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M Nogami

Publications and source records attributed to M Nogami.

At least 55 records · Page 3Linked to original sources
PubMed1995

Isolation and characterization of the HC8 subunit gene of the human proteasome.

For study of the molecular basis of regulation of proteasome gene expression, we isolated the gene encoding the alpha-type HC8 subunit of the human proteasome. About 2.3 kb of the 5' flanking region of this gene was tested for promoter function by chloramphenicol acetyltransferase assay. This analysis revealed that CAAT and TATA boxes, but not a GC box, are essential for its promoter activity. These results differed from previous findings that the genes for the alpha-type HC3 and beta-type HC5 subunits of the human proteasome have a TATA-less promoter and that two or three GC boxes function as the promoter sequences (Tamura, T. et al. (1994) J. Mol. Biol. 244, 1117-1124). We mapped the HC8 gene at q23 on human chromosome 14, which differs from the chromosomal locations of nine other proteasomal subunit genes mapped so far.

Animals↗
PubMed1995

Assignment of the 36.5-kDa (RFC5), 37-kDa (RFC4), 38-kDa (RFC3), and 40-kDa (RFC2) subunit genes of human replication factor C to chromosome bands 12q24.2-q24.3, 3q27, 13q12.3-q13, and 7q11.23.

Replication factor C is a multimeric primer-recognition protein consisting of five subunits (p145, p40, p38, p37, and p36.5) and is essential for the processive elongation of DNA chains catalyzed by DNA polymerase delta or epsilon in human cells. We have mapped the locations on human chromosomes of the genes coding for the four smaller subunits [p36.5 (RFC5), p37 (RFC4), p38 (RFC3), and p40 (RFC2)] using both PCR amplification from DNAs of a panel of somatic hybrids and fluorescence in situ hybridization to bands 12q24.2-q24.3, 3q27, 13q12.3-q13, and 7q11.23, respectively.

Base Sequence↗
PubMed1995

Lysophosphatidic acid regulation of cyclic AMP accumulation in cultured human airway smooth muscle cells.

The effects of the simple bioactive lipid mediator lysophosphatidic acid (LPA) on cAMP accumulation were investigated in cultured human airway smooth muscle cells (ASMC). Pretreatment of cells with LPA induced an increase in subsequent stimulation of cAMP accumulation by forskolin and by isoproterenol. When included during the assay of cAMP accumulation rather than as a pretreatment, LPA inhibited forskolin stimulation but enhanced isoproterenol stimulation. Both effects of LPA on forskolin stimulation were completely blocked by pertussis toxin treatment, whereas the effects on isoproterenol stimulation appeared relatively insensitive to pertussis toxin. The protein kinase C activator phorbol-12-myristate-13-acetate (PMA) sensitized forskolin stimulation to a similar extent as did LPA, and the combination of LPA plus PMA caused markedly more sensitization than either agent alone. In contrast, PMA inhibited isoproterenol stimulation and markedly decreased the sensitization induced by LPA. Serum also induced sensitization, and sensitization by LPA plus serum was no greater than that with LPA alone. LPA-induced sensitization appeared to be independent of protein kinase C activation because it was unchanged in cells treated to down-regulate protein kinase C. LPA also stimulated polyphosphoinositide hydrolysis, and this stimulation was partially inhibited by pertussis toxin treatment. These results suggest that LPA activates receptors coupled to both the pertussis toxin-sensitive G protein Gi and the pertussis toxin-insensitive G protein Gq. The complex effects of LPA, PMA, and pertussis toxin on cAMP accumulation in these cells are consistent with the expression of the type 2 isozyme of adenylyl cyclase in these cells.

Cells, Cultured↗
PubMed1994

Molecular cloning of cDNA encoding human DNA helicase Q1 which has homology to Escherichia coli Rec Q helicase and localization of the gene at chromosome 12p12.

