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K Tanabe

Publications and source records attributed to K Tanabe.

At least 433 records · Page 24Linked to original sources
PubMed1989

The maximum and minimum water content and cell volume of human erythrocytes in vitro.

The maximum and minimum water contents of human erythrocytes were measured after exposure to various osmotic pressures. Within a range of osmolarities, at which no haemolysis occurred, the water content reached its maximum, 78.1%, at 180 mosM and its minimum, 54.8%, at 800 mosM. Simultaneously, the mean cell volume increased to 98.5 microns 3 at 180 mosM and decreased to 77.2 microns 3 at 800 mosM.

Erythrocyte Volume↗
PubMed1989

Protein kinase C phosphorylation of desmin at four serine residues within the non-alpha-helical head domain.

We reported that phosphorylation by either cAMP-dependent protein kinase or protein kinase C (Ca2+/phospholipid-dependent enzyme) in vitro induces disassembly of the desmin filaments (Inagaki, M., Gonda, Y., Matsuyama, M., Nishizawa, K., Nishi, Y., and Sato, C. (1988) J. Biol. Chem. 263, 5970-5978). For this subunit protein, Ser-29, Ser-35, and Ser-50 within the non-alpha-helical head domain were shown to be the sites of phosphorylation for cAMP-dependent protein kinase (Geisler, N., and Weber, K. (1988) EMBO J. 7, 15-20). In the present work, we identified the sites of desmin phosphorylated in vitro by other protein kinase which affects the filament structure. The protein kinase C-phosphorylated desmin was hydrolyzed with trypsin, and the phosphorylated peptides were isolated by reverse-phase chromatography. Sequential analysis of the purified phosphopeptides, together with the known primary sequence, revealed that Ser-12, Ser-29, Ser-38, and Ser-56 were phosphorylated by protein kinase C. All four sites are located within the non-alpha-helical head domain of desmin. Ser-12, Ser-38, and Ser-56, specifically phosphorylated by protein kinase C, have arginine residues at the carboxyl-terminal side (Arg-14, Arg-42, and Arg-59, respectively). Ser-29 phosphorylated by both protein kinase C and cAMP-dependent protein kinase has arginine residues at the amino and carboxyl termini (Arg-27 and Arg-33). These findings support the view that the head domain-specific phosphorylation strongly influences desmin filament structure; however, each protein kinase differed with regard to site recognition on this domain.

Amino Acid Sequence↗
PubMed1989

Domain- and sequence-specific phosphorylation of vimentin induces disassembly of the filament structure.

We reported that stoichiometric phosphorylation by either cAMP-dependent protein kinase or protein kinase C induces disassembly of vimentin filaments [Inagaki, M., Nishi, Y., Nishizawa, K., Matsuyama, M., & Sato, C. (1987) Nature 328, 649-652; Inagaki, M., Gonda, Y., Matsuyama, M., Nishizawa, K., Nishi, Y., & Sato, C. (1988) J. Biol. Chem. 263, 5970-5978]. In the present work, we attempted to identify the sites of vimentin phosphorylated by each protein kinase. Sequential analysis of the purified phosphopeptides, together with the known primary sequence, revealed that Ser-8, Ser-9, Ser-20, Ser-25, Ser-33, and Ser-41 were specifically phosphorylated by protein kinase C, whereas Ser-46 was phosphorylated preferentially by cAMP-dependent protein kinase. Both kinases reacted with Ser-6, Ser-24, Ser-38, Ser-50, and Ser-65. Specific phosphorylation sites for protein kinase C are mostly located close to the amino-terminal side of arginine while those for cAMP-dependent protein kinase are located close to the carboxyl-terminal side of arginine. The phosphorylation sites exclusively occur in the amino-terminal non-alpha-helical head domain, particularly at the beta-turn region. These results provide clues to the molecular mechanisms of phosphorylation-dependent disassembly of vimentin filaments.

Amino Acid Sequence↗
PubMed1989

Phylogenetic association of Pneumocystis carinii with the 'Rhizopoda/Myxomycota/Zygomycota group' indicated by comparison of 5S ribosomal RNA sequences.

The cytoplasmic 5S ribosomal RNA (5S rRNA) sequence from Pneumocystis carinii was determined. A sequence comparison matrix of 382 eukaryote 5S rRNA sequences and an evolutionary tree were constructed to establish the phylogenetic position of Pneumocystis. The data suggest that Pneumocystis is associated with the Rhizopoda/Myxomycota/Zygomycota group (= 'Protista fungi') but not with common fungi, such as Ascomycota or Basidiomycota, nor with other protozoa.

