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Y Minami

Publications and source records attributed to Y Minami.

At least 289 records · Page 16Linked to original sources
PubMed1985

Amino acid sequence of a ferredoxin from thermoacidophilic archaebacterium, Sulfolobus acidocaldarius. Presence of an N6-monomethyllysine and phyletic consideration of archaebacteria.

The amino acid sequence of a ferredoxin from a thermoacidophilic archaebacterium, Sulfolobus acidocaldarius, was determined by a combination of various conventional methods to be as follows: Gly-Ile-Asp-Pro-Tyr-Arg-Thr-His-Lys-Pro-Val-Val-Gly-Asp-Ser-Ser-Gly-His- Lys-Ile -Tyr-Gly-Pro-Val-Glu-Ser-Pro-Lys(Me)-Val-Leu-Gly-Val-His-Gly-Thr-Ile-Val -Gly-Va l-Asp-Phe-Asp-Leu-Cys-Ile-Ala-Asp-Gly-Ser-Cys-Ile-Thr-Ala-Cys-Pro-Val-As n-Val-P he-Gln-Trp-Tyr-Glu-Thr-Pro-Gly-His-Pro-Ala-Ser-Glu-Lys-Lys-Ala-Asp-Pro-V al-Asn- Glu-Gln-Ala-Cys-Ile-Phe-Cys-Met-Ala-Cys-Val-Asn-Val-Cys-Pro-Val-Ala-Ala- Ile-Asp -Val-Lys-Pro-Pro. It was composed of 103 amino acid residues giving a molecular weight of 10,908 excluding Fe and S atoms. This ferredoxin contained an N6-monomethyllysine residue at position 29 which was determined by a comparison of the elution profile of the acid hydrolysates of the protein and peptides on an amino acid analyzer with three methyl derivatives of lysine and also by field desorption mass spectrometry of a purified peptide. The ferredoxin has only 7 cysteine residues, which probably participate in constructing the Fe-S clusters of this ferredoxin, indicating the presence of a unique chelate structure. Comparison of this ferredoxin with other archaebacterial ferredoxins indicated that the archaebacteria might have multiple origins in an evolutionary tree.

Amino Acid Sequence↗
PubMed1985

Ferredoxin from a liverwort, Marchantia polymorpha. Purification and amino acid sequence.

Marchantia polymorpha ferredoxin was purified by DE-52 and Sephadex G-75 column chromatographies to homogeneity. The complete amino acid sequence of the carboxymethylated (Cm) ferredoxin was determined by conventional methods to be as follows. Thr-Phe-Lys- Val-Thr-Leu-Asn-Thr-Pro-Thr-Gly-Gln-Ser-Val-Ile-Asp-Val-Glu-Asp- Asp-Glu-Tyr-Ile-Leu-Asp-Ala-Ala-Glu-Glu-Ala-Gly-Leu-Ser-Leu-Pro- Tyr-Ser-Cys-Arg-Ala-Gly-Ala-Cys-Ser-Ser-Cys-Ala-Gly-Lys-Val-Thr- Ala-Gly-Glu-Val-Asp-Gln-Ser-Asp-Glu-Ser-Phe-Leu-Asp-Asp-Asp-Gln- Met-Asp-Glu-Gly-Tyr-Val-Leu-Thr-Cys-Ile-Ala-Tyr-Pro-Thr-Ser-Asp- Leu-Thr-Ile-Asp-Thr-His-Gln-Glu-Glu-Ala-Leu-Ile. The total number of amino acid residues was 95 and the molecular weight was calculated to be 10,174, excluding iron and sulfur atoms. The distribution of the four cysteine residues chelating the two iron atoms was identical to those of other [2Fe-2S] ferredoxins. The relationship between M. polymorpha and other plants was discussed in terms of plant phylogeny.

Amino Acid Sequence↗
PubMed1985

Intestinal absorption of ursodeoxycholic, glycoursodeoxycholic and tauroursodeoxycholic acids in rats.