A complementary DNA encoding DNA-dependent ATPase Q1 possessing DNA helicase activity, which is the major DNA-dependent ATPase in human cell extracts, was cloned from a cDNA library of human KB cells. The predicted amino acid sequence has seven consecutive motifs conserved in the RNA and DNA helicase super family and DNA helicase Q1 belongs to DEXH helicase family. A homology search indicated that helicase Q1 had 47% homology in the seven conserved regions with Escherichia coli RecQ protein. Three RNA bands of 4.0, 3.3, and 2.2 kilobases were detected in HeLa cells by Northern blotting. Analysis of the genomic DNA indicated the presence of a homologous gene in mouse cells. The DNA helicase Q1 gene was localized on the short arm of human chromosome 12 at 12p12.

Adenosine Triphosphatases↗
PubMed1994

TGF-beta 1 modulates beta-adrenergic receptor number and function in cultured human tracheal smooth muscle cells.

Pretreatment of cultured human tracheal smooth muscle cells with transforming growth factor-beta 1 (TGF-beta 1) decreased adenosine 3',5'-cyclic monophosphate (cAMP) accumulation by intact cells stimulated with the beta-adrenergic agonist isoproterenol. The maximal inhibition of isoproterenol-stimulated cAMP accumulation by TGF-beta 1 was 31 +/- 3%, and the mean effective concentration (EC50) of TGF-beta 1 was approximately 1.5 pM. TGF-beta 1 decreased the maximal response to isoproterenol but did not change the EC50 value of isoproterenol. TGF-beta 1 did not change cAMP accumulation stimulated by forskolin. TGF-beta 1 pretreatment decreased isoproterenol-stimulated adenylyl cyclase activity measured in broken cell preparations, but did not change the fluoride-stimulated adenylyl cyclase activity. Together these results suggest that the TGF-beta 1 effect is not by direct inhibition of adenylyl cyclase or by decreased activity of the stimulatory GTP-binding protein. Saturation binding experiments with the beta-adrenergic receptor radioligand [125I]iodopindolol showed that TGF-beta 1 pretreatment decreased the beta-adrenergic receptor number. The protein synthesis inhibitor cycloheximide abolished the effect of TGF-beta 1 on both cAMP accumulation and on beta-adrenergic receptor number, indicating that protein synthesis is involved. These results suggest that TGF-beta 1 in the lung could play a role in changing the responsiveness of airway smooth muscle cells to endogenous catecholamines and to beta-adrenergic agonists used in therapy.

Adenylyl Cyclases↗
PubMed1994

T cells are the cellular target of the proliferation-augmenting effect of chronic low-dose ionizing radiation in mice.

The proliferative response to mitogenic stimulation by splenocytes can be augmented by exposing mice to whole-body, chronic, intermittent low doses of ionizing radiation, referred to here as low-dose irradiation. The purpose of this study was to identify the cell(s) in the spleen which is responsive to the proliferation-augmenting effect of low-dose irradiation, i.e., the cellular target. C57BL/6 mice were subjected to low-dose irradiation (0.04 Gy/exposure/day, 5 consecutive days/week, 2 weeks) or to sham irradiation. Three days after the last exposure, spleens were removed, separated into cell fractions which were nonadherent and adherent to plastic surfaces and reconstituted in various combinations, and their proliferative responses to various mitogens were determined. Highly purified T cells were also used in place of the nonadherent cell fraction in the reconstitution studies. The target cells were shown to be T cells. The target T cells of low-dose-irradiated mice possessed elevated constitutive levels of HSP-70 mRNA and HSP-72, and they responded to T-cell receptor-specific anti-CD3 stimulation by producing more HSP-70 mRNA and HSP-72 and by proliferating more extensively than T cells of sham-irradiated mice.

Animals↗
PubMed1993

Agonist-induced desensitization of beta-adrenoceptors of bovine bronchial epithelial cells.