Animals↗
PubMed1989

An alpha-specific gene, SAG1 is required for sexual agglutination in Saccharomyces cerevisiae.

Seven alpha-specific mutants specifically defective in sexual agglutinability were isolated. The other alpha mating functions exhibited by these mutants, designated sag mutants, such as the production of alpha pheromone and response to a mating pheromone, were normal. While the MAT alpha sag1 cells did not agglutinate with wild-type a cells, the MATa sag1 cells did, indicating that the SAG1 gene is expressed only in alpha cells. The mutations were semi-dominant and fell into a single complementation group, SAG1, which was mapped near met3 on chromosome X. Complementation analysis showed that sag1 and ag alpha 1, the latter being a previously reported alpha-specific mutation, were mutations in the same gene.

Genes, Fungal↗
PubMed1989

Chloroquine, a lysosomotropic agent, inhibits zygote formation in yeast.

Haploid cells of opposite mating type of Saccharomyces cerevisiae conjugate to form zygote. During the conjugation process, the degradation or reorganization of the cell wall and the fusion of the two plasma membranes take place. Since chloroquine inhibits cellular events associated with the reorganization of the plasma membrane, the effect of the drug on conjugation was studied. Chloroquine at a concentration, at which cell growth was not retarded, inhibited zygote formation, while it did not affect other mating functions, such as sexual agglutination, production of and response to mating pheromone. Cells in a mating culture containing chloroquine formed no "prezygote" suggesting that they were not prepared for entering into fusion process. The inhibitory effect of chloroquine was reversible as cells formed zygote when they were washed after treatment with chloroquine. Zygote formation was unaffected in cells possessing chloroquine within vacuoles after incubation with the drug in complete medium (YPD) at pH 7.5, followed by washing. This suggests that chloroquine inhibits zygote formation by adsorbing to the plasma membrane of S. cerevisiae.

Adsorption↗
PubMed1989

Induction of DNA double-strand breaks in Chinese hamster V79 cells by 2-chlorodeoxyadenosine.

2-Chlorodeoxyadenosine was found to induce DNA double-strand breaks as well as cell death in log-phase Chinese hamster V79 cells. The induction of DNA double-strand breaks, measured by a neutral elution technique, was observed after a 2-h incubation of the cells in the presence of 5 microM of 2-chlorodeoxyadenosine, but these breaks were almost rejoined by a subsequent 1-h incubation, even though this drug was present in the medium during incubation. This repair was prevented by the addition of nicotinamide, which is known to inhibit poly(ADP-ribose) synthesis that is strongly associated with the DNA ligation, but not prevented by the addition of 9-beta-D-arabinofuranosyladenine (araA), which is known to inhibit DNA polymerization. These results suggest that the repair of CdA-induced double-strand breaks is achieved by ligation alone without DNA polymerization. When 35 microM of cycloheximide and 1.3 mM of dibutyryl cAMP were added to the medium, it was found that the induction of double-strand breaks by 2-chlorodeoxyadenosine was suppressed, while the cytotoxicity of 2-chlorodeoxyadenosine measured by colony-forming ability was not interfered with. These results suggest that the induction of DNA double-strand breaks is not associated with the cytotoxicity of this drug.

2-Chloroadenosine↗
PubMed1989

Rapid clearance of Plasmodium yoelii-infected erythrocytes after exposure to the ionophore A23187.

1. The effects of Ca2+ and the calcium ionophore A23187 on the intraerythrocytic development of the asexual forms of Plasmodium yoelii were examined. 2. Erythrocyte-free parasites obtained by saponin lysis of infected cells remained viable after exposure to 1 mM Ca2+. 3. A23187 inhibited the growth of P. yoelii and the inhibition was augmented by Ca2+ in cells infected with parasites at young stage of development. 4. A23187-treated infected cells disappeared from the circulation shortly after intravenous injection and this disappearance was profound in infected cells treated with the ionophore in the presence of Ca2+.

Animals↗
PubMed1989

Transport processes of 2-deoxy-D-glucose in erythrocytes infected with Plasmodium yoelii, a rodent malaria parasite.