We examined the intestinal absorption of ursodeoxycholic acid (UDC), glycoursodeoxycholic acid (GUDC) and tauroursodeoxycholic acid (TUDC) using an everted gut sac technique. UDC was absorbed throughout rat small intestine almost to the same extent. Absorption of both GUDC and TUDC, however, varied between jejunum and ileum. Absorption of these conjugated bile acids in the jejunal segments was less than that of UDC. While, absorption of GUDC and TUDC in the terminal ileum was more efficient than UDC. Although 2,4-dinitrophenol had no effect on the jejunal uptake, ileal uptake of these three bile acids was inhibited by 2,4-dinitrophenol.

Animals↗
PubMed1985

[Clinical experience with cefmenoxime (CMX) in complicated urinary tract infections].

Cefmenoxime (CMX) was intravenously administered to 106 patients with complicated urinary tract infection at a daily dose of 2-4 g for 5 days. An excellent response in overall clinical efficacy was seen in 15 cases (18.3%), a moderate response in 46 cases (56.1%) and poor response in 21 cases (25.6%). Pyuria was cleared in 20 cases (24.4%), decreased in 22 cases (26.8%) and unchanged in 40 cases (48.8%). Bacteriuria was eliminated in 41 cases (50.0%), decreased in 17 cases (20.7%), relapsed in 7 cases (8.5%) and unchanged in 17 cases (20.7%). Bacteriologically, 74 (76.8%) of the 95 strains isolated were eradicated by CMX, and 22 (23.2%) persisted. Side effects were observed in 3 (abdominal pain, diarrhea and elevation of trans amylase) of the 106 cases. Judging from the above results, CMX is considered to be a useful drug in the treatment of complicated urinary tract infections.

Adolescent↗
PubMed1984

Effect of high doses of synthetic estrogen on lipid metabolism in castrated male rats.

The mechanism by which high doses of estrogen influences lipid metabolism was studied with a microtubular blocking agent. Castrated male rats received oral injection daily for 14 days of 3 mg hexestrol in olive oil, or oil alone as controls. About half of the animals in each group were injected intraperitoneally with 4 mg/100 g body weight colchicine 3 hr before they were killed. Hexestrol treatment caused an accumulation of esterified cholesterol in the liver while it decreased those in serum. Triglyceride concentrations slightly decreased in the liver but were unaffected in serum. On polyacrylamide-gel disc electrophoresis, the peaks of high density lipoproteins (HDL) and low density lipoproteins (LDL) were decreased remarkably. Electron microscopic examination of hepatocytes revealed electron-lucent lipid droplets in the cytoplasm. After a colchicine treatment of the control animals, concentrations of esterified cholesterol and triglycerides markedly increased in the liver, while those in serum decreased. Electron microscopic examination of hepatocytes revealed numerous secretory vesicles filled with nascent VLDL. In hexestrol-treated animals, the colchicine treatment was associated with marked decreases in serum-esterified cholesterol and triglyceride as seen in the controls. However, there were no further increases of esterified cholesterol in the liver, and the increase of triglycerides was slight. Electron microscopic examination showed less secretory droplets than in the controls. These data suggest that very low density lipoproteins (VLDL) synthesis in the liver of hexestrol treated rats was inhibited. An accumulation of esterified cholesterol with a marked decrease in serum could not be accounted for by the inhibition of lipoproteins secretion, but rather by their enhanced entry into the liver.

Animals↗
PubMed1984

Ferredoxins from the photosynthetic purple non-sulfur bacterium Rhodopseudomonas palustris. Isolation and amino acid sequence of ferredoxin I.

Two ferredoxins, ferredoxins I and II, were prepared from Rhodopseudomonas palustris. They were separated on a Sephadex column after carboxymethylation and ferredoxin I, the major component, was subjected to an amino acid sequence study. The protein was composed of 63 amino acid residues and the sequence was as follows: (sequence; see text). The molecular weight was calculated to be 6,718, excluding iron and sulfur atoms. The distribution of the nine cysteine residues was similar to but clearly distinct from those of ferredoxins of other photosynthetic bacteria. Comparison of this ferredoxin with those of other bacteria suggests that the photosynthetic bacteria evolved on separate lines. Ferredoxin II was also subjected to analyses of amino acid composition and terminal sequences, but no further study was possible due to the limited material. Although the composition was different from that of ferredoxin I, the terminal sequences were exactly the same as those of ferredoxin I.