1. Cultured bovine bronchial epithelial cells express a large number of beta-adrenoceptors of the beta 2 subtype which are coupled to activation of adenylate cyclase and synthesis of cyclic AMP. The mechanisms involved in agonist-induced desensitization of beta-adrenoceptor function in these cells were investigated. 2. Preincubation of cells with the beta-adrenoceptor agonist isoprenaline induced a rapid desensitization of adenylate cyclase activity stimulated by isoprenaline (40% at 30 min) with little or no decrease in forskolin stimulation or in the number of beta-adrenoceptors detected by radioligand binding, indicating that uncoupling of beta-adrenoceptors from adenylate cyclase had occurred. 3. Uncoupling of beta-adrenoceptors from the stimulatory guanine-nucleotide-binding protein Gs was indicated by the loss of GTP effects on agonist competition for radioligand binding. Results from subcellular fractionation by sucrose density gradient centrifugation suggest that rapid internalization or sequestration of beta-adrenoceptors occurred along with the desensitization. 4. Preincubation with isoprenaline for longer times led to a marked decrease in total receptor number (85% at 18 h), indicating that receptor down-regulation also occurs. Recovery of receptors after down-regulation was prevented by cycloheximide and by actinomycin D, suggesting that degradation of both receptor protein and receptor mRNA may be involved in down-regulation.

Adenylyl Cyclases↗
PubMed1993

Mice chronically exposed to low dose ionizing radiation possess splenocytes with elevated levels of HSP70 mRNA, HSC70 and HSP72 and with an increased capacity to proliferate.

The purpose of this study was to determine whether the enhanced proliferative activity of splenocytes induced by exposing mice to whole body, chronic, intermittent low doses of ionizing radiation is associated with an increase in the expression of stress protein genes. Mice were exposed to a gamma-irradiation protocol of 0, 0.04 or 0.10 Gy/day for 5 consequent days/week, for 4 weeks. Splenocytes were then assessed for their levels of heat shock protein (HSP) 70 mRNA, glyceraldehyde 3-phosphate dehydrogenase (GAPD) mRNA, HSC70 (a constitutively-expressed isoform of HSP70) and HSP72 (an inducible isoform of HSP70), before and 1 day after mitogenic stimulation. Splenocytes from mice exposed to 0.04 Gy/exposure contained elevated constitutive levels of HSP70 mRNA, HSC70 and HSP72. These splenocytes responded to T, but not B, cell mitogens by further increasing their levels of HSP70 mRNA, HSC70 and HSP72 and by mounting a heightened proliferative response. However, an exposure of 0.10 Gy was ineffective. Thus, the constitutive levels of HSP70 mRNA, HSC70 and HSP72 and the mitogen-stimulated levels of HSC70 and HSP72 of splenocytes from mice exposed to 0.10 Gy/exposure were comparable with those of sham-irradiated mice. Moreover, their proliferative activity in response to mitogenic stimulation was also comparable with that of splenocytes from sham-irradiated mice.

Animals↗
PubMed1991

The effect of CV-3988 and CV-6209 on the acute gastric erosions of rats due to water-immersion and restraint stress.

CV-3988 and CV-6209 inhibited gastric erosions in rats due to water-immersion and restraint stress in a dose-dependent manner. The above inhibitory effects of CV-3988 were observed in the presence of indomethacin, which may indicate that the inhibition is not prostaglandin dependent. The studies indicate that platelet-activating factor may be involved in the formation of erosions in rats under water-immersion and restraint stress.

Analysis of Variance↗
PubMed1991

T-cell-dependent accumulation of eosinophils in the lung and its inhibition by monoclonal anti-interleukin-5.

The transnasal administration of an extract of the parasite Ascaris suum to C57BL/6 mice for 3 weeks produced marked eosinophilia in the bronchoalveolar lavage (BAL) fluid. The oral administration of ciclosporin significantly suppressed the pulmonary eosinophilia. Athymic C57BL/6-nu/nu mice failed to develop pulmonary eosinophilia. These data indicate that the pulmonary eosinophilia caused by this parasite extract is T-cell-dependent. Genetically mast-cell-deficient (WB x C57BL/6) F1-W/Wv (W/Wv) mice developed marked eosinophilia in the BAL, which shows that mast cells are not necessary in the formation of lung eosinophilia in this model. Monoclonal antimurine interleukin-5 injected intraperitoneally clearly inhibited the infiltration of eosinophils in the lung, suggesting that T-cell-derived interleukin-5 is essential.

