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K Hidaka

Publications and source records attributed to K Hidaka.

At least 145 records · Page 8Linked to original sources
PubMed1983

Secondary mutation resistant to 7-ketocholesterol rescues a sterol metabolic defect in amphotericin B-resistant Chinese hamster cell line.

Amphotericin B-resistant mutants isolated from Chinese hamster V79 cells (1) are defective in cholesterol synthesis and more sensitive to an oxygenated sterol analog, 7-ketocholesterol, than their parental cell line. We isolated 7-ketocholesterol-resistant mutants from an amphotericin B-resistant mutant, AMBR-1. The 7-ketocholesterol-resistant mutants had regained increased level of free cholesterol, and they showed somewhat similar dose-response curves to amphotericin B as that of V79. Sterol synthesis from acetate, but not from mevalonate, in 7-ketocholesterol-resistant clones was threefold higher than that of AMBR-1. 7-Ketocholesterol-resistant clone, unlike AMBR-1, could form colonies in the presence of lipoprotein-depleted serum. The results are discussed in terms of probable change in the sterol biosynthetic pathway by the different lesions.

Amphotericin B↗
PubMed1982

Expression of bacterial beta-galactosidase in animal cells.

A recombinant plasmid containing the gene for bacterial beta-galactosidase, situated close to the simian virus 40 early promoter, has been constructed. Transfection of CHO, L, and COS-1 cells with this plasmid led to the expression and appearance of the enzyme. Using this system, we have developed a series of promoter cloning vehicles capable of accepting promoter signals for animal genes.

Animals↗
PubMed1981

Amphotericin B resistance is recessive in Chinese hamster hybrid cells.

Previous studies from our laboratory have shown that Chinese hamster V79 cells mutated to high level resistance to amphotericin B have a lower cellular level of cholesterol, the target molecule for the polyene antibiotic. Two amphotericin B-resistant (AMBR) mutants were each hybridized to their parental amphotericin B-sensitive (AMBS) V79 cells. All the hybrids derived from AMBR/AMBS fusions were as sensitive to polyene antibiotics (amphotericin B, filipin, and pimaricin) as AMBS cells or AMBS/AMBS hybrids. The AMBR/AMBS hybrids were found to contain cholesterol per phospholipids that is comparable to those in AMBS or AMBS/AMBS. The analysis of hybrids formed between mutant and wild-type cells thus indicated that resistance to amphotericin B is a recessive marker, and that the cellular level of cholesterol is compensated in the AMBS/AMBR hybrids. Hybrids of AMBR and AMBR cells were all resistant, so that the three AMBR mutants all fell into a single complementation group.

Amphotericin B↗
PubMed1980

Hemoglobin takamatsu (beta 120 (GH 3) Lys leads to Gln): a new abnormal hemoglobin detected in three unrelated families in the takamatsu area of shikoku.

A survey of hemoglobinopathies which was carried out in the Takamatsu district during the period from January to August 1979 detected six families with abnormal hemoglobins. Approximately 6010 inhabitants were screened. Three of these families had the same new Hb variant (Hb Takamatsu beta 120 Lys leads to Gln) that has not been previously reported. Existence of a blood relationship among these three families could not be established even after careful family studies. This abnormal hemoglobin was not associated with adverse symptoms and gave normal hematologic findings in the carriers. The isopropranol test was negative, oxygen affinity was within the normal range, and biosynthetic ratio in reticulocytes was around 1.0. One of the difficulties in the structural analysis of this hemoglobin was related to complete superposition of abnormal beta XT-12b,13 on a beta T-8,9 peptide in the fingerprint of the trypsin digest of aminoethylated aberrant beta X chain. This was overcome by collection of abnormal tryptic beta core (beta XT-10-13) from unmodified beta X chain, and subsequent digestion by chymotrypsin. Edman analysis of the chymotryptic peptides thus obtained successfully confirmed the substitution to be beta 120 Lys leads to Gln.

Adult↗
PubMed1979

Control of permeation of bleomycin A2 by polyene antibiotics in cultured Chinese hamster cells.

