Disease relevance of SMR3A

• The transport of the viral PB1 protein, nucleocapsid protein, hemagglutinin, membrane protein, and M2 mRNAs was not affected by the NS1 protein [1].
• The RNA-dependent RNA polymerase of influenza virus is composed of three viral P proteins (PB1, PB2, and PA) and involved in both transcription and replication of the RNA genome [2].
• We have established a simultaneous expression system of three P proteins in various combinations using recombinant baculoviruses, and isolated the PA-PB1-PB2 ternary (3P) complex and two kinds of the binary (2P) complex, PA-PB1 and PB1-PB2 [2].
• Antisera to recombinant human immunodeficiency virus (HIV) proteins containing the entire envelope, gp160, or the central portion of the envelope, PB1, can inhibit fusion of virally infected cells in culture [3].
• We also used reverse genetics to generate a reassortant virus containing the PB1 gene of the A/PR/8/34 virus, with all other genes representing A/WSN/33 [4].

Psychiatry related information on SMR3A

• The three dimensions of care, overprotection, and authoritarianism also explained the underlying structure of the NCS-modified, eight-item PBI that is now part of the NCS public use dataset available to psychopathology researchers [5].
• The Spanish version of the PBI has psychometric features similar to those described in other cultures [6].
• The goal of the study was to examine the reliability and validity of a clinician-report PBI, and to provide a preliminary examination of the relation between personality disorder (PD) symptoms and parental bonding in a national sample of patients in treatment in the community [7].
• The Factor 1 score was significantly and negatively correlated with the Extraversion subscale of the EPQ and the Paternal Care subscale of the PBI [8].
• BACKGROUND: Study of the contribution of retrospective perceptions of dysfunctional parenting in relation to adult psychopathology has been greatly facilitated by the development of the 25-item Parental Bonding Instrument (PBI; Parker et al. 1979) [5].

High impact information on SMR3A

• Further, phorbol ester treatment renders the fibronectin-mediated adhesion process less sensitive to inhibitors, including GRGDSP peptide and PB1, a monoclonal anti-FnR antibody [9].
• This report presents evidence that a reduced pyrrolo[1,2-a]benzimidazole (PBI) cleaves DNA as a result of phosphate alkylation followed by hydrolysis of the resulting phosphate triester [10].
• The base-pair specificity of the phosphate alkylation results from Hoogsteen-type hydrogen bonding of the reduced PBI in the major groove at only A.T and G.C base pairs [10].
• Recently, a novel 87-amino acid influenza A virus protein with proapoptotic properties, PB1-F2, has been reported that originates from an alternative reading frame in the PB1 polymerase gene and is encoded in most known human influenza A virus isolates [11].
• This aggregation phenotype was not altered on removal of the N-terminal PB1 dimerization domain, implying that aggregate formation is not wholly mediated by interaction through the PB1 domain [12].

Chemical compound and disease context of SMR3A

• Degradation of hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) by Stenotrophomonas maltophilia PB1 [13].
• The observed down-regulation of transcription by C4 nucleotide is consistent with its potential role in segment-specific regulation of influenza virus gene expression, especially PB1, PB2 and PA proteins, during virus infection [14].
• A pattern of high values of PBI and T3-test and relatively low values of cholesterol in most of the patients with hydatidiform mole, and in almost one third of the patients with hyperemesis was found [15].
• The thyroid function tests, serum protein-bound iodine (PBI), serum triiodothyronine reaction (T3-test) and serum cholesterol were measured in three groups of pregnant women: 1) 57 with normal pregnancy, 2) 35 with hyperemesis and 3) 14 with hydatidiform mole [15].
• In a euthyroid patient, the association of an elevated serum PBI concentration (with an abnormally large butanol-insoluble iodine fraction) with a diffuse goiter that became nodular and calcified may be unique [16].