The transport processes of D-glucose in Plasmodium yoelii-infected mouse erythrocytes were investigated using 2-deoxy-D-glucose (2DOG), a non-metabolizable analogue of D-glucose. Infected cells showed an increase in the uptake of 2DOG compared to uninfected controls, and an effect which was more prominent in cells with mature-stage parasites. Kinetic studies measuring the initial rates of 2DOG uptake revealed two components in infected cells with late trophozoite and schizont-stage parasites: a simple diffusion system and a carrier (transporter)-mediated system. The transporter was common for D-glucose and 2DOG and had a kinetic constant indicating a high affinity for 2DOG (the Km = 0.18 mM and the Vmax = 0.61 mmol/10(10) cells/min), as compared to the constant of the mouse erythrocyte carrier (the Km = 10 mM and the Vmax = 1.8 mmol/10(10) cells/min). Determination of the distribution of [3H]2DOG in infected cells and experiments with metabolic inhibitors indicated that the simple diffusion system localizes in the membrane of host cells and the transporter in the parasite plasma membrane. The parasite glucose transporter was much less sensitive to cytochalasin B than that of the host cells and the uptake of 2DOG via the transporter was dependent on energy. Based on these findings, the following features emerge: D-glucose first gains access to the cytosol of infected erythrocytes via the simple diffusion system, which appears after infection by the parasite, and an active uptake against the concentration gradient takes place at the parasite plasma membrane via the parasite glucose transporter in an energy dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Glycoproteins composed of major surface immunodeterminants of Pneumocystis carinii.

Pneumocystis carinii is a pathogen which causes fatal pneumonia in patients with acquired immune deficiency syndrome. To facilitate the basic study of P. carinii, we analyzed the major surface proteins by immunochemical and biochemical methods. The major protein components of both cysts (resting form) and trophozoites (vegetative form) are part of a group of proteins called P115 with apparent masses of 105 to 120 kilodaltons. They represent an unusually large portion of the total proteins of this organism. The purified proteins exhibited six isoelectric variants when analyzed by two-dimensional gel electrophoresis. A monoclonal antibody raised against cysts recognized all six variants and reacted with epitopes that were located in the cell wall, thereby indicating that P115 is an immunoreactive surface component. Data are presented that the isoelectric variants contain identical or closely related protein components and that they are mannose-rich glycoproteins. Deglycosylated P115 migrates primarily as a single more acidic protein in two-dimensional gels, suggesting that the isoelectric variants may be due primarily to differences in glycosylation. The majority of sera tested from humans with diagnosed pneumocystosis reacted strongly with the P115 proteins.

Animals↗
PubMed1989

Induction of repressible acid phosphatase by unsaturated fatty acid in Saccharomyces cerevisiae.

We studied the induction of acid phosphatase (APase) by fatty acids in Saccharomyces cerevisiae. S. cerevisiae has two types of APase: constitutive and repressible enzymes. The synthesis of the latter APase is normally derepressed by depletion of inorganic phosphate (Pi) in the incubation medium. Of the saturated and unsaturated fatty acids tested, linoleic, linolenic and arachidonic acids induced the synthesis of APase even in the presence of a high concentration of Pi, whereas palmitic, stearic and oleic acids did not. De novo protein synthesis but not stimulation of secretion of the enzyme was required for the induction. Genetic analyses using plasmids carrying the genes, PHO5 and PHO3, that code for repressible APase and constitutive APase, respectively, showed that linolenic acid induced the formation of repressible APase. Linolenic acid inhibited the uptake of exogenous 32Pi and simultaneously lowered the intracellular level of Pi. These circumstances indicate that linolenic acid-induced derepression of repressible APase is primarily caused by a fall in the intracellular level of Pi. However, cells that had been preincubated in the presence of a high concentration of Pi produced APase shortly after the addition of linolenic acid. It is, therefore, suggested that, as well as a normal regulatory mechanism for derepression of repressible APase, a mechanism independent of the external level of Pi participates in the induction of repressible APase by linolenic acid.

Acid Phosphatase↗
PubMed1989

Binding of hydrochlorothiazide to erythrocytes.

Hydrochlorothiazide (HCT) was administered orally to healthy volunteers and intravenously to rabbits. HCT concentrations in plasma (Cp) and erythrocytes (Ce) were determined by a high-performance liquid chromatographic method. Ce was about 9-fold that of Cp 24 h after the administration to volunteers, and 8-fold 6 h after the administration to rabbits. From the results of the in vitro binding study which was done with rabbit erythrocytes, at least the presence of three kinds of binding site for HCT was expected. The first binding site was characterized by extremely high affinity and very low capacity, and was unaffected by acetazolamide, known as a carbonic anhydrase inhibitor. The second one was characterized by medium affinity and medium capacity, and disappeared under the presence of acetazolamide and may be due to the carbonic anhydrase of erythrocytes. The third one was characterized by low affinity, but its binding capacity was extremely high and apparently unsaturable in the HCT concentration range studied (0.5-100 micrograms/ml = 1.68-336 microM). The binding of HCT to erythrocytes seems to be dominated by the second binding site in the therapeutic range (under 1 microgram/ml of plasma).

Adult↗
PubMed1989

Study of cardiac hypertrophy--humoral factors that stimulate protein metabolism of cultured rat heart cells.

