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)

The product of phage P22 gene c1 has two functions: (1) it promotes synthesis of repressor and (2) during the first minutes of infection it retards expression of some lytic genes. We call the second, negative function "c1 retardation". We investigated c1 retardation in a mutant host of Salmonella typhimurium that is resistant to rifampicin and carries an altered RNA polymerase. No c1 retardation of DNA synthesis was detectable in this host after infection with wild-type phages. This elimination of the normally detectable c1 function leads to the conclusion that the mutant RNA polymerase interferes with the expression of c1 gene activity. Wild-type genes form clear plaques on the mutant host. Mutants of P22 called cly were isolated by others. These mutants form turbid plaques on the altered RNA polymerase host. Infections with P22 cly in the mutant host resulted in detectable c1 retardation. The cly mutation therefore restores c1 activity in a host which wild-type c1 is not expressed. Two spontaneous mutants were isolated from the mutant host. These two strains allowed partial expression of c1 retardation, although they remained rifampicin resistant. We interpret our data to indicate that expression of the normal functions of the gene c1 product requires an interaction of that product with the host RNA polymerase.
Mol Gen Genet 1977 Jun 08
PMID:Effect of mutant host RNA polymerase on the bifunctional activities of P22 gene c1. 32 18

We described a strategy which facilitates the identification of cell mutants which are restricted in DNA synthesis in a temperature-dependent manner. A collection of over 200 cell mutants temperature-sensitive for growth was isolated in established Chinese hamster cell lines (CHO and V79) by a variety of selective and nonselective techniques. Approximately 10% of these mutants were identified as ts DNA- based on differential inhibition of macromolecular synthesis at the restrictive temperature (39 degrees C) as assessed by incorporation of [3H]thymidine and [35S]methionine. Nine such mutants, selected for further study, demonstrated rapid shutoff of DNA replication at 39 degrees C. Infections with two classes of DNA viruses extensively dependent on host-cell functions for their replication were used to distinguish defects in DNA synthesis itself from those predominantly affecting other aspects of DNA replication. All cell mutants supported human adenovirus type 2 (Ad2) and mouse polyomavirus DNA synthesis at the permissive temperature. Five of the nine mutants (JB3-B, JB3-O, JB7-K, JB8-D, and JB11-J) restricted polyomavirus DNA replication upon transfection with viral sequences at 33 degrees C and subsequent shift to 39 degrees C either before or after the onset of viral DNA synthesis. Only one of these mutants (JB3-B) also restricted Ad2 DNA synthesis after virion infection under comparable conditions. No mutant was both restrictive for Ad2 and permissive for polyomavirus DNA synthesis at 39 degrees C. The differential effect of these cell mutants on viral DNA synthesis is expected to assist subsequent definition of the biochemical defect responsible.
Mol Cell Biol 1986 Dec
PMID:Identification of temperature-sensitive DNA- mutants of Chinese hamster cells affected in cellular and viral DNA synthesis. 379 11

Rats were immunized with mouse lymphocytes enriched by the absorption-elution technique with specific suppressor T-cells (STC) immune to antigens of the H-2 complex. The anti-suppressor sera (ASS) obtained being absorbed with mouse erythrocytes and lymph node cells killed in the presence of complement about 30 per cent of the STC-enriched cell population and inactivated the STC in vitro function in a selective fashion, not affecting the function of other T-cell subclasses, killers and MIF-producers, immune to the same H-2 antigens. The STC inactivating ASS action occurred partly in the absence of complement irrespective of the STC strain origin, STC immunological specificity in the H-2 system and the intensity of the STC activity. This ASS action was abolished by exhaustion of antibodies only with STC containing cell suspensions. In contrast, intact (non-enriched) mouse STC appeared to be able to induce a mixture of rat antibodies inactivating partly all three T-cell subclasses assayed. Infections of ASS to mice prevented them from the in vivo STC generation and gave rise to inhibition of the syngeneic tumor growth in the specifically preimmunized mice.
Mol Biol (Mosk)
PMID:[Selective inactivation of specific T-suppressors immune to H-2 complex antigens and prevention of their generation in vivo by antisuppressor xenogenic antibodies]. 645 78