Amino Acid Sequence↗
PubMed1984

Participation of 200K or 150K subunit of neurofilament in construction of the filament core with 70K subunit and promotion of tubulin polymerization by incorporated 200K subunit.

We have already reported that neurofilaments are capable of stimulating microtubule assembly and causing gelation. After separation of each of the triplet proteins of neurofilaments it was demonstrated that only the 200K subunit shows the activity to promote tubulin polymerization (Minami, Y. & Sakai, H. (1983) J. Biochem. 94, 2023-2033). The separation of each subunit protein led us to attempt the reconstitution of filaments from the 200K and 70K subunits or from the 150K and 70K subunits. It was found that both the 200K and 150K subunits independently contribute to the formation of intermediate-sized filaments, provided that each subunit was combined with the 70K subunit before removing urea by dialysis for reconstitution. On the other hand, the 200K subunit alone formed a very short thread-like structure after removal of urea, and the 150K subunit formed a filamentous structure, both incapable of being incorporated into filaments made of the 70K subunit alone. These observations suggest that the 200K and 150K subunits are not peripherally attached to a filament core made of 70K protein, but they take part in the formation of the core. Moreover, both proteins can co-polymerize with the 70K protein at a weight ratio of about 1 : 1 at least, which is in excess of that of the intact neurofilament. We investigated whether or not the 200K subunit incorporated with the 70K subunit into filaments could also stimulate tubulin polymerization. Low-shear viscometry measurements suggested that the 200K subunit retains the activity to initiate tubulin polymerization. This was confirmed by measuring viscosity changes with an Ostwald-type viscometer. In contrast, filaments reconstituted from the 70K and 150K proteins were incapable of increasing low-shear viscosity when mixed with tubulin. These observations suggest that the domain of the 200K protein embedded in the core of intermediate-sized filament is separate from the site responsible for promotion of tubulin polymerization.

Animals↗
PubMed1984

Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil to 5-fluorouracil.

Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)). FT was converted into 5-fluorouracil (5-FU) in the reconstituted system, and its rate was 71 pmol 5-FU formed/min/nmol P-4501 and 45 pmol 5-FU/min/nmol P-448(1). Cytochrome P-450, NADPH-cytochrome P-450 reductase and NADPH were required for 5-FU production. Inhibitors of cytochrome P-450 such as carbon monoxide and metyrapone markedly decreased the rate. FT was found to interact with the purified cytochrome P-450, causing a reverse type I spectral change. From these observations, we concluded that the hepatic microsomal cytochrome P-450-dependent mixed function oxidase system participates in the oxidative cleavage of FT.

Animals↗
PubMed1983

Hepatic microsomal cytochrome p-450-dependent N-demethylation of methylguanidine.

Cytochrome P-450-dependent N-demethylation of methylguanidine, a uremia toxin, was investigated. Methylguanidine was stoichiometrically converted into equal amounts of guanidine and formaldehyde by aerobic incubation with phenobarbital-induced microsomes and NADPH. The guanidine formation in the incubation mixture followed Michaelis-Menten kinetics and required the presence of molecular oxygen and NADPH. Methimazole, a non-formaldehyde-producing substrate specific for FAD-containing monooxygenase, did not inhibit significantly formaldehyde formation, suggesting that microsomal FAD-containing monooxygenase does not play a significant role in N-demethylation of methylguanidine. The direct involvement of cytochrome P-450 in the N-demethylation is supported by the observations that addition of methylguanidine to purified cytochrome P-450 preparation caused a type I spectral change and that inhibitors of cytochrome P-450, such as carbon monoxide and metyrapone, markedly decreased the rate of demethylation. Neither superoxide anion nor hydrogen peroxide was directly involved in the demethylation reaction. In addition, guanidine formation was observed in the reconstituted system containing purified cytochrome P-450. Thus, these findings indicate that the hepatic microsomal mixed function oxidase system catalyzes N-demethylation of methylguanidine to guanidine.

Animals↗