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

The poststress activation of peroxide oxidation reaction (POL) of lipids from brain tissue of the mice CBA and FI (CBA X C57 Black) has been confirmed. The principal difference in the nature of malonic dialdehyde level dynamics in brain tissue determined by a form of infectious process induced by influenza strain A/PR/8/34 pathogenic for mice has been found. The sublethal dose has been shown to activate while the lethal dose to suppress the POL process. Progression of influenza infection at the stress background was accompanied by a sharp unidirectional increase in MDA content in mice brain tissue. The increase was mostly expressed in case of mice infection with a lethal dose of the virus. The data obtained suggest a membrane mechanism for barrier damage as a reason of severing influenza infection by the stress background.
Mol Gen Mikrobiol Virusol 1988 Feb
PMID:[Dynamics of peroxidation of brain tissue lipids in mice infected with influenza virus in the presence of immobilization stress]. 283 24

Two synthetic peptides from different regions of the glycoprotein D of herpes simplex virus (HSV) have been used to determine whether or not anti-peptide IgG responses can be generated in the absence of adjuvant. Based on an earlier demonstration (Carayanniotis and Barber, 1987) that protein antigens could be made immunogenic in the absence of adjuvant, if coupled to MAbs specific for the recipient's class II major histocompatibility complex (MHC) antigens, the HSV synthetic peptides were photocoupled to avidin and mixed with biotinylated anti-class II or control antibodies. Peptide-specific IgG responses were obtained when avidin-peptide conjugates coupled to an anti-I-Ak MAb were injected into (H-2k x H-2b) F1 mice, but not when injected into H-2b mice. The same avidin-peptide conjugates were non-immunogenic when coupled to a control anti-influenza virus nucleoprotein antibody or biotinylated bovine serum albumin. These data indicate that targeting synthetic peptides to class II bearing cells in vivo can elicit peptide-specific IgG responses without the need for adjuvant. These findings offer a new approach to the design and delivery of adjuvant-independent vaccine agents based on synthetic peptide antigens.
Mol Immunol 1988 Sep
PMID:Delivery of synthetic peptides by anti-class II MHC monoclonal antibodies induces specific adjuvant-free IgG responses in vivo. 285 Apr 98

Virosomes were prepared by using the zwitterion detergent sulfobetaine-12. The virosomes included the surface antigens and virus-specific lipids of influenza virus, strain A/PR/8/34. Immunogenic and protective properties of the surface antigens in the micellar form and as a complex with the virosomes were studied. The surface antigens of this complex, like the intact virus, were found to possess the high immunogenic and protective activity in relation to the following infection with the homologous pathogenic virus.
Mol Gen Mikrobiol Virusol 1988 Dec
PMID:[Use of the zwitterion detergent Sulfobetain-12 for preparation of virosomes and investigation of their immunogenic and protective properties]. 285 92

The interferon-regulated mouse Mx gene encodes the 72-kilodalton nuclear Mx protein that selectively inhibits influenza virus replication. Mice carrying Mx+ alleles synthesize Mx protein and resist influenza virus infection, whereas mice homozygous for Mx- alleles fail to synthesize Mx protein and, as a consequence, are influenza virus susceptible. Southern blot analysis allowed us to define the following three distinct Mx restriction fragment length polymorphism (RFLP) types among classical inbred strains: RFLP type 1 in the Mx+ strains A2G and SL/NiA, RFLP type 2 in BALB/c and 33 other Mx- strains, and RFLP type 3 in CBA/J and 2 other Mx- strains. cDNA clones of Mx mRNAs from BALB/c and CBA/J cells were isolated, and their sequences were compared with that of the wild-type Mx mRNA of strain A2G. Mx mRNA of BALB/c mice has 424 nucleotides absent from the coding region, resulting in a frame shift and premature termination of Mx protein. The missing sequences correspond exactly to Mx exons 9 through 11. These three exons, together with some flanking intron sequences, are deleted from the genomes of all Mx RFLP type 2 strains. The Mx- phenotype of the Mx RFLP type 3 strain CBA/J is due to a point mutation that converts the lysine codon in position 389 to a termination codon. Mx RFLP type 3 strains have an extra HindIII site which maps to an intron and thus probably does not affect the coding capacity of Mx mRNA. We further show that the Mx mRNA levels in interferon-treated BALB/c and CBA/J cells are about 15-fold lower than in similarly treated Mx+ cells. This is probably due to decreased metabolic stabilities of the mutant mRNAs.
Mol Cell Biol 1988 Oct
PMID:Influenza virus-susceptible mice carry Mx genes with a large deletion or a nonsense mutation. 290 37

