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Biomedical subjects

S Osada

Publications and source records attributed to S Osada.

At least 109 records · Page 6Linked to original sources
PubMed1991

SF-B that binds to a negative element in glutathione transferase P gene is similar or identical to trans-activator LAP/IL6-DBP.

We have previously identified a silencer (negative enhancer) in glutathione transferase P (GST-P) gene which is strongly and specifically induced during hepatocarcinogenesis of the rat. At least three trans-acting factors bind to multiple cis-elements located in this silencer. One of these factors, SF-B (Silencer Factor B) specifically binds to GPS1 (GST-P Silencer 1) and has been cloned by a Southwestern protocol. Analysis of DNA and deduced amino acid sequence reveals that SF-B clone is most likely identical to an IL-6 inducible trans-activator LAP/IL6-DBP. Binding efficiency of SF-B to GPS1 is indistinguishable from that to IL6-responsive element found in C-reactive protein gene. The possibility that SF-B/LAP/IL6-DBP functions as a dual positive and negative regulator is discussed.

Amino Acid Sequence↗
PubMed1991

Silencer binding proteins function on multiple cis-elements in the glutathione transferase P gene.

The glutathione transferase P (GST-P) gene is specifically expressed during chemical hepatocarcinogenesis of the rat, whereas mRNA of this gene is virtually undetectable in normal liver. We have previously identified a stretch of DNA, that acted negatively in transcription, at 400 bp upstream from the cap site of the rat GST-P gene. Further characterization has revealed that this negative fragment functions in an orientation and position independent manner, suggesting that it is acting as a silencer. This silencer consists of multiple negative elements to which nuclear factors bind. This silencer is active not only in rat non-hepatoma and hepatoma cells but also in human and mouse cell lines, suggesting that these elements function as general regulators of basal gene expression. At least two proteins bind to this silencer fragment, one of which, designated SF-A (Silencer Factor A), has been partially purified. SF-A binds to several regions in this silencer, and likely plays an important role on negative regulation of this gene.

Animals↗
PubMed1991

Structural and functional diversities of a family of signal transducing protein kinases, protein kinase C family; two distinct classes of PKC, conventional cPKC and novel nPKC.

Recent molecular cloning and biochemical experiments on the nature of protein kinase C (PKC) have revealed the existence of two distinct classes of phorbol ester (and diacylglycerol) receptor/protein kinase, conventional PKC (cPKC) and novel PKC (nPKC). Each of these classes contains multiple related molecules expressed in tissues and cells in a type-specific manner. Although nPKC does not show the typical PKC activity ascribable to conventional PKCs and thus was neglected in earlier studies, several lines of evidence suggest that nPKCs are involved in a variety of cell responses to physiological stimuli and phorbol esters. It is possible that in some cases nPKC is the major mediator of the so-called PKC-activators, such as phorbol esters, mezerein, and bryostatins. In addition to the clear difference between cPKC and nPKC, functional diversity among conventional PKCs has also been demonstrated; PKC gamma differs in its competence to mediate the signal toward transcriptional activation through TPA-responsive cis-acting elements from cPKC alpha and nPKC epsilon. The differences between cPKC and nPKC and among the individual members of each of these two classes, and their specific pattern of distribution in tissues and cells, provide a rationale by which to explain the specificity and diversity of cellular responses to external stimuli generating DAG and to phorbol esters. The results presented here also provide a means to dissect the complex signaling pathway in cells and to analyze the molecular basis underlying the signal transduction processes mediated by this family of protein kinases.

Animals↗
PubMed1990

A phorbol ester receptor/protein kinase, nPKC eta, a new member of the protein kinase C family predominantly expressed in lung and skin.

Protein kinase C (PKC)-related cDNA clones isolated from mouse epidermis cDNA library encoded a 78-kDa protein, nPKC eta. nPKC eta contains a characteristic cysteine-rich repeat sequence (C1 region) and a protein kinase domain sequence (C3 region), both of which are conserved among PKC family members. However, nPKC eta lacks a putative Ca2+ binding region (C2 region) that is seen in conventional PKCs (alpha, beta I, beta II, gamma), but not in novel PKCs (nPKC delta, -epsilon, -zeta). nPKC eta shows the highest sequence similarity to nPKC epsilon (59.4% identity). The similarity extends to the NH2-terminal sequence (E region) which corresponds to one of the divergent regions (D1 region). Northern blot analysis showed that the mRNA for nPKC eta is highly expressed in the lung and skin but, in contrast to other members of the PKC family, only slightly expressed in the brain. nPKC eta expressed in COS cells shows phorbol ester binding activity with a similar affinity to nPKC epsilon. Antiserum raised against a COOH-terminal peptide of nPKC eta identified an 82-kDa protein in mouse lung extract as well as in an extract from COS cells transfected with the nPKC eta-cDNA expression plasmid. Autophosphorylation of nPKC eta immunoprecipitated with the specific antiserum was observed, indicating that nPKC eta is a protein kinase. These results clearly demonstrate the existence and the possible importance of nPKC eta as a member of the phorbol ester receptor/protein kinase, PKC, family.

