ドイツにおける都市型商業集積としてのパサージュ,ガレリー －小売「製品」概念の外延的展開によせて

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教育相談活動報告

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Incidentally identified ductus arteriosus aneurysm in eight adults: a case series

BJR Case Reports. 2021, 7 (4), 20200097journal articl

In vitro characterization of missense mutations associated with quantitative protein Sdeficiency

名古屋大学NAGOYA University博士(医療技術学)Objective: To elucidate the molecular consequences of hereditary protein S (PS) deficiency, we investigated the in vitro synthesis of the PS missense mutants in COS-1 cells and their activated protein C (APC) cofactor activities. Patients: Four patients with quantitative PS deficiency suffering from venous thrombosis were examined. Results: We identified three distinct novel missense mutations, R275C, P375Q and D455Y, and two previously reported missense mutations, C80Y and R314H. The P375Q and D455Y mutations were found in one patient and observed to be in linkage on the same allele. The R314H mutant showed the lowest level of expression (32.7%), and the C80Y, P375Q + D455Y, and R275C mutants exhibited a moderate impairment of expression, that is, 43.8%, 49.5%, and 72.3% of the wild type, respectively. Furthermore, pulse-chase experiments demonstrated that all mutants showed impaired secretion and longer half-lives in the cells than the wild type PS. In the APC cofactor assays, the C80Y mutant showed no cofactor activity, and the R275C mutant showed reduced activity, 62.3% of the wild type PS, whereas the R314H and P375Q + D455Y mutants exhibited normal cofactor activity. Conclusion: These data indicate that the C80Y and R275C mutations affect the secretion and function of the PS molecule, and that the R314H and P375Q + D455Y mutations are responsible for only secretion defects, causing the phenotype of quantitative PS deficiency observed in the patients.名古屋大学博士学位論文 学位の種類:博士（医療技術学）（課程）学位授与年月日:平成19年3月23日In vitro characterization of missense mutations associated with quantitative protein Sdeficiency Schattauer, v.4, iss.9, pp.2003-2009を、博士論文として提出したもの。doctoral thesi

Observation of the DsJ(2317) and DsJ(2457) in B Decays

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EIGENVALUES OF THE LAPLACIAN AND RIEMANNIAN SUBMERSIONS

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人倫の「形而上学」 : 倫理を示す「礼」の考察

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Tat reverses the HEXIM1-mediated inhibition of P-TEFb transcriptional activity

<p><b>Copyright information:</b></p><p>Taken from "Tat competes with HEXIM1 to increase the active pool of P-TEFb for HIV-1 transcription"</p><p></p><p>Nucleic Acids Research 2007;35(6):2003-2012.</p><p>Published online 6 Mar 2007</p><p>PMCID:PMC1874611.</p><p>© 2007 The Author(s)</p> HeLa cells were co-transfected with the reporter plasmid pSLIIBCAT (0.2 μg) and the plasmids coding for the various effectors (Rev-CycT1: 0.6 μg; F-HEXIM1: 0.6 μg; Tat-F: 0.8 μg; TatC22G-F: 0.8 μg) as indicated. The chloramphenicol acetyltransferase (CAT) enzyme activities in cell lysates were measured and the error bars represent the mean +/− SD. Lower panel shows the expression levels of the co-transfected F-HEXIM1 and Tat-F as revealed by western blotting

Tat displaces HEXIM1-TBD from CycT1 due to its higher affinity for CycT1

<p><b>Copyright information:</b></p><p>Taken from "Tat competes with HEXIM1 to increase the active pool of P-TEFb for HIV-1 transcription"</p><p></p><p>Nucleic Acids Research 2007;35(6):2003-2012.</p><p>Published online 6 Mar 2007</p><p>PMCID:PMC1874611.</p><p>© 2007 The Author(s)</p> () A schematic diagram of the main steps of the fluorescence competition assay. GST-T1 was first added to HEXIM1-TBD* (step I), followed by the addition of Tat (step II). () Fluorescence emission spectra of the two-step titrations as diagrammed in A. To 1.0 µM HEXIM1-TBD* (black curve), 1.0 µM of GST-T1 was added (red), followed by an excess of 5.0 µM Tat (green). () Dissociation of the HEXIM1-TBD* from GST-T1 by increasing concentrations of Tat. The displacement of HEXIM1-TBD* from GST-T1 by Tat was observed by equilibrium fluorescence titration. To a preformed complex of 2.0 µM HEXIM-TBD* and 1.0 µM GST-T1, Tat was added at concentrations from 0.2–4 µM. () Kinetics of the Tat- or Tat/TAR-mediated displacement of HEXIM1-TBD* from GST-T1 as measured by stopped flow techniques. To a pre-equilibrated solution of 5 µM GST-T1 and 5 µM dimeric HEXIM1-TBD*, Tat or Tat/TAR was injected at a concentration of 10 (2×) or 20 µM (4×) to displace HEXIM1-TBD* over the indicated time periods (in seconds). The displacement caused by buffer alone or 10 µM (2×) unlabeled HEXIM1-TBD (labeled as TBD) is also presented as a comparison

HEXIM1 inhibits Tat-independent but not Tat-dependent transcriptional activation from the HIV-1 LTR

<p><b>Copyright information:</b></p><p>Taken from "Tat competes with HEXIM1 to increase the active pool of P-TEFb for HIV-1 transcription"</p><p></p><p>Nucleic Acids Research 2007;35(6):2003-2012.</p><p>Published online 6 Mar 2007</p><p>PMCID:PMC1874611.</p><p>© 2007 The Author(s)</p> () HL3T1 cells containing an integrated HIV-1 LTR-driven luciferase reporter construct were transfected with an empty vector or the plasmids encoding Tat-F and/or F-HEXIM1. Where indicated, the cells were also stimulated by PMA. Luciferase activities in cell lysates were measured and the error bars represent the mean +/− SD. Lower panels show the expression levels of the co-transfected F-HEXIM1 and Tat-F as revealed by western blotting