Biological context of SMR3A

• Nucleotide sequence of gene PBI encoding a protein homologous to salivary proline-rich protein P-B [17].
• PBI is 6.4 kb long and contains 3 exons [17].
• A strong correlation was observed between a functional PA binding site on PB1 and P activity [18].
• The role of the minimal PB1 domain alpha in influenza virus gene expression and genome replication was subsequently analyzed by evaluating the activity of a set of PB1 mutants in a model reporter minigenome system [18].
• These results indicate that the ability of PB1 and PB2 to form a complex is an intrinsic property of these two proteins that does not require the participation of other influenza viral gene products [19].

Anatomical context of SMR3A

• The proteins recognized by these cell lines included the nucleoprotein (NP), matrix protein (M1), nonstructural protein 1 (NS1), polymerases (PB1 and PB2), and hemagglutinin (HA) [20].
• Mixtures of 5 X 10(4) B (PB1 or TG) cells, 2 X 10(4) CD4+ (PB or TG) cells, and 5 X 10(3) macrophages (PB or TG) were cultured with various numbers of CD8+ (PB) or CD8+ (TG) cells for 7 days with pokeweed mitogen, and IgG synthesis was determined by solid phase RIA [21].
• A series of compounds that increase the activity of delta-aminolevulinic acid synthase (ALAS) in chick embryo hepatocyte cultures were studied for their effects on steady-state levels of mRNA for ALAS and phenobarbital-inducible cytochrome PB1 P450 [22].
• Serum thyroxine (T4), triiodothyronine (T3), reverse T3 (rT3), thyroid stimulating hormone (TSH), protein-bound iodide (PBI), and total iodide concentrations, serum T3-charcoal uptake, and 24-hour urinary iodide excretion were measured on Days 1, 8, and 15 [23].
• METHODS: Human oocytes with an extruded polar body I (PBI) were cryopreserved using a slow-cooling method including 1.5 mol/l propane-1,2-diol (PrOH) and alternative sucrose concentrations (either 0.1 or 0.3 mol/l) in the freezing solution [24].

Associations of SMR3A with chemical compounds

• Serum PBI was 9.7 micrograms/dl, and more than 90% was not extractable with butanol [25].
• Interaction of NP with PB1 and PB2 was confirmed by both coimmunoprecipitation and histidine tagging of the NP-PB1 and NP-PB2 complexes [26].
• Markedly elevated serum PBI levels occur after therapy with povidone-iodine (Betadine), an iodine-polyvinylpyrrolidone iodophor [27].
• Most of the PBI was in albumin, and hydrolysis of the serum proteins with proteases released 35% of the PBI as monoiodotyrosine, 3.2% as diiodotyrosine, 0.01% as T3, and 2.5% as T4, as determined by competitive radioassays, anion exchange, and reversed phase high pressure liquid chromatography [27].
• Diagnosis of defective Tg gene expression was based on findings of normal PBI and low serum T4, low or normal serum T3, negative perchlorate discharge test, and virtual absence of the serum Tg response to challenge by bovine TSH [28].

Other interactions of SMR3A

• PBI appears to code for the precursor of a proline-rich protein which we have designated P-B1 [17].

Analytical, diagnostic and therapeutic context of SMR3A

• We identified the N-terminal region of PB1 protein as responsible for the interaction with the PA subunit by two-hybrid assays in mammalian cells [29].
• Subsequently, we used site-directed mutagenesis to identify the critical amino acid residues of PB1 for interaction with PA in vivo [18].
• Evaluation of a child with goiter includes historical review, physical examination, and measurement of serum concentrations of PBI, T4 and T3RU, TSH, and titers of antithyroglobulin and antithyroid microsomal antibodies [30].
• We report a longitudinal study examining three measures of parental style (EE; Parental Bonding Instrument or PBI; and interviewer ratings) [31].
• The composition of the large helical internal components of influenza virus was investigated by immunogold labeling/electron microscopy with antibodies to the nucleoprotein (NP), matrix protein (M), and polymerase complex (PB1, PB2, and PA) of the virus [32].

References