Infections, trauma and inflammatory processes induce a host response with increases in a large group of structurally and functionally diverse plasma proteins. Parental administration of foreign proteins also induce an increase in plasma fibrinogen. Interleukin-6 (IL-6) is a monocyte-derived mediator and has regulatory effects on acute phase protein genes which result in the induction of fibrinogen synthesis in primary hepatocytes, while the addition of interleukin-1 (IL-1) exerts a negative modulating influence on the IL-6-stimulated fibrinogen. In order to understand the mechanisms by which IL-1 inhibits IL-6-stimulated fibrinogen transcription and translation, and since IL-1 is believed to act through PGE2 stimulation, we have studied the influence of PGE2 in IL-6 or IL-1, alone and in combination, on Fg mRNA expression (by Northern blot analysis) and the influence of PGE2, indomethacin, and arachidonic acid on Fg secretion. Moreover, since human recombinant interleukin-1 receptor antagonist (hrIL-1ra) is a strong inhibitor of IL-1 induced IL-1 transcription and translation and has an inhibitory effect on PGE2, we have studied the effects of IL-1ra on the down-regulation of IL-6 stimulated fibrinogen by IL-1, using an Fg ELISA method.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Biochem 1995 Jan 26
PMID:The down-regulation of IL-6-stimulated fibrinogen steady state mRNA and protein levels by human recombinant IL-1 is not PGE2-dependent: effects of IL-1 receptor antagonist (IL-1RA). 777 69

We have conducted a retrospective study of 100 HIV-infected patients enrolled in an AZT monotherapy clinical study at the Medical College of Georgia (MCG) in Augusta, Georgia. When compared to the national trends, our results confirm previous studies that describe an overall increase in the burden of HIV infections among blacks, and, in particular, black women in the rural Southeast. In our cohort, infections due to homosexual contact accounted for approximately 40% of all cases while heterosexual contact and intravenous drug use (IDU) comprised 33% and 13%, respectively. Infections attributable to all other risk factors accounted for the remaining 14%. Relative to national surveillance data, we observed an increase in the prevalence of HIV infections among blacks, and heterosexually acquired infections, particularly among black women. Our analysis illustrates the dynamic nature of the current U.S. epidemic which appears to be shifting both in terms of its demographic and epidemiological profile. These data may indicate that national surveillance data may not reflect the dynamic nature of current demographic trends in HIV incidence, particularly as evidenced in the rural Southeast. This suggests that hospital or laboratory based cross-sectional studies, like ours, that analyze demographic variables of HIV-infected clinic attendees may be necessary to more accurately assess the leading edge of the HIV epidemic in rural, non-metropolitan areas.
Cell Mol Biol (Noisy-le-grand) 1997 Nov
PMID:Epidemiology of HIV-1 infection in rural Georgia: demographic trends and analysis at the Medical College of Georgia. 944 42

Infections of the eye and genital tract with the bacterium Chlamydia trachomatis are a major cause of morbidity worldwide and are costly to treat. Development of a vaccine capable of protecting against infection or severe disease presents special challenges but would be the most effective long-term option for control of chlamydial disease. Progress has been made in understanding protective and pathological immune mechanisms in these infections, and a number of potential vaccine candidates have been developed.
Mol Med Today 1998 Apr
PMID:Vaccines against Chlamydia: approaches and progress. 957 58

Infections caused by rickettsial pathogens persist in vertebrate hosts for long periods of time, despite the active host immune response. We recently described the multigene locus encoding 28 kDa surface antigen proteins (28 kDa SAPs) for two closely related rickettsials, Ehrlichia chaffeensis and Ehrlichia canis (Reddy, G. R., et al. (1998) Biochem. Biophys. Res. Commun. 247, 636-643), that share extensive structural homology to antigenic variant surface protein genes of Neisseria and Borrelia species. In this study, we describe motifs for recombinase binding sites and a high frequency of repeat elements in the cloned 28 kDa SAP genes. The locus for two newly established E. chaffeensis isolates also was characterized, and immunological specificity of the 28 kDa SAPs was investigated. The study identified variant forms of the 28 kDa SAPs and extensive restriction fragment length polymorphisms among isolates. The molecular data suggest that the locus is influenced by short-term evolutionary changes such as genetic recombinations leading to the generation of antigenic variants. Antigenic variation could contribute to the mechanism of immune evasion and the emergence of new diseases.
Mol Cell Biol Res Commun 1999 Jun
PMID:Variability in the 28-kDa surface antigen protein multigene locus of isolates of the emerging disease agent Ehrlichia chaffeensis suggests that it plays a role in immune evasion. 1042 22

