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T Satoh

Publications and source records attributed to T Satoh.

At least 487 records · Page 27Linked to original sources
PubMed1996

Nucleotide sequence of the genes, encoding the pentaheme cytochrome (dmsC) and the transmembrane protein (dmsB), involved in dimethyl sulfoxide respiration from Rhodobacter sphaeroides f. sp. denitrificans.

The nucleotide sequence of the genes encoding a pentaheme cytochrome (dmsC) and a transmembrane protein (dmsB) were determined upstream of the dmsA gene encoding dimethyl sulfoxide reductase from Rhodobacter sphaeroides f. sp. denitrificans. dmsC and dmsB encode proteins of 404 and 226 amino acid residues, which show 40% and 26% identity to the pentaheme cytochrome TorC and the transmembrane protein TorD, respectively, of the trimethylamine N-oxide reduction system in Escherichia coli.

Amino Acid Sequence↗
PubMed1996

Negative regulation of the gene for the preprothyrotropin-releasing hormone from the mouse by thyroid hormone requires additional factors in conjunction with thyroid hormone receptors.

To gain additional insights into the negative gene regulatory action by triiodothyronine (T3), we isolated a 2-kilobase pair 5'-flanking region of the mouse preprothyrotropin-releasing hormone (ppTRH) gene and characterized the DNA elements mediating inhibitory regulation by T3 in the promoter region. In GH4C1 cells, the expression of the 2-kilobase pair mouse ppTRH 5'-flanking region fused to the luciferase reporter gene occurred by transfection and was significantly suppressed by T3. In contrast, T3 suppression was not observed in T3 receptor (T3R)-deficient CV-1 cells, suggesting that T3Rs were required for the negative regulation. Cotransfected mouse T3R alpha1, beta1, and beta2 possessed indistinguishable potency for the negative regulation. Deletion analysis localized the element mediating the negative regulation to the region between -83 and +46, and the sequence downstream of the transcription start site (TSS) between +12 and +46 was found to be essential for the inhibitory regulation. In mobility shift assays, only T3R monomers bound to the element containing a T3 response element half-site at -57. No apparent T3R binding was observed to the element downstream of TSS. Neither the T3 response element half-site nor the element downstream of the TSS confer T3 suppression individually in heterologous promoters. These results indicate that the negative regulation of murine ppTRH gene by T3 might be mediated by the cooperation of T3R monomers with unknown factor(s) interacting with the element downstream of the TSS.

Animals↗
PubMed1996

Survival factor-insensitive generation of reactive oxygen species induced by serum deprivation in neuronal cells.

To investigate the involvement of reactive oxygen species (ROS) in neuronal apoptosis, we performed confocal and flow cytometric analysis with a ROS-specific fluorogen, 6-carboxy-2', 7'-dichorodihydrofluorescein diacetate, di(acetoxymethyl ester) (C-DCDHF-DA). Serum deprivation significantly increased the level of ROS in PC12 cells and rat cortical neurons. N,N'-diphenyl-p-phenylenediamine (DPPD), an antioxidant, reduced ROS production induced by serum deprivation and recovered cell survival. However, some survival factors such as nerve growth factor and Bcl-2, which prevented the apoptosis of PC12 cells, did not affect the up-regulation of ROS induced by serum deprivation. Epidermal growth factor which prevented the apoptosis of cortical neurons, did not affect the increase of ROS. These data suggest that survival factors rescue the serum deprivation induced apoptosis independently of ROS production.

Animals↗
PubMed1996

Genomic organization and promoter function of the human thyrotropin-releasing hormone receptor gene.

We isolated and characterized the gene for the human thyrotropin-releasing hormone receptor. The gene spanned more than 30 kilobases and contained three exons and two introns. Intron 1 exists in the 5'-untranslated region, and intron 2 is more than 25 kilobases in length which interrupts the coding region before the beginning of the putative sixth transmembrane domain. Exon 3 encodes the rest of the coding region and the entire 3'-untranslated region. The 3'-flanking region contains four potential polyadenylation signals, and 3'-rapid amplification of cDNA ends studies showed that only a signal at 2076 base pairs downstream of the stop codon was functional in the anterior pituitary. Primer extension and anchor-polymerase chain reaction studies indicated a transcriptional start site at 344 base pairs upstream of the translational start site. The promoter region does not contain either a TATA box or a CAAT box in the appropriate location. Transient transfection study revealed significant activity of the promoter in GH4C1 cells, and the region between -338 and -933 bp from the transcriptional start site worked as a negative regulator. Knowledge of the genomic organization and the promoter region of thyrotropin-releasing hormone (TRH) receptor gene will allow further studies of possible disorders of the TRH receptor, as well as facilitate elucidation of transcriptional control of the human TRH receptor gene.

