Search PubMed⌕ Search

Biomedical subjects

M Imoto

Publications and source records attributed to M Imoto.

At least 91 records · Page 5Linked to original sources
PubMed1990

Inhibition of phosphatidylinositol kinase by toyocamycin.

We have screened toyocamycin as an inhibitor of phosphatidylinositol kinase. It inhibited the enzyme of A431 cell membrane with an IC50 of 3.3 micrograms/ml. Adenosine and formycin A also inhibited the enzyme, but other 6 related nucleosides did not. Although orobol and 2,3-dihydroxybenzaldehyde that inhibit phosphatidylinositol kinase inhibited in situ phosphatidylinositol turnover, toyocamycin did not.

1-Phosphatidylinositol 4-Kinase↗
PubMed1989

Modification of cellular membrane functions by pendolmycin.

Pendolmycin is a new indole alkaloid isolated from Nocardiopsis as an inhibitor of phosphatidylinositol turnover. Structurally, pendolmycin is similar to teleocidin B and lyngbyatoxin A. Pendolmycin, teleocidin B and 12-O-tetradecanoylphorbol-13-acetate all inhibited phosphatidylinositol turnover in A431 cells. Pendolmycin inhibited binding of epidermal growth factor, activated arachidonic acid release and hexose transport, and inhibited binding of phorbol-12,13-dibutylate in C3H10T1/2 cells. Thus, pendolmycin was as potent as teleocidin B and phorbol ester tumor promoters in modification of cell membrane functions, while having the simplest structure among them.

Alkaloids↗
PubMed1989

Effect of histamine H1-receptor antagonist on the regulation of carbohydrate and lipid metabolism in rat liver.

In order to elucidate the role of histamine in the liver, we studied the effect of a histamine H1-receptor antagonist on the carbohydrate and lipid metabolism in the rat liver. The administration of the H1-receptor antagonist decreased significantly the contents of glycogen and malonyl-CoA in the liver. However, it did not affect the levels of serum glucose and free fatty acid. These results suggest that histamine may play a part in the regulation of metabolism of carbohydrates and lipids in the liver.

Animals↗
PubMed1989

In situ distribution of enolase isozymes in chronic liver disease.

Liver biopsy specimens with or without chronic liver diseases were examined immunohistochemically to determine the distribution of enolase isozymes (alpha, beta, and gamma). In normal liver, alpha-enolase was positively stained in almost all hepatocytes and bile duct cells. beta- and gamma-enolases were localized in hepatocytes and bile duct cells, respectively. Electron microscopic studies revealed that Kupffer cells and sinusoidal endothelial cells had both alpha- and gamma-enolases. In chronic active hepatitis and cirrhosis, proliferated biliary ductular cells had both alpha- and gamma-enolases, but did not express beta-enolase. This is almost the same localization pattern of enolase isozymes as in preexisting bile duct cells. gamma-Enolase was detected in some hepatocytes in eight of 12 cases with chronic active hepatitis and six of 12 cases with cirrhosis. These hepatocytes were small, showed a cobblestone pattern, and binucleate cells were frequent. On the other hand, rosette-formed hepatocytes adjacent to a regenerating bulging lobule were not stained for gamma-enolase. These results suggest that regenerating hepatocytes have gamma-enolase and that, with maturation, hepatocytes lose it.

Chronic Disease↗
PubMed1989

Changes in endogenous prostaglandin levels during D-galactosamine-induced liver injury.

The role of prostaglandins (PGs) in liver injury induced by D-galactosamine was investigated in the rat. The contents of PGD2 and PGF2 alpha in the liver were significantly increased from 3 h and 24 h after the D-galactosamine administration, respectively, but that of PGE2 was not significantly changed. Administration of 16,16-dimethyl PGE2, a long acting derivative of PGE2, or indomethacin, but not 16,16-dimethyl PGF2 alpha, a long acting derivative of PGF2 alpha, significantly depressed the increase in the serum transaminase activities induced by D-galactosamine. The protective effect of indomethacin was not disturbed by the 16, 16-dimethyl PGF2 alpha administration. These results indicate that PGE2 has a cytoprotective effect against the D-galactosamine induced liver injury and suggest that the protective effect of indomethacin is ascribable to its suppression of synthesis of PGs other than PGE2 or PGF2 alpha, e.g., PGD2.

