Search PubMed⌕ Search

Biomedical subjects

M Satake

Publications and source records attributed to M Satake.

At least 307 records · Page 17Linked to original sources
PubMed1981

Effect of vinblastine on distribution of murine leukemia virus-derived membrane-associated antigens.

The effect of vinblastine on the distribution of murine leukemia virus-derived membrane-associated antigens was examined by using the indirect immunofluorescence of 3.7% formaldehyde-fixed MJD-54 (Moloney murine leukemia virus-infected) cells. On fixed, non-drug-treated cells, p30 antigen was distributed homogeneously and diffusely over the cell membrane. When cells were incubated with 10 microM vinblastine for 1 hr before fixation, the distribution of p30 antigen was greatly changed, fluorescence now being collected into poles (cap-like formation). In contrast to this distribution pattern for p30 antigen, gp70 antigen was distributed in a micropunctate pattern on the cell surface, with or without vinblastine pretreatment. These observations indicate that the distribution patterns of p30 and gp70 membrane antigens are completely different and that they are differently controlled by cytoplasmic microtubules. In addition, because the p30 membrane antigen visualized in these studies most likely represents viral Pr65gag precursor molecules which are localized directly under and associated with the plasma membrane, these results suggest that, under special conditions of fixation, it is possible to obtain a cap-like phenomenon for cytoplasmic (internal) membrane-oriented proteins.

Animals↗
PubMed1980

A novel sphingophosphonoglycolipid containing 3-O-methylgalactose isolated from the skin of the marine gastropod Aplysia kurodai.

A novel sphingophosphonolipid was isolated from the skin of a marine gastropod, Aplysia kurodai. It was composed of one mol each of sphingosine base, fatty acid, glucose, galactosamine, and an unknown sugar and two mol each of galactose and aminophosphonic acid. The unknown sugar was identified as 3-O-methylgalactose by GC-mass spectrometry of the alditol acetate derivative and by GLC of the trimethylsilyl methylglycoside derivative. The aminophosphonic acid was identified as 2-aminoethylphosphonic acid by TLC of the free acid and the dinitrophenyl (DNP-) compound and by GLC of the O-di-trimethylsilyl-N-isothiocyanate compound. Thus, a ceramide bis(2-aminoethylphosphono)-pentaoside structure having an oligosaccharide chain consisting of one mol each of glucose, 3-O-methylgalactose and galactosamine and two mol of galactose was proposed.

Aminoethylphosphonic Acid↗
PubMed1980

Further studies on the smooth-surfaced membranes isolated from rat brain.

The light and heavy smooth-surfaced membranes (LSM and HSM), which had densities corresponding to 1.08 M and 1.28 M sucrose, respectively, were isolated from rat brain and some of their biochemical properties were investigated. Both LSM and HSM showed high Na+,K+-ATPase activity and, in particular, in HSM the activity was four times (21.55 mumol/mg protein/h) higher than that of the brain homogenate. High 2',3'-cyclic nucleotide 3'-phosphodiesterase activity (293.4 mumol/mg protein/h) was characteristic of LSM. 5'-Nucleotidase and acetylcholinesterase activities were also higher in LSM than in HSM. SDS-polyacrylamide gel electrophoresis showed that LSM and HSM had many protein component and that low molecular weight proteins such as proteolipid protein and basic protein were almost absent, in contrast with myelin and myelin-like membrane. GM1 ganglioside constituted the major class of total ganglioside in both LSM and HSM. These biochemical findings suggested that LSM is a membrane that has not previously been described, or a membrane fraction related to the oligodendroglial plasma membrane.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1979

Effect of neocarzinostatin on microtubules.

Effect of Neocarzinostatin (NCS) on microtubules was examined both in vitro and in vivo. Although NCS had no effect on microtubule assembly in vitro nor dissociated cytoplasmic microtubular network in vivo, microtubular network appeared to be changed to coarse form in NCS-treated 3T3 and HeLa cells. Effect of NCS on microtubules was discussed in comparison with colchicine.

Animals↗
PubMed1978

Biochemical characterization of the submicrosomal membrane of the rat brain. Selective solubilization of the components of the light smooth-surfaced membrane by lysophosphatidylcholine.

The light smooth-surfaced membrane, one of the three membrane fractions derived from the rat brain microsomal fraction, was fractionated into its soluble and insoluble parts by the use of lysophosphatidylcholine and the chemical composition of these was investigated. Under the condition whereby the maximal amount of the membrane protein was solubilized by lysophosphatidylcholine (0.5% lysophosphatidylcholine at 37 degrees C for 10 min), the insoluble residue, which accounted for approximately 30% of the membrane protein, was ultracentrifugally homogeneous and showed a granular structure under the electron microscope. The lipid composition of the soluble and insoluble fractions, as well as their protein composition, revealed a preferential and limited solubilization of the constituents of the membrane by lysophosphatidylcholine.

Animals↗
PubMed1978

Involvement of microtubules in cytopathic effects of animal viruses: early proteins of adenovirus and herpesvirus inhibit formation of microtubular paracrystals in HeLa-S3 cells.