Recent extensive studies suggested that some humoral factors may contribute to the development and/or reversal of cardiac hypertrophy in hypertension. The purpose of this study is to examine whether there exists humoral factor(s) for cardiac hypertrophy in experimental perinephritic hypertension in dogs. Hypertension was induced by the method of Page with some modifications. Humoral factors were studied using a microassay system that was independent of pressure overload, hemodynamic effects, and other factors. L(-)-isoproterenol (ISO) and angiotensin II (AngII) increased the uptake of 3H-uridine into 10-day-old cultured heart cells. The maximal response to ISO or AngII was obtained by 10(-5) M ISO or 10(-10) M AngII, and the percent increments in the uptake of 3H-uridine was 38.4 +/- 20.4%, and 45.1 +/- 22.5%, respectively. Moreover, ISO, DL-noradrenaline, and AngII stimulated protein synthesis of 7-day-old or 14-day-old cultured heart cells in this order (9.5 +/- 1.5, 7.3 +/- 1.2, 2.0 +/- 0.5 micrograms/6 x 10(5) by 7-day-old heart cells; 23.8 +/- 8.3, 19.0 +/- 9.4, 4.4 +/- 1.1 micrograms/6 x 10(5) by 14-day-old heart cells). Heart and kidney extracts were obtained from experimental perinephritic hypertensive dogs and sham-operated dogs. The heart extract obtained from hypertrophied left ventricle (LV) of the experimental hypertensive dogs, but not of the sham-operated dogs, increased the uptake of 3H-uridine into 10-day-old heart cells. The mean percent increment in uptake of 3H-uridine induced by the hypertrophied LV heart extract at a final concentration of 5 x 10(-3)% V/V (1-3 micrograms) in different experiments was about 15%. High performance liquid chromatography (HPLC) demonstrated that the LV heart extract obtained from the perinephritic hypertensive dogs contained at least 16 molecules. Among them, one with a molecular weight of approximately 11,200 daltons stimulated uptake of both 3H-uridine and 14C-leucine into cultured heart cells. These results demonstrated that heart extract obtained from hypertrophied LV of perinephritic hypertensive dogs contained at least one factor which may induce and/or modulate myocardial hypertrophy in this model for hypertension.

Angiotensin II↗
PubMed1989

[Infectious diseases in kidney transplant recipients treated with cyclosporin].

Cyclosporin (CYA) is now recognized as an effective immunosuppressant to lead to a marked improvement in graft survival in organ transplant recipients. Although the incidence of infection in the CYA group has been decreased compared with that in the azathioprine group, infectious diseases in 400 kidney transplant recipients treated with CYA were noted in our single center. Treatment strategy for infectious diseases: Antibiotics and/or gamma-Globulin were administered to all recipients with bacterial infections. Aciclovir was added in recipients with herpes simplex virus (HSV) infection or varicella zoster virus (VZV) infection. Human interferon-beta (HuIFN-beta) was used in recipients who had life-threatening viral infection, especially cytomegalovirus (CMV) pneumonitis. Glycyrrhizin was used for acute hemorrhagic cystitis and nephropathy due to adenovirus (AV). Trimethoprim sulfamethoxazole and/or pentamidine were added in recipients complicated with Pneumocystis carinii (Pc) pneumonitis or in order to prevent Pc pneumonitis. Infectious diseases: One hundred and six recipients had infectious diseases 129 times in this series, seventy-six percent of all infections occurred during the first 4 months after the transplantation. Urinary tract infection (UTI), herpes zoster and pulmonary infection were the most common infectious diseases, occurring in 28.7%, 24.0% and 23.2%, respectively. Septicemia or bacteremia developed in 9 recipients, secondary to UTI in 8 and to surgical wound infection in one. Sixty-one symptomatic viral infections occurred in 57 recipients. A total of 5 recipients (1.3%) died of interstitial pneumonitis. Infectious organisms: Viral and bacterial infections were most common, occurring in 47.3% and 41.9%, respectively. Viral species detected in these recipients with the frequency were HSV 14 times, CMV 9 times, VZV 31 times and AV 7 times. 1) The incidence of viral infections in kidney transplant recipients treated with CYA is relatively high compared to bacterial infections. 2) HuIFN-beta therapy is effective in the treatment of serious opportunistic herpes virus infections, especially CMV pneumonitis. 3) Glycyrrhizin therapy is effective in the treatment of acute hemorrhagic cystitis and nephropathy due to AV and hepatic dysfunction. 4) Aerosolised pentamidine therapy is very useful for prophylaxis of Pc pneumonitis.

Adolescent↗