Disease relevance of P7Ehs1

• Monoclonal or polyclonal IgG or IgM and the IgM-FC5 mu fragment of human myeloma protein combined with the protein B thereby inhibiting protein B-induced hemolysis in the CAMP reaction [1].
• Targeted disruption of the surfactant protein B gene disrupts surfactant homeostasis, causing respiratory failure in newborn mice [2].
• The adaptor protein B cell lymphoma 10 (Bcl10) plays an essential role in the functions of the AgRs in T and B cells [3].
• Surface expression of an immunodominant malaria protein B cell epitope by yellow fever virus [4].
• Decreased surfactant protein-B expression and surfactant dysfunction in a murine model of acute lung injury [5].

High impact information on P7Ehs1

• Epileptic seizures caused by inactivation of a novel gene, jerky, related to centromere binding protein-B in transgenic mice [6].
• The protein B/Ig complex can be dissociated with 1% Triton or guanidine-HCl (6 M) [1].
• Intratracheal treatment with exogenous surfactant protein B improved survival and lung histology in Stat-3-deleted mice during hyperoxia [7].
• The hyperreactivity to bronchoconstriction observed in the Aqp5(-/-) mice was not due to differences in tracheal smooth muscle contractility in isolated preparations or to altered levels of surfactant protein B. These data suggest a novel pathway by which AQP5 influences bronchoconstriction [8].
• The binding domain is similar to the two tandemly arranged homeodomain-like helix-turn-helix DNA binding motifs of centromere binding protein B. The putative helix-turn-helix motifs of Jerky can also bind double-stranded DNA and represent a novel mammalian RNA/DNA binding domain [9].

Biological context of P7Ehs1

• The lung-specific surfactant protein B gene promoter is a target for thyroid transcription factor 1 and hepatocyte nuclear factor 3, indicating common factors for organ-specific gene expression along the foregut axis [10].
• Furthermore, competitor containing the YY1 consensus sequence competed for protein B binding, whereas competitor containing a perfect yeast ABF-1 consensus sequence did not.(ABSTRACT TRUNCATED AT 400 WORDS)[11]
• The -447/-419 region of this promoter contains two binding sites for orphan nuclear receptors that are required for activation by SF-1, nerve growth factor-inducible protein B, and cAMP [12].
• Protein A (about 115 kDa) and protein B (about 15 kDa) were made transiently at early times after transfection, whereas a large amount of protein alpha (43 kDa), the precursor to the two viral coat proteins, was made continuously starting later in the infectious cycle [13].
• Four different E1A-Mer chimeras (ME, EM, E(DeltaNLS)M, MEM) were constructed and inserted into the adenoviral genome under control of a lung-specific surfactant protein B promoter [14].

Anatomical context of P7Ehs1

• These reagents down-regulated surfactant protein B gene expression in respiratory epithelial cells at the transcriptional level in both cell line and whole lung explant systems [15].
• Deficiency in the adaptor protein B cell linker protein (BLNK) results in a substantial but incomplete block in B cell development, suggesting that alternative pathways exist for B lineage differentiation [16].
• We also demonstrate the exclusive induction of the IkappaB protein B cell lymphoma 3 (Bcl-3) in tolerant T cells as well as its specific binding to the NFkappaB site [17].
• Surfactant protein B (SP-B) mRNA and protein are restricted to alveolar Type II and Clara cells in the respiratory epithelium [18].
• Plasminogen-related protein B, which antagonizes various endothelial cell activities, also elicited a significant inhibition of neoplastic growth, albeit with reduced effectiveness [19].

Associations of P7Ehs1 with chemical compounds

• In this report, the functional role of the neutral lipid metabolites, 15-deoxy-Delta12,14-prostaglandin J2 and 9-hydroxyoctadecanoic acids, and peroxisome proliferator-activated receptor gamma was evaluated in surfactant protein B gene regulation [15].
• Tumor necrosis produced by combination therapy of ET-743 and recombinant plasminogen-related protein B was also significantly greater than that produced by conventional doxorubicin treatment, further corroborating the efficacy of combination therapy [19].
• Cysteine protease activity is required for surfactant protein B processing and lamellar body genesis [20].
• Nitric oxide inhibits surfactant protein B gene expression in lung epithelial cells [21].
• Alveolar and lung tissue saturated phosphatidylcholine and surfactant protein B concentrations were significantly decreased after treatment with aerosolized GM-CSF [22].

Physical interactions of P7Ehs1

• Allelic diversity of the two transferrin binding protein B gene isotypes among a collection of Neisseria meningitidis strains representative of serogroup B disease: implication for the composition of a recombinant TbpB-based vaccine [23].

Regulatory relationships of P7Ehs1

• Absence of heme oxygenase-1 expression in the lung parenchyma exacerbates endotoxin-induced acute lung injury and decreases surfactant protein-B levels [24].
• In contrast, incorporation of the Th-cell epitope into BT-MAP induced a strong humoral response towards the class 1 protein B-cell epitope [25].

Other interactions of P7Ehs1

• We found that the anti-apoptotic protein B-cell leukemia/lymphoma 2 (Bcl-2) was increased in the GM3-reconstituted cells [26].
• Tumor necrosis factor-alpha decreases surfactant protein B mRNA in murine lung [27].
• In contrast, surfactant protein B and CCSP expression was decreased or was absent in hypertrophic epithelial cells lining the conducting airways of transgenic mice [28].
• Although surfactant protein A, B, and C content and surfactant protein-B mRNA expression in Stat3(DeltaDelta) mice were similar, TUNEL staining and caspase-3 were increased in alveolar type II epithelial cells of Stat3(DeltaDelta) mice after exposure to virus [29].
• Synergy between signal transducer and activator of transcription 3 and retinoic acid receptor-alpha in regulation of the surfactant protein B gene in the lung [30].

Analytical, diagnostic and therapeutic context of P7Ehs1

• Mice infected intraperitoneally with sublethal doses of group B streptococci (GBS) and that received seven repeated intravenous injections of highly purified protein B during the first 9 h of infection developed fatal septicemia within 24 h with colony counts of up to 10(8) CFU/ml in the blood [1].
• The expression of surfactant protein B mRNA was unaffected, whereas surfactant protein B in bronchoalveolar lavage increased [31].
• The apoptotic activity of alveolar epithelial type II cells, determined by combined TUNEL labeling and anti-surfactant protein B immunohistochemistry, showed a dramatic increase during the perinatal transition (type II cell apoptotic index <0.1% at E17, 1.5% at P1-P3, and 0.3% at P5) [32].

References