In order to examine the involvement of microtubules in the virus-induced cytopathic effect (c.p.e.), the effect of virus infection on the formation of microtubular paracrystals (PC) induced by 10 microgram/ml of vinblastine sulphate in HeLa-S3 cells was examined by phase-contrast microscopy. In poliovirus-infected cells, c.p.e. (cell rounding) and the inhibition of PC formation proceeded in parallel, starting 4 h post-infection. In Sendai virus-infected cells, however, PC formation was not inhibited even 24 h post-infection when most infected cells clearly showed c.p.e. (syncytial formation). In adenovirus-infected cells, the inhibition of PC formation was observed 9 h before the appearance of c.p.e. Cytosine arabinoside (ara C) did not block the inhibition of PC formation in infected cells, but blocked the appearance of late c.p.e. (nuclear alteration). Cycloheximide blocked both the inhibition of PC formation and the induction of late c.p.e. These results suggest that an early protein synthesized de novo by adenovirus is required for direct or indirect inhibition of the microtubular PC formation. Furthermore, on ultraviolet (u.v.) inactivation of adenovirus both activities (induction of early c.p.e. shown by shrinkage of cytoplasm, and inhibition of PC formation) followed the same inactivation curve and were inactivated at a slower rate than viral infectivity and the activity leading to late c.p.e. The u.v. light sensitive target responsible for the induction of early c.p.e. and the inhibition of PC formation is about 20% of that for infectivity and is in accord with the genome size of the early functioning virus genes. In herpes simplex virus (HSV)-infected cells, the inhibition of PC formation, the appearance of c.p.e. (cell rounding and disappearance of nucleoli) and the synthesis of V antigen proceeded in parallel. These three functions of HSV were not blocked in infected cells even when the de novo synthesis of virus DNA was inhibited by ara C or phosphonoacetic acid (PAA), whereas these three functions were blocked by cycloheximide, suggesting that a protein coded by the input virus genome early after infection inhibits the microtubular PC formation and is responsible for c.p.e. From the u.v. inactivation curve of HSV, it was confirmed that only one-tenth of virus genome was responsible for both activities (induction of c.p.e. and inhibition of PC formation).

Adenoviruses, Human↗
PubMed1977

Biochemical characterization of the neuron. ATPase and acetylcholinesterase activities of neuronal cell bodies isolated in bulk from the pig brain stem.

Nerve cell bodies, large and multipolar, were isolated in bulk with the least possible contamination from the pig brain stem. The activities of two neurobiologically important membrane enzymes, Na+, K+-ATPase, and acetylcholinesterase, in the isolated cell bodies were estimated. Na+, K+-ATPase [EC 3.6.1.4], more accurately called ouabain-sensitive ATPase of the nerve cell body, hydrolyzed 94 micronmoles of ATP per h per 100 mg of protein. This activity was one-fourth that in the brain stem. Nerve cell bodies contained a large amount of Ca2+, 275 micronmoles per 100 mg of protein, about half of which was calculated to exist as compounds other than calcium orthophosphate. However, the Na+, K+-ATPase of the nerve cell bodies was not stimulated by EGTA, in contrast to that of the brain stem. Acetylcholinesterase [EC 3.1.1.7] and cholinesterase [EC 3.1.1.8] activities were estimated separately by the use of the specific inhibitors Persidol and BW 284C51 dibromide. Acetylcholinesterase was almost completely responsible for the hydrolysis of acetylcholine in the nerve cell bodies isolated from the brain stem and little cholinesterase activity was detected. 1300-1400 micronmoles of acetylcholine was hydrolyzed per h per 100 mg of protein of the neuronal cell bodies; this activity was about four times higher than that in the brain stem. The differences between the specific activities of Na+, K+-ATPase, and acetylcholinesterase in theneuronal cell bodies and the brain stem are discussed in the light of electron microscopic analysis of the distribution of these enzymes and the preservation of the plasma membrane of the isolated cell bodies.

Acetylcholinesterase↗
PubMed1977

Inhibition of surface immunoglobulin centeral capping of Daudi cells and cell spreading of HeLa-S3 cells by neocarzinostatin.

The effects of an antitumor antibiotic, neocarzinostatin (NCS), on the surface immunoglobulin central capping induced by anti-immunoglobulin M antibody on Daudi cells and on the cell spreading of trypsinized HeLa-S3 cells were examined. Pretreatment of Daudi cells and HeLa-S3 cells with NCS, 5 to 30 micrograms/ml, for 4 hr inhibited cap formation and cell spreading, respectively. It was shown that there is a direct relationship between the dose and the degree of inhibition. Inhibitors of DNA synthesis such as bleomycin, mitomycin C, and 1-beta-D-arabinofuranosylcytosine showed no inhibitory effect on cap formation or cell spreading. However, known microtubule-acting agents such as colchicine and vinblastine sulfate completely inhibited both capping and cell spreading at a dose of 10 micrograms/ml. In view of the fact that 10 micorograms NCS per ml also inhibit the formation of microtubular paracrystals induced by vinblastine sulfate in HeLa-S3 cells and that other agents known to influence microtubule function such as local anesthetics and calcium ionophores also inhibit both paracrystal formation and cap formation, these new observations add further support to our hypothesis that NCS affects microtubular proteins transmembranously in vivo.

Anesthetics, Local↗