Amino Acid Sequence↗
PubMed1996

Synthetic peptides derived from the fourth domain of CD4 antagonize off function and inhibit T cell activation.

We have developed synthetic peptide analogs to analyze novel surface structures of the human CD4 protein potentially involved in T cell activation. Linear and cyclic peptides derived from the FG and CC' loops of the membrane proximal fourth domain of CD4 displayed inhibitory activities in a CD4-dependent immunological assay. These results suggest that the fourth domain of CD4 plays an important role in T cell activation. In addition, we report the synthesis of a highly stable CD4 peptide analog cyclized by the formation of an amide bond between amino and carboxyl termini. Serum stability studies showed that this main-chain cyclic CD4 peptide was highly resistant to proteolytic degradation while the linear and disulfide cyclic peptides were much less stable. The strategy of main chain cyclization of CD4 peptides may represent a promising approach to generate proteolytically stable, orally active immunoregulatory agents.

Amino Acid Sequence↗
PubMed1996

Rapid rates during bradycardia prolong ventricular refractoriness and facilitate ventricular tachycardia induction with cesium in dogs.

BACKGROUND: Bradycardia can promote the development of some ventricular techycardias (VTs). We investigated whether relative bradycardia per se or the transition from a rapid to a slower ventricular rate might be important in developing VT. METHODS AND RESULTS: We studied groups of anesthetized closed-chest dogs that had AV produced by radiofrequency catheter ablation of the AV junction. One group had uninterrupted AV block; the other group underwent a period of rapid left ventricular pacing. Both groups then received incremental doses of CsCl until sustained VT resulted. We also measured ventricular effective refractory period (V-ERP) and QT interval in separate groups of dogs that had AV block for 1 week or 3 days with and without rapid pacing (pacing cycle length [PCL] = 500 or 250 ms) for 1 hour or 30 minutes. Finally, we investigated the effects of rapid pacing on V-ERP by testing the effects of verapamil and autonomic denervation on these changes. We found that CsCl induced larger early afterdepolarizations and a greater prevalence of VT in dogs with rapid pacing than in dogs without. In dogs that had AV block for 1 week, 1 hour of rapid pacing prolonged V-ERP and QT interval compared with V-ERP and QT interval before pacing. Changes persisted for at least 3 hours. Rapid pacing for only 30 minutes and at a PCL of 250 ms, as well as superimposition on sinus rhythm, each prolonged V-ERP but to a lesser extent. Only 3 days of complete AV block and autonomic denervation did not affect the prolongation of V-ERP produced by rapid pacing, whereas verapamil significantly blunted but did not eliminate the prolongation. CONCLUSIONS: At the same PCLs, the heart exposed to transient tachycardia superimposed on bradycardia exhibited a longer V-ERP, QT interval, and monophasic action potential duration and greater ease for developing VT than the heart exposed only to bradycardia. The prolongation of refractoriness lasted for at least 3 hours, and the delta-ERP was influenced by the heart rate before pacing, the duration of pacing, and the PCL. The mechanism for this response to rapid rates appears to involve calcium, at least in part.

Animals↗
PubMed1996

A YAC contig of the human CC chemokine genes clustered on chromosome 17q11.2.