Control of permeation of bleomycin A2, a well-known antitumor antibiotic, in combination with various polyene macrolide antibiotics was analyzed in cultured Chinese hamster cells in vitro. Three polyene antibiotics, filipin, pentamycin, and pimaricin, were found to enhance the action of bleomycin A2 remarkably, while amphotericin B or nystatin could not. Although DNA synthesis and colony-forming activity of polyene-sensitive Chinese hamster V79 cells were synergistically inhibited by the combination of filipin and bleomycin A2, in a polyene-resistant subline (AMBR-1) derived from V79, they were only slightly affected in the presence of both drugs. The cellular uptake of [14C]bleomycin A2 by V79 was enhanced 2- to 4-fold in the presence of increasing doses of filipin or pentamycin, but not in the presence of amphotericin B. The treatment of V79 cells with filipin for 20 to 30 min was enought to block DNA synthesis almost completely when combined with 20 microgram belomycin A2 per ml. The pretreatment of the hamster cells with 6 microgram filipin per ml for 60 min continued to enhance the inhibitory action by bleomycin A2 of DNA synthesis up to 5 hr after the removal of filipin from the cultured medium.

Amphotericin B↗
PubMed1978

Isolation and characterization of amphotericin B-resistant cell lines in Chinese hamster cells.

Amphotericin B is a polyene macrolide antibiotic which interacts specifically with sterols in mammalian cell membranes. Amphotericin B-resistant (AMBr) lines of stable phenotype have been isolated from cultured Chinese hamster (V79) cells. Three AMBr clones (AMBr-1, -2 and -3) isolated independently after treatment with nitrosoguanidine were resistant to greater than or equal to microgram/ml of the antibiotic, while DNA synthesis as well as the colony-forming ability of the parental V79 cells was blocked by greater than 80% of control in the presence of 20--50 microgram/ml amphotericin B. The AMBr cell line also exhibited increased resistance to other polyene macrolide antibiotics such as nystatin and pentamycin. Other agents, however, such as cytosine arabinoside or ricin, blocked DNA synthesis in AMBr cells to the same extent as in V79 cells. The amphotericin B resistance phenotype was stably retained even after AMBr cells were cultured in the absence of the drug for over 200 generations. The control of free cholesterol or its esters was significantly decreased in all three resistant clones. Furthermore, cholesterol synthesis from acetate as well as mevalonate was partly defective in AMBr cells, compared with that in V79 cells.

Amphotericin B↗
PubMed1978

Hemoglobin Hoshida (beta43 (cd-2) Glu leads to Gln), a new hemoglobin variant discovered in Japan.

An electrophoretically G-like hemoglobin variant, Hb Hoshida, was detected from a ten year old girl and her mother. No clinical and hematological abnormalities were seen in the individuals heterozygous for this mutant gene. Structural studies of this abnormal hemoglobin demonstrated a previously undescribed substitution of beta43 (CD-2) Glu leads to Gln. The proportion of the abnormal hemoglobin in hemolysate was 42.1 per cent. The hemoglobin revealed neither instabilities nor functional abnormalities.

Child↗
PubMed1978

Mode of mutagenic action of methylnitrosocyanamide, a potent carcinogen.

A potent carcinogen, methylnitrosocyanamide was used to induce revertants in a strain of Escherichia coli carrying an amber mutation in a gene for tryptophan (trp) biosynthesis and an ochre mutation in a gene for alkaline phosphatase biosynthesis. Trp+ revertants were purified and classified into seven categories based on their ability to support the growth of particular nonsense mutants of phage lambda and on their content of alkaline phosphatase. About 90% of the Trp+ revertants induced by methylnitrosocyanamide were due to mutations in suppressor genes, and 85% of the suppressor mutations occurred in gene supE. Intragenic reversion cannot occur by a GC leads to AT base substitution mutation, whereas this is the obligate mode of mutation in gene supE. We conclude that methylnitrosocyanamide preferentially induces GC leads to AT transition mutations but that other base substitution mutations are also induced at about 10% of this frequency. N-Methyl-N-nitrosourea and, particularly, N-methyl-N'-nitro-N-nitrosoguanidine also preferentially induce GC leads to AT transition mutations.

Codon↗