Animals↗
PubMed1988

A novel enhancement of SV40 enhancer activity by treatment of mouse neuroblastoma N18TG2 with protein kinase inhibitor H-7.

To determine the role of protein phosphorylation in transcription regulation, we have treated mouse neuroblastoma N18TG2 cells with the protein kinase inhibitor H-7 and tested its effect on transcription. After the preculture and transfection in the presence of H-7, the cell preparation was divided in half and cultured with and without H-7. The level of CAT expression of pSV2-CAT was found to be higher in the cells cultured in the absence of H-7 than in those cultured in the presence of H-7. This difference was observed only after pretreatment of the cells with H-7, suggesting that withdrawal of H-7 from the culture medium after preculture with H-7 gave an enhancing effect on CAT expression. This phenomenon was also observed with transformants that expressed the CAT gene of pSV2-CAT stably. The 72 base-pair (bp) repeat of SV40 DNA was responsible for this difference in CAT expression. A similar effect of H-7 on the SV40 enhancer activity was observed in mouse neuroblastoma x rat glioma hybrid NG108-15 cells, but not in rat glioma C6-BU-1 cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Inhibition of cellular phosphatidylinositol turnover by psi-tectorigenin.

Psi-tectorigenin, an isoflavonoid, was isolated from a culture filtrate of actinomycetes as an inhibitor of epidermal growth factor-induced phosphatidylinositol turnover in cultured A431 cells. It inhibited phosphatidylinositol turnover with an IC50 of about 1 microgram/ml; thus, its inhibitory activity was 6-times stronger than that of genistein or orobol. When added to cultured A431 cells psi-tectorigenin inhibited phosphatidylinositol turnover without inhibiting epidermal growth factor receptor tyrosine protein kinase. Thus, psi-tectorigenin is a specific inhibitor of phosphatidylinositol turnover and may be a useful tool for the functional analysis of phosphatidylinositol turnover.

Actinomycetales↗
PubMed1988

Purification and analysis of the structure of alpha-galactosidase from Escherichia coli.

Alpha-Galactosidase, the product of the melA gene, was purified from a strain of Escherichia coli harboring a plasmid carrying melA, which over-produced the alpha-galactosidase. An apparent molecular weight was determined to be 50 kDa. The amino acid composition of this enzyme was determined. The result indicates that this enzyme is a hydrophilic and acidic protein. We have subjected the purified enzyme to 20 cycles of N-terminal sequence analysis. This verified the translation start site of the melA gene and the predicted N-terminal sequence.

Amino Acid Sequence↗
PubMed1988

Immunohistochemical studies on the distribution of nerve fibers in chronic liver diseases.

Innervation of the liver with or without chronic liver disease was immunohistochemically studied. In normal liver tissues, gamma-enolase [neuron-specific enolase (NSE)]- and S-100 protein (S-100)-positive nerve fibers were found around hepatic arteries, portal veins, and bile ductules in the portal area, along the sinusoid, and around central veins inside the hepatic lobule. Neuropeptide Y (NPY)-immunoreactive (IR) nerve fibers were detected in close contact with hepatic arteries and portal veins in the portal area and along the sinusoid in the parenchyma. Vasoactive intestinal polypeptide (VIP)-IR nerve fibers were found in the portal area but were scarce in the parenchyma. VIP-IR nerve fibers were much fewer than NPY-IR fibers. In patients with chronic active hepatitis, NSE- and S-100-positive nerve fibers, as well as NPY-IR nerve fibers, proliferated in the enlarged portal area. In cirrhotic liver, NSE- and S-100-positive nerve fibers and NPY-IR fibers increased remarkably in the fibrous septa, whereas they decreased or vanished inside the pseudolobules. These findings suggest that, in chronic liver disease, intrahepatic nerve fibers change their distribution, accompanying the structural changes in the hepatic lobules.

Humans↗