CC chemokines are cytokines that attract and activate leukocytes. The human genes for the CC chemokines are clustered on chromosome 17. To elucidate the genomic organization of the CC chemokine genes, we constructed a YAC contig comprising 34 clones. The contig was shown to contain all 10 CC chemokine genes reported so far, except for one gene whose nucleotide sequence is not available. The contig also contains 4 CC chemokine-like genes, which were deposited in GenBank as ESTs and are here referred to as NCC-1, NCC-2, NCC-3, and NCC-4. Within the contig, the CC chemokine genes were localized in two regions. In addition, the CC chemokine genes were more precisely mapped on chromosome 17q11.2 using a somatic cell hybrid cell DNA panel containing various portions of human chromosome 17. Interestingly, a reciprocal translocation t(Y;17) breakpoint, contained in the hybrid cell line Y1741, lay between the two chromosome 17 chemokine gene regions covered by our YAC contig. From these results, the order and the orientation of CC chemokine genes on chromosome 17 were determined as follows: centromere-neurofibromatosis 1-(MCP-3, MCP-1, NCC-1, I-309)-Y1741 breakpoint-RANTES-(LD78gamma, AT744.2, LD78beta)-(NCC-3, NCC-2, AT744.1, LD78alpha)-NCC-4-retinoic acid receptor alpha- telomere.

Animals↗
PubMed1996

NMR studies of the effects of the 5'-phosphate group on conformational properties of 5-methylaminomethyluridine found in the first position of the anticodon of Escherichia coli tRNA(Arg)4.

5-Methylaminomethyluridine (mnm5U) exists in the first position of the anticodon (position 34) of Escherichia coli tRNA4Arg for codons AGA/AGG. In the present study, the temperature dependence of the ribose-puckering equilibrium of pmnm5U was analyzed by proton NMR spectroscopy. Thus, the enthalpy difference (delta H) between the C2'-endo and C3'-endo forms was obtained at 0.65 kcal.mol-1. By comparison of the delta H values of pU and pmnm5U, the 5-substitution was found to increase the relative stability of the C3'-endo form over the C2'-endo form significantly (by 0.56 kcal.mol-1). Furthermore, this conformational "rigidity" was concluded to depend on the 5'-phosphate group, because nucleoside U exhibits only a negligible change in the ribose-puckering equilibrium upon the 5-methylaminomethyl substitution. Further NMR analyses and molecular dynamics calculations revealed that interactions between the 5-methylaminomethyl and 5'-phosphate groups of pmnm5U restrict the conformation about the glycosidic bond to a low anti form, enhancing steric repulsion between the 2-carbonyl and 2'-hydroxyl groups in the C2'-endo form. This intrinsic conformational rigidity of the mnm5U residue in position 34 may contribute to the correct codon recognition.

Anticodon↗
PubMed1996

Tyrosine phosphorylation of ACK in response to temperature shift-down, hyperosmotic shock, and epidermal growth factor stimulation.

The mammalian Cdc42 protein regulates various kinds of cellular responses, including formation of filopodia, polarization of T cells, and cell cycle progression. A non-receptor tyrosine kinase ACK, which specifically binds to the GTP-bound form of Cdc42, was isolated as a putative target of Cdc42. Here we show the induction of tyrosine phosphorylation of ACK in response to temperature shift-down to 25 degrees C, and hypertonic shock, as well as stimulation with epidermal growth factor (EGF) in human embryonic kidney (HEK) 293 cells. The increased tyrosine phosphorylation level upon temperature shift-down was sustained for at least 60 min, whereas reversion of the temperature to 37 degrees C caused rapid tyrosine dephosphorylation to the initial level. The responses to EGF and the high osmolarity were transient. Furthermore, we observed association of ACK with an adaptor protein Grb2, which may suggest the involvement of Grb2 in EGF receptor-mediated tyrosine phosphorylation of ACK.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Correlated discharges of two neurons in rat gustatory cortex during gustatory stimulation.

During application of tastants into the oral cavity correlated activities were observed in 27 of 64 neuron pairs recorded simultaneously in the gustatory cortex of anesthetized rats. The mean frequency of correlated discharges as assessed from the size of the peak appearing in the cross-correlogram was lower (0.2-0.33 spikes/s) and the mean width of the peaks was wider (8 ms) as compared to those reported in the gustatory relay stations in the brainstem. In a few cases troughs were formed or peaks appeared with a long delay.

Animals↗
PubMed1996

Cytogenetic effects of a food mutagen, 2-amino-1-methyl-6-phenylimidazo[4,5-beta]pyridine (PhIP), and its metabolite, 2-hydroxyamino-1-methy-6-phenylimidazo[4,5-beta]pyridine (N-OH-PhIP), on human and Chinese hamster cells in vitro.