Determining the mechanisms by which B cells develop that culminates in the generation of a diverse repertoire is critical to our understanding of how the immune response is regulated. The B cell specificity repertoire appears to be developmentally acquired in a predetermined, temporally ordered fashion. Thus, in the Balb/c mouse, the ontogenetic appearance of functional B cells specific for various hapten probes occurs in the order of dinitrophenol (DNP), fluorescein (Fl), and phosphorylcholine (PC). In addition, when the influenza virus hemagglutinin molecule was used as an antigen probe, similar conclusions were drawn regarding a patterned acquisition of the specificity repertoire. More recently, we have used a fetal organ culture system to show that hapten-responsive B cells appear in the same predictable, temporal order in vitro. The importance of these studies was that the effects of environmental influences were minimized in the absence of circulation and cell migration, and therefore the results indicated that the patterned emergence of the specificity repertoire observed was largely the result of genetic regulatory processes. Recent molecular findings may relate to such genetic regulatory processes. The VH genes in Balb/c mice have been grouped into eight families based on sequence homology, and have been mapped relative to the constant region genes. Yancopoulos et al. and Perlmutter et al. have shown that the VH gene segments closest to the JH cluster, the VH1B 7183 family, are preferentially utilized in transformed fetal pre-B cell lines and in fetal B cell hybridomas. This led to the hypothesis that the developmental control of the expression of VH gene segments is related to chromosomal organization. A logical extension of these findings is that the programmed appearance of particular clonotypes in ontogeny may be explained, in part, by the preferential use of particular VH gene segments. However, to what extent the transformed B cell lines represent members of the functional expressed repertoire could not be evaluated. In the studies described herein, the fetal organ culture system was used to assess the early expressed repertoire at the clonotypic level using idiotypic analysis. Anti-DNP secreting clones were derived from fetal organ cultures and tested for the presence of two idiotypes, 36 and MOPC 460 (460). The 36 idiotype is a predominant DNP clonotype of the neonatal repertoire, while the 460 idiotype is a major cross-reactive idiotype of the adult DNP response.(ABSTRACT TRUNCATED AT 400 WORDS)
J Mol Cell Immunol 1986
PMID:Clonotypic analysis of the fetal B cell repertoire: evidence for an early and predominant expression of idiotypes associated with the VH 36-60 family. 290 78

Specific resistance of Mx+ mice to influenza virus is due to the interferon (IFN)-induced protein Mx. The Mx gene consists of 14 exons that are spread over at least 55 kilobase pairs of DNA. Surprisingly, the Mx gene promoter is induced as efficiently by Newcastle disease virus as it is by IFN. The 5' boundary of the region required for maximal induction by both IFN and Newcastle disease virus is located about 140 base pairs upstream of the cap site. This region contains five elements of the type GAAANN, which occurs in all IFN- and virus-inducible promoters. The consensus sequence purine-GAAAN(N/-)GAAA(C/G)-pyrimidine is found in all IFN-inducible promoters.
Mol Cell Biol 1988 Aug
PMID:Organization of the murine Mx gene and characterization of its interferon- and virus-inducible promoter. 297 22

We have investigated the site of surface expression of the neuraminidase (NA) glycoprotein of influenza A virus, which, in contrast to the hemagglutinin, is bound to membranes by hydrophobic residues near the NH2-terminus. Madin-Darby canine kidney or primary African green monkey kidney cells infected with influenza A/WSN/33 virus and subsequently labeled with monoclonal antibody to the NA and then with a colloidal gold- or ferritin-conjugated second antibody exhibited specific labeling of apical surfaces. Using simian virus 40 late expression vectors, we also studied the surface expression of the complete NA gene (SNC) and a truncated NA gene (SN10) in either primary or a polarized continuous line (MA104) of African green monkey kidney cells. The polypeptides encoded by the cloned NA cDNAs were expressed on the surface of both cell types. Analysis of [3H]mannose-labeled polypeptides from recombinant virus-infected MA104 cells showed that the products of cloned NA cDNA comigrated with glycosylated NA from influenza virus-infected cells. Both the complete and the truncated glycoproteins were found to be preferentially expressed on apical plasma membranes, as detected by immunogold labeling. These results indicate that the NA polypeptide contains structural features capable of directing the transport of the protein to apical cell surfaces and the first 10 amino-terminal residues of the NA polypeptide are not involved in this process.
Mol Cell Biol 1985 Sep
PMID:Surface expression of influenza virus neuraminidase, an amino-terminally anchored viral membrane glycoprotein, in polarized epithelial cells. 301 20