Amino Acid Sequence↗
PubMed1990

Characterization of metallothionein cDNAs induced by cadmium in the nematode Caenorhabditis elegans.

cDNAs of metallothioneins (MTs) in the nematode Caenorhabditis elegans were characterized. The MT-II clone encodes 62 amino acid residues and the predicted Mr is 6462. The MT-I clone contains an additional 12 residues at the C-terminal end, and the predicted Mr is 7959. There is a considerable similarity between MT-I and MT-II. Both of these proteins are cysteine-rich and, with a few exceptions, show a good alignment of cysteine residues. No obvious sequence relationship in the coding region was discernible between C. elegans MTs and mammalian MTs, aside from Cys-Cys, Cys-Xaa-Cys, and Cys-Xaa-Xaa-Xaa-Cys segments. However, 3'-untranslated region of cDNAs of C. elegans MT-I and -II have some consensus sequences found in mammalian MT cDNAs, suggesting that these regions may have some roles in the regulation of MT-gene expression.

Amino Acid Sequence↗
PubMed1990

A case of infantile acute monocytic leukemia caused by vertical transmission of the mother's leukemic cells.

A case of infantile acute monocytic leukemia (AMoL), which was probably transmitted from a pregnant woman with leukemia to her unborn infant, is presented. A woman had AMoL when her third infant was born. This infant, who was a boy, also suffered from AMoL when he was 20 months of age. The infant's leukemic cells had the same cytochemical and immunophenotypic patterns as the mother's leukemic cells. By cytogenetic analysis, the majority of the infant's leukemic marrow cells had the 46,XX karyotype and showed no Y body by quinacrine staining. Moreover, the phenotype for human major histocompatibility system, HLA-A, HLA-B, and HLA-DR of the infant's leukemic cells was consistent with that of the mother's lymphocytes. Thus, the infant's leukemic clone was found to be identical to the mother's leukemic clone. His lymphocytes could not react with the mother's leukemic cells or his own leukemic cells in mixed lymphocyte culture, suggesting that the HLA homozygosity of the mother may have played a role in inducing immunologic tolerance to the immigrated leukemic cells in the infant. This is the first report of an infantile leukemia transmitted from a mother with leukemia, supposedly through the placenta.

Adult↗
PubMed1990

Mechanism of specific expression of glutathione transferase P gene during hepatocarcinogenesis.

The mechanism of specific expression of glutathione transferase P gene during hepatocarcinogenesis of the rat has been investigated by cloning the gene and determining the upstream regulatory sequences. Two enhancers and a silencer are located within 3 kb upstream of the promoter. The stronger enhancer designated GPEI has two TPA (12-O-tetradecanoyl phorbol 13-acetate)-response element (TRE)-like sequences arranged in a palindrome at a 3 base pairs spacing. This special combination was found to form a very strong enhancer which could act efficiently even in F9 cells where the collagenase enhancer with a singlet TRE cannot work due to the low c-jun content. Whether this structure is operating with a very low concentration of c-jun/c-fos heterodimer or with any other proteins remains to be determined. These findings suggest that new and more efficient enhancers evolve by a combination of basic enhancer elements. The silencer region consists of several sequences that can bind specific protein(s) and works cooperatively.

Animals↗
PubMed1988

Assignment of a gene coding for a human T-cell antigen with a molecular weight of 40,000 daltons to chromosome 17.

Hybrid human-mouse T-cell clones reactive with Tp40 antibody, which detects cluster of differentiation (CD)7 antigen on human T lymphocytes, were established. Karyotype analysis showed that human chromosome 17 was essential for the expression of CD7 antigen. The presence of this chromosome was confirmed by enzyme analysis of galactokinase, which is coded by a gene on human chromosome 17.

Animals↗
PubMed1976

Mechanism of supraventricular tachycardia and pharmacological effects on it.

Electrophysiologic study in 30 patients with documented SVT, 16 of whom had preexcitation, and in 24 control subjects were reported. The mechanism of SVT were found to be various and to include reentry confined to the AV node, SA node or the atrium, reentry through accessory pathway and ectopic atrial automaticity. It was noted that some of SVT might use concealed accessory pathway in VA direction while the some of SVT in WPW syndrome might not utilize accessory pathways. Electrophysiological properties in cases with SVT did not differ from those observed in controls. There were no differences in the mode of electrophysiological action of drugs between XVT and control groups. Both propranolol and procaine amide slightly depressed AV conduction. However, the action of the drugs on echo zone were not the same. The basic mechanisms of the action of the drugs in SVT were discussed.

Heart Conduction System↗