2-Amino-1-methyl-6-phenylimidazo[4,5-beta]pyridine (PhIP) induced structural chromosomal aberrations (CAs) and sister-chromatid exchanges (SCEs) in human lymphocytes and human diploid fibroblasts (TIG-7) at concentrations above 12.5 microgram /ml in the presence of rat S9 mix. PhIP also elevated the frequencies of SCEs in human lymphocytes in the presence of rat S9 at concentrations above 2.0 microgram/ml with dose-dependency. A proximate form of metabolites of PhIP, 2-hydroxy-amino-1-methyl-6-phenylimidazo[4,5-beta]pyridine (N-OH-PhIP), caused CAs in human and Chinese hamster fibroblast cells in the absence of S9 mix at concentrations above 0.75 microgram/ml and 1.25 microgram/ml, respectively, which were 10 times lower than the effective concentration of PhIP. No marked differences were observed in the cytogenetic sensitivity to N-OH-PhIP between human and Chinese hamster cells, except between lymphocytes obtained from different donors.

Adult↗
PubMed1996

Analysis of the T-cell activation signaling pathway mediated by tyrosine kinases, protein kinase C, and Ras protein, which is modulated by intracellular cyclic AMP.

T-cell receptor (TCR) triggering by an anti-CD3 antibody or phytohemagglutinin (PHA) as well as the treatment with phorbol myristate acetate (PMA), a direct activator of protein kinase C (PKC), induces activation of Ras in T-lymphocytes (Downward, J. et al. (1990)) Nature 364, 719-723). In this paper, we studied the role of Ras in the process of TCR-mediated T-cell activation using a human lymphomic Jurkat cell line. The stimulatory effect of TCR cross-linking on Ras activation was inhibited by herbimycin A, a specific inhibitor of protein tyrosine kinases (PTKs), whereas PMA-induced Ras activation was not affected. On the other hand, calphostin C, a specific inhibitor of PKC, blocked not only PMA-induced, but also TCR-mediated formation of Ras.GTP. Furthermore, down-regulation of PMA-sensitive PKC severely impaired the activation of Ras in response to TCR-stimulation. Tyrosine-phosphorylation and translocation to the particulate fraction of phospholipase C-gamma 1 (PLC-gamma 1) were observed upon T-cell activation. Subcellular localization of PKC was also changed when the cells were stimulated with an anti-CD3 antibody or PMA. While TCR-stimulated translocation of PKC was observed only transiently, PMA-induced translocation of PKC was more sustained. These results suggest that the activation of PLC-gamma 1 by PTK and subsequent activation of PKC are important for TCR-mediated Ras activation in Jurkat cells. An activated form of Ras enhanced the activation of interleukin 2 (IL-2) promoter by TCR stimulation or PMA treatment, although the activated Ras by itself was insufficient for IL-2 promoter activation. On the other hand, a dominant-inhibitory Ras diminished almost completely the activation of IL-2 promoter induced by PMA plus calcium ionophore, indicating that Ras is essential for transduction of T-cell activation signals. Cholera toxin (CTX), which directly activates Gs alpha, is shown to inhibit the activation of IL-2 promoter. TCR-mediated Ras activation, tyrosine phosphorylation and translocation of cellular proteins including ZAP-70, PLC-gamma 1 , and PKC. An activated Gs alpha mutant as well as dibutylyl cAMP (dBcAMP) also showed similar inhibitory effects.

Cell Compartmentation↗
PubMed1996

Comparison of the inhibitory action of synthetic capsaicin analogues with various NADH-ubiquinone oxidoreductases.