The potential role of respiratory infections in altering the development of atopy and asthma is complex. Infections have been suggested to be effective in preventing the induction of T-helper 2-polarized allergen-specific immunity in early life, but also to exacerbate asthma in older, sensitized individuals. The mechanism(s) underlying these effects are poorly defined. The aim of this work was to determine the influence of lipopolysaccharide (LPS) exposure on the development of sensitization to allergen and the response to allergen challenge in vivo. Piebald-Virol-Glaxo rats were exposed to a single aerosol of LPS 1 d before or 1, 2, 4, 6, 8, or 10 d after sensitization with ovalbumin (OVA). On Day 11 animals were exposed to 1% OVA and responses to allergen were measured 24 h later, monitoring inflammatory cell influx and microvascular leakage into bronchoalveolar lavage (BAL) fluid as well as pulmonary responses to methacholine using the forced oscillation technique. Histologic analysis was included to complement the BAL results. Single aerosol exposure to LPS 1 d before and up to 4 d after intraperitoneal injection of OVA protected against the development of OVA-specific immunoglobulin (Ig) E. LPS exposure 6, 8, or 10 d after sensitization further exacerbated the OVA-induced cellular influx, resulting in neutrophilia and increased Evans Blue dye leakage with no effect on serum IgE levels. In addition, LPS abolished the OVA-induced hyperresponsiveness in sensitized animals when given 18 h after OVA challenge. This study demonstrates that exposure to LPS can modify the development of allergic inflammation in vivo by two independent mechanisms. Exposure early in the sensitization process, up to Day 6 after exposure to allergen, prevented allergen sensitization. Exposure to LPS after allergen challenge in sensitized animals abolished the hyperresponsiveness and modified the inflammatory cell influx characteristic of late-phase response to allergen.
Am J Respir Cell Mol Biol 2000 May
PMID:Modification of the inflammatory response to allergen challenge after exposure to bacterial lipopolysaccharide. 1078 33

Patients with neutropenia, especially neutropenia following aggressive myeloablative therapy, are at high risk for developing infectious complications caused by bacteria and opportunistic fungi. Infections remain one of the leading causes of treatment failure in patients with cancer. Thus, new and innovative therapeutic strategies are needed for management of neutropenic patients with infection. Because neutrophils represent the first line of host defense, granulocyte transfusion therapy should be a logical therapeutic approach. Although such therapy has been employed sporadically for several decades, clinical benefit has been compromised by technical problems and low granulocyte yields resulting from inadequate donor stimulation. The discovery of granulocyte colony-stimulating factor (G-CSF) as a means to elevate blood neutrophil counts when administered to normal donors has rekindled interest in granulocyte transfusion therapy. Extensive experience has been gained worldwide with G-CSF in clinical practice, and adverse events have been minimal when G-CSF has been administered to patients or healthy persons in human trials. This review focuses on the use of G-CSF in granulocyte transfusion therapy, including technical considerations of granulocyte leukapheresis and storage, donor selection and stimulation, as well as treatment results and associated risks.
Cytokines Cell Mol Ther 2000 Jun
PMID:Use of G-CSF for granulocyte transfusion therapy. 1110 74

The hepatitis C viruses (HCVs) are a group of small enveloped RNA viruses that have been viewed as a leading cause of chronic hepatitis in humans. Infections by HCV represent a serious global health problem, because millions of people worldwide are infected and no efficient treatment is available at the present time. Since HCV was identified in 1989, considerable effort has been devoted to the discovery and development of novel molecules to treat HCV-related diseases. One of the approaches is the development of novel inhibitors that interrupt the normal functions of HCV NS5B, an RNA-dependent RNA polymerase essential to HCV replication. This review summarizes recent advances in the biochemical and structural understanding of HCV NS5B polymerase as well as in the development of antiviral agents targeting this important enzyme.
Cell Mol Life Sci 2002 Jun
PMID:RNA-dependent RNA polymerase encoded by hepatitis C virus: biomedical applications. 1216 21


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