Animals↗
PubMed1990

The effect of platelet-activating factor on [14C]aminopyrine uptake by isolated guinea pig parietal cells.

C16- and C18- platelet-activating factor (PAF) at 10(-6) M enhanced the uptake of [14C]aminopyrine (AP) by isolated guinea pig parietal cells. This increase was inhibited by a PAF antagonist CV-6209. In a medium with a low calcium (Ca2+) concentration (2 uM), this increase was not observed, which indicates that the increase of AP uptake by PAF is dependent on extracellular Ca2+. PAF and lyso-PAF showed no effect on AP uptake in the presence of histamine or carbachol.

Aminopyrine↗
PubMed1990

Experimental pulmonary eosinophilia in mice by Ascaris suum extract.

The transnasal administration of an extract of the parasite Ascaris suum (Asc) to C57BL/6 mice for 3 wk produced marked eosinophilia in the bronchoalveolar lavage (BAL) fluid. This pulmonary eosinophilia was not accompanied by blood eosinophilia. The oral administration of cyclosporin, 50 mg/kg body weight, every other day significantly suppressed the pulmonary eosinophilia. Athymic C57BL/6-nu/nu mice failed to develop pulmonary eosinophilia. These data indicate that pulmonary eosinophilia caused by this parasite extract is T-cell-dependent. Genetically mast-cell-deficient (WB X C57BL/6)F1-W/WV (W/WV) mice developed marked eosinophilia in the BAL, which shows that mast cells are not necessary in the formation of eosinophilia in BAL in this model. C57BL/6, W/WV, and Balb-C mice that developed eosinophilia in the BAL also showed elevated total IgE levels and IgE titers against Asc in the sera. On the other hand, C57BL/6-nu/nu mice and IgE low-responder SJL mice, which developed little eosinophilia, did not show elevated total IgE levels and IgE titers against Asc in the sera. However, oral administration of cyclosporin, 50 mg/kg, which inhibited eosinophilia in the BAL in C57BL/6 mice, did not significantly inhibit the elevation of total IgE or IgE against Asc in the sera. This indicates that serum IgE production is not required for the formation of eosinophilia.

Animals↗
PubMed1989

Studies on medicinal resources from livestock. I. Anti-allergic effects of pig bile. (1).

Anti-allergic activities of animal biles and commercially available bile acids were evaluated in experimental allergic disease models. Pig bile exhibited marked preventive effects on the models of delayed-type hypersensitivity (type IV allergy), picryl chloride-induced contact dermatitis (PC-CD) and sheep red blood cells (SRBC)-induced footpad swelling in mice. Fel ursi (dried bear gallbladder) also had an inhibitory effect on PC-CD, whereas ox bile, chicken bile and bile acids had no effect on ether of the models.

Animals↗
PubMed1988

Experimental hypersensitivity pneumonitis in the mouse: histologic and immunologic features and their modulation with cyclosporin A.

A murine model of hypersensitivity pneumonitis (HP) was established with transnasally administered Thermoactinomyces vulgaris (Tv) bacilli. Bronchoalveolar lavage (BAL) of experimental animals revealed marked increase in the total cell, lymphocyte, and macrophage numbers; the findings were similar to those in human HP. The BAL lymphocytes were mostly Thy 1.2 positive. Lyt-1 positive cells predominated Lyt-2 positive cells. Anti-Tv IgG antibodies and delayed-type hypersensitivity footpad reactions against Tv were detected in animals with HP. Cyclosporin A (CyA), a potent immunosuppressive drug, had marked effects on the development of HP in this model. When CyA was administered throughout the course of Tv inoculations, the granulomatous pneumonitis was markedly suppressed, and an increase in BAL lymphocytes, Thy 1.2 positive cells, was suppressed. When CyA was administered only during the first half period of the Tv treatment, suppression of the disease was minimal; when CyA was administered in the latter half, both the HP lesions and the increase in BAL cell lymphocyte numbers were significantly suppressed. These results indicate that a series of transnasal administration of Tv in mice may provide a good model for human HP.

Alveolitis, Extrinsic Allergic↗