Capsaicin is a new naturally occurring inhibitor of proton-pumping NADH-ubiquinone oxidoreductase (NDH-1), that competitively acts against ubiquinone. A series of capsaicin analogues was synthesized to examine the structural factors required for the inhibitory action and to probe the structural property of the ubiquinone catalytic site of various NADH-ubiquinone reductases, including non-proton-pumping enzyme (NDH-2), from bovine heart mitochondria, potato tuber (Solanum tuberosum, L) mitochondria and Escherichia coli (GR 19N) plasma membranes. Some synthetic capsaicins were fairly potent inhibitors of each of the three NDH-1 compared with the potent rotenone and piericidin A. Synthetic capsaicin analogues inhibited all three NDH-1 activities in a competitive manner against an exogenous quinone. The modification both of the substitution pattern and of the number of methoxy groups on the benzene ring, which may be superimposable on the quinone ring of ubiquinone, did not drastically affect the inhibitory potency. In addition, alteration of the position of dipolar amide bond unit in the molecule and chemical modifications of this unit did not change the inhibitory potency, particularly with bovine heart and potato tuber NDH-1. These results might be explained assuming that the ubiquinone catalytic site of NDH-1 is spacious enough to accommodate a variety of structurally different capsaicin analogues in a dissimilar manner. Regarding the moiety corresponding to the alkyl side chain, a rigid diphenyl ether structure was more inhibitory than a flexible alkyl chain. Structure-activity studies and molecular orbital calculations suggested that a bent form is the active conformation of capsaicin analogues. On the other hand, poor correlations between the inhibitory potencies determined with the three NDH-1 suggested that the structural similarity of the ubiquinone catalytic sites of these enzymes is rather poor. The sensitivity to the inhibition by synthetic capsaicins remarkably differed between NDH-1 and NDH-2, supporting the notion that the sensitivity against capsaicin inhibition correlates well with the presence of an energy coupling site in the enzyme (Yagi, T. (1990) Arch. Biochem. Biophys. 281, 305-311). It is noteworthy that several synthetic capsaicins discriminated between NDH-1 and NDH-2 much better than natural capsaicin.

Animals↗
PubMed1996

Risk of progression and dying of clinically localized prostate cancer in Japan.

Study was made of the conservative management of 107 men with clinically localized prostate cancer. Distant metastasis developed more frequently in patients with poorly differentiated tumors than in those with well- and moderately differentiated counterparts (P < 0.01). Poorly differentiated histology was strongly associated with cancer-specific death (P < 0.01). The progression-free and cancer-specific survival of patients with stage T1a disease was significantly better than that of patients with stages T1b, T2a-b, and T2c tumors (P < 0.05). Available data clearly demonstrate that prostate cancer is a progressive disease when managed conservatively. Long-term follow-up data indicate the natural history of prostate cancer not to differ significantly according to race, despite noteworthy differences in prevalence and mortality. Patients with localized prostate cancer would be candidates for expectant therapy if they had lower-grade tumors and a life expectancy of 10 years or less. For patients with a 10-year or greater life expectancy and any grade of disease definitive therapy should be applicable.

Aged↗
PubMed1996

Relationship between acetone exposure concentration and health effects in acetate fiber plant workers.

In order to clarify the effects of acetone (AC) exposure on health, a cross-sectional study was carried out in 110 male AC-exposed and 67 male nonexposed shift workers. The AC workers ranged in age from 18.7 to 56.8 years (mean: 37.6 years) and in length of AC exposure from 0.5 to 34.3 years (mean: 14.9 years). The nonexposed workers ranged in age from 20.7 to 57.5 years (mean: 41.9 years). AC exposure levels assessed by personal passive monitors and biological monitoring indices measured at the end of the workshift were 19.6-1018 ppm in the breathing zone (AC-E, mean: 364 ppm), 2.5-422 ppm in alveolar air (AC-A, mean: 97.3 ppm) 4-220 mg/l in blood (AC-B, mean 66.0 ppm), and 0.75-170 mg/l in urine (AC-U, mean: 37.8 mg/l). Symptoms at the end of the workshift with good exposure-response relationships were eye irritation, tearing, and acetone odor, and symptoms within the previous 6 months with good exposure-response relationships were heavy, vague, or faint feeling in the head, nausea, loss of weight, and slow healing of an external wound. In the 30-44 year age range, simple reaction time and digit span scores in a short computerized neuro-behavioral test battery were significantly lower in AC workers, but exposure-response relationships were not clear. Manifest Anxiety Scale scores, Self-rating Depression Scale scores, R-R interval variation on the ECG, hematological examinations, serum biochemistry examinations for liver function, and phagocytic activity of peripheral neutrophils did not show any AC-related differences between the two groups. In view of the reported findings, the current occupational exposure limit of 750 ppm recommended by many governmental and academic associations seems to be too high to prevent the health effects of AC observed in this study.

Acetone↗