During influenza virus infection, protein synthesis is maintained at high levels and a dramatic switch from cellular to viral protein synthesis occurs despite the presence of high levels of functional cellular mRNAs in the cytoplasm of infected cells (M. G. Katze and R. M. Krug, Mol. Cell. Biol. 4:2198-2206, 1984). To determine the step at which the block in cellular mRNA translation occurs, we compared the polysome association of several representative cellular mRNAs (actin, glyceraldehyde-3-phosphate dehydrogenase, and pHe7 mRNAs) in infected and uninfected HeLa cells. We showed that most of these cellular mRNAs remained polysome associated after influenza viral infection, indicating that the elongation of the proteins encoded by these cellular mRNAs was severely inhibited. Because the polysomes containing these cellular mRNAs did not increase in size but either remained the same size or decreased in size, the initiation step in cellular protein synthesis must also have been defective. Several control experiments established that the cellular mRNAs sedimenting in the polysome region of sucrose gradients were in fact associated with polyribosomes. Most definitively, puromycin treatment of infected cells caused the dissociation of polysomes and the release of cellular, as well as viral, mRNAs from the polysomes, indicating that the cellular mRNAs were associated with polysomes that were capable of forming at least a single peptide bond. A similar analysis was performed with HeLa cells infected by adenovirus, which also dramatically shuts down cellular protein synthesis. Again, it was found that most of the cellular mRNAs, which were translatable in reticulocyte extracts, remained associated with polysomes and that there was a combined initiation-elongation block to cellular protein synthesis. In cells infected by both adenovirus and influenza virus, influenza viral mRNAs were on larger polysomes than were several late adenoviral mRNAs with comparably sized coding regions. In addition, after influenza virus superinfection of cells infected by the adenovirus mutant dl331, a situation in which there is a limitation in the amount of functional initiation factor eIF-2 (M. G. Katze, B. M. Detjen, B. Safer, and R. M. Krug, Mol. Cell. Biol. 6:1741-1750, 1986), influenza viral mRNAs, but not late adenoviral mRNAs, were on polysomes. These results indicate that influenza viral mRNAs are better initiators of translation than are late adenoviral mRNAs.
 ...
PMID:Cellular mRNA translation is blocked at both initiation and elongation after infection by influenza virus or adenovirus. 302 55

The membrane orientation of the NB protein of influenza B virus, a small (Mr, approximately 18,000) glycoprotein with a single internal hydrophobic domain, was investigated by biochemical and genetic means. Cell fractionation and protein solubility studies indicate NB is an integral membrane protein, and NB has been shown to be a dimer under nonreducing conditions. Treatment of infected-cell surfaces with proteinase K and endoglycosidase F and immunoprecipitation with a site-specific antibody suggests that the 18-amino-acid NH2-terminal region of NB is exposed at the cell surface. Oligonucleotide-directed mutagenesis to eliminate each of the four potential sites of N-linked glycosylation and expression of the mutant NB proteins in eucaryotic cells suggest that the two sites adjacent to the NH2 terminus are glycosylated. This provides further evidence that NB, which lacks a cleavable NH2-terminal signal sequence, has an exposed NH2 terminus at the cell surface.
Mol Cell Biol 1986 Dec
PMID:Determination of the orientation of an integral membrane protein and sites of glycosylation by oligonucleotide-directed mutagenesis: influenza B virus NB glycoprotein lacks a cleavable signal sequence and has an extracellular NH2-terminal region. 302 52

Incomplete reproduction cycle of influenza virus A/134/17/57, the attenuation donor being used for preparation of recombinant vaccine strains, hs been analyzed with the use of molecular biology methods. Virus A/134/17/57 with two mutations in P3, NP and M genes remains capable of synthesis of viral polypeptides that are devoid of ability to be inserted into cellular plasma membrane, when the virus is propagated in MDCK culture at non-permissive temperature. The process is preceded by defects in the process of formation of RNP structures connected, evidently, with deficient synthesis of viral RNA due to mutations in the gene coding for P3 protein.
Mol Gen Mikrobiol Virusol 1985 Feb
PMID:[Characteristics of incomplete reproduction cycle of ts-mutant of influenza virus A at non-permissive temperature]. 302 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>