacements at the VP1 coding segment was 6 x 10(-3) substitutions per nt per year. Only small differences in the rate of evolution were observed between subsegments within the VP1 gene. The observation of a relatively constant rate of evolution during a disease episode was unexpected. We propose that such constancy may be a consequence of random sampling of mutants from the FMDV quasispecies, followed by their amplification in susceptible hosts (to generate a new quasispecies). Successive sampling and amplification events may result in a steady accumulation of mutations.
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PMID:Fixation of mutations at the VP1 gene of foot-and-mouth disease virus. Can quasispecies define a transient molecular clock? 165 54

Hybridomas producing monoclonal antibodies of different isotypes were isolated from BALB/c antibody responses to the capsid protein VP1 of the foot-and-mouth disease virus (FMDV) strain O1. According to antigen binding measured by ELISA a weak-binding (81D10, IgM) and a strong-binding antibody (113C12, IgG2a) were selected. As RNA sequencing of productive immunoglobulin VH and VK genes turned out, both chains of the weak-binding antibody (81D10) are encoded by germline (i.e. not mutated) genes whereas the gene encoding the strong-binding antibody (113C12) k chain is mutated at several sites. Therefore, rearranged VH and VK genes of 81D10 were cloned, expressed in immunoglobulin non-producing plasmacytoma cells, and mice transgenic for the 81D10 k gene were produced. These mice provide a first step in the development of a transgenic mouse model for genetical investigations in the affinity maturation of anti-viral immunoglobulin variable genes.
Mol Immunol 1991 Nov
PMID:Immunoglobulin VH and VK genes of the BALB/c anti-foot-and-mouth disease virus (O1) VP1 response: cloning, characterization and transgenic mice. 172 May 3

A technique was developed for identifying peptides with high affinity for a given antibody. By testing a monoclonal antibody directed against a discontinuous antigenic determinant on foot-and-mouth disease virus, peptides mimicking the determinant were identified even though the tertiary structure of the proteins comprising the virus capsid is unknown. The allowable variations in spacing and stereochemistry of the peptides shown to mimic this epitope suggest protein folding in which amino acid residues from three regions, distant from one another in the primary sequence, are brought into close proximity at this epitope. The technique has potential for identification of peptides which will bind with high affinity to receptors other than antibody molecules.
Mol Immunol 1986 Jul
PMID:A priori delineation of a peptide which mimics a discontinuous antigenic determinant. 243 10

Antibodies were raised against synthetic peptides of two regions of the surface protein VP1 of foot-and-mouth disease virus. The peptides were conjugated with keyhole limpet hemocyanin via C- or N-terminal amino acid residues by use of different coupling agents. The fine specificity of the resulting antibodies was determined by PEPSCAN methods. In general, amino acid residues specific for antibody recognition tended to be located opposite to those used for coupling with the carrier protein. Depending on the method of conjugation, the orientation of the peptide at the carrier protein changes and directs the immune response. Thus, the method of conjugation can be used to manipulate the immune response and to improve the antiviral activity of antipeptide antibodies. The PEPSCAN method is an effective monitor in this process.
Mol Immunol 1989 Jan
PMID:Manipulation of antipeptide immune response by varying the coupling of the peptide with the carrier protein. 253 27

The nucleotide sequence of the 3D (polymerase) gene of eight epidemiologically related isolates of foot-and-mouth disease virus of serotype C1 is reported. The genetic heterogeneity of 3D RNA is compared with that of the VP1-coding RNA of the same viruses. Regression lines of substitutions per nucleotide that distinguish any pair of viruses as a function of the time interval between the corresponding isolations show: (1) the slope (substitutions/nucleotide per month) is 2.1 times larger for the VP1 RNA than for the 3D RNA region; (2) the intercept with the ordinate (substitutions/nucleotide) for VP1 RNA is indistinguishable from that for 3D RNA. Thus, the average heterogeneity of the VP1-coding region is very similar to that of the 3D-coding region only among co-circulating viruses. Nine mutations and points of heterogeneity occurred within nucleotide residues 883 to 1026, which encode an amino acid segment, extremely conserved among many different RNA viruses. The results suggest that, rather than due to inherently lower mutability, the conservation of 3D genes is caused by a limitation in the fixation of substitutions in viable genomes.
J Mol Biol 1988 Dec 05
PMID:3D gene of foot-and-mouth disease virus. Conservation by convergence of average sequences. 322 50

The cDNA fragments complementary to RNA-polymerase gene and 3'-untranslated genome region of attenuated foot-and-mouth disease virus strain A(22)645 have been synthesized and cloned into a plasmid vector pUC19 in E. coli JM109. The cloned cDNA fragments were characterized as to their size, orientation towards the plasmid, and localization in the virus genome. Restriction maps for complete gene and two cDNA clones were constructed.
Mol Gen Mikrobiol Virusol
PMID:[Cloning fragments of the RNA polymerase gene of an attenuated variant of the foot-and-mouth disease virus A22]. 747 32

A model for the topology of the PhoE porin has been proposed according to which the polypeptide traverses the outer membrane sixteen times mostly as amphipathic beta-sheets, thereby exposing eight loops at the cell surface. Until now, no evidence has been obtained for the surface exposure of the third loop. Recently, the structure of porin of Rhodobacter capsulatus has been determined. The proposed model of PhoE is very similar to the structure of the R. capsulatus porin, which has an 'eyelet' region, extending into the interior of the pore. The proposed third external loop of PhoE might form a similar 'eyelet' region. To determine the location of the predicted third external loop of PhoE, multiple copies of an oligonucleotide linker encoding an antigenic determinant of VP1 protein of foot-and-mouth disease virus (FMDV) were inserted. All hybrid proteins were properly inserted in the outer membrane. The monoclonal antibody MA11, directed against the linear FMDV epitope, was able to bind only to intact cells expressing a hybrid PhoE protein with at least three copies of the FMDV epitope present. Antibiotic sensitivity tests and single-channel conductance measurements revealed that the insertions influenced the channel size. These results are consistent with a location of the third loop of PhoE within the pore channel.
Mol Microbiol 1993 Jan
PMID:Topology of PhoE porin: the 'eyelet' region. 767 70

We have constructed a mycobacterial integrative vector by placing two copies of the insertion sequence IS900 flanking a kanamycin-resistance gene into a 'suicide' vector unable to replicate in mycobacteria. The Mycobacterium leprae gene encoding the M. leprae 18 kDa protein was cloned between the two copies of IS900 to provide expression signals. Constructs were introduced into Mycobacterium species smegmatis, vaccae and bovis BCG by electroporation and selection for kanamycin resistance. The expression of the 18 kDa gene was analysed by Western blotting. Integration of the vector into the M. smegmatis chromosome was analysed by Southern blotting. One to five copies of the vector were detected in each transformant. The SIV gag p27 gene and the foot-and-mouth disease virus VP1 140-160 epitope were successfully cloned into the 18 kDa gene and expression in M. smegmatis was obtained.
Mol Microbiol 1993 Dec
PMID:Construction and use of integrative vectors to express foreign genes in mycobacteria. 793 74


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