Mastoparan inhibits phosphoinositide hydrolysis via pertussis toxin-intensive G-protein in human astrocytoma cells

AbstractMastoparan inhibited [3H]inositol phosphate accumulation induced by carbachol as well as cyclic AMP accumulation induced by isoproterenol in 1321N1 human astrocytoma cells. Mastoparan inhibited GTPγS-induced, but not Ca2+-induced, [3H]inositol phosphate accumulation in membrane preparations with an IC50 of approximately 10 μM. The inhibitory effect of mastoparan on carbachol-induced [3pH]inositol phosphate accumulation was resistant to pertussis toxin (IAP) treatment in intact cells. These results suggest that mastoparan inhibits phospholipase C in human astrocytoma cells via a GTP binding protein, which is not a substrate for IAP

The Teaching of Singing in Meiji Period : Mainly on the contents of teaching

Additional file 3: Fig. S4. Spontaneous gp120 shedding from cell surface. The susceptibility of gp41 mutants to spontaneously shed gp120 was determined by flow cytometry and ELISA as described previously [79]. Briefly, culture medium of transiently transfected envelope expressing cells was exchanged for fresh medium containing Brefeldin A (BioLegend) and 0.2 % Sodium azide. Cells were then incubated for 15 h at 37˚C, 5 % CO2. (a) Level of envelope expression before and after incubation was compared by staining with 2G12. (b) Amount of gp120 released during incubation was determined by gp120 capture ELISA. As a positive control, cells expressing WT envelope was incubated with 20 µg/ml sCD4, which trigger gp120 shedding. Cells expressing SIV Env (SIV) and no Env (No Env) were used as negative control. The results are shown as the means ± standard errors of four replicas

ホブ切り性能向上に関する基礎的研究

第1章 緒論 第2章 平歯車のホブ切り機構の解析 第3章 舞いツールによるホブの耐久力試験法 第4章 ホブ摩耗に及ぼすホブ材質の影響 第5章 ホブ摩耗および仕上げ面粗さに及ぼす不水溶性切削油の効果 第6章 切削油添加剤としてのアルコールの効果 第7章 ホブ切り用水溶性切削油剤の効果 第8章 オーステンパ球状黒鉛鋳鉄歯車のホブ切り基礎試験 第9章 結論Made available in DSpace on 2012-09-05T01:45:41Z (GMT). No. of bitstreams: 3 matsuoka1.pdf: 11373276 bytes, checksum: 3f5aea4c6b9d2a505d2ec2f3a041f3f9 (MD5) matsuoka2.pdf: 12130320 bytes, checksum: c24107b398bbe4e02bf3dea01ae06f2b (MD5) matsuoka3.pdf: 11968984 bytes, checksum: d71ba009f776a7613b4e999cd66210b0 (MD5) Previous issue date: 1997-12-24主1-参1工学_機械科

ホブ切り性能向上に関する基礎的研究

第1章 緒論 第2章 平歯車のホブ切り機構の解析 第3章 舞いツールによるホブの耐久力試験法 第4章 ホブ摩耗に及ぼすホブ材質の影響 第5章 ホブ摩耗および仕上げ面粗さに及ぼす不水溶性切削油の効果 第6章 切削油添加剤としてのアルコールの効果 第7章 ホブ切り用水溶性切削油剤の効果 第8章 オーステンパ球状黒鉛鋳鉄歯車のホブ切り基礎試験 第9章 結論主1-参1工学_機械科

The Gibberellin Signaling Pathway Is Regulated by the Appearance and Disappearance of SLENDER RICE1 in Nuclei

The slender rice1 mutant (slr1) shows a constitutive gibberellin (GA) response phenotype. To investigate the mode of action of SLR1, we generated transgenic rice expressing a fusion protein consisting of SLR1 and green fluorescent protein (SLR1-GFP) and analyzed the phenotype of the transformants and the subcellular localization of GFP in vivo. SLR1-GFP worked in nuclei to repress the GA signaling pathway; its overproduction caused a dwarf phenotype. Application of GA(3) to SLR1-GFP overproducers induced GA actions such as shoot elongation, downregulation of GA 20-oxidase expression, and upregulation of SLR1 expression linked with the disappearance of the nuclear SLR1-GFP protein. We also performed domain analyses of SLR1 using transgenic plants overproducing different kinds of truncated SLR1 proteins. The analyses revealed that the SLR1 protein can be divided into four parts: a GA signal perception domain located at the N terminus, a regulatory domain for its repression activity, a dimer formation domain essential for signal perception and repression activity, and a repression domain at the C terminus. We conclude that GA signal transduction is regulated by the appearance or disappearance of the nuclear SLR1 protein, which is controlled by the upstream GA signal

Isolation and Molecular Characterization of a Nelfinavir (NFV)-Resistant Human Immunodeficiency Virus Type 1 That Exhibits NFV-Dependent Enhancement of Replication

During the use of a phenotypic anti-human immunodeficiency virus type 1 (HIV-1) drug resistance assay in a large set of clinical virus isolates, we found a unique variant (CL-4) that exhibited a high level of nelfinavir (NFV) resistance and rather enhanced replication under subinhibitory concentrations of NFV (0.001 to 0.1 μM). Comparison of gag-pol sequences of the CL-4 variant and its predecessor virus isolates showed a stepwise accumulation of a total of 19 amino acid substitutions in protease (PR) and Gag p17 during 32-month NFV-containing antiretroviral therapy, while other Gag regions including the cleavage sites of the p55 precursor remained highly conserved. To understand the relationship between the genetic and phenotypic changes in CL-4, we constructed chimeric viruses using pNL4-3, replacing the PR, p24PR, or p17PR gene segment of CL-4 or its predecessor. A series of tissue culture infections with the chimeras in the absence or presence of increasing concentrations of NFV demonstrated that only the p17PR segment of CL-4 could confer the NFV-dependent replication enhancement phenotype on NL4-3. Our data suggest a novel adaptation mechanism of HIV-1 to NFV, in which coevolution of Gag and PR genes generates a variant that replicates more efficiently in the cellular environment in the presence of NFV than without the drug