Journal of receptor research最新文献_第4页

Homologous regulation of the MSH receptor in melanoma cells. 黑色素瘤细胞中MSH受体的同源调控。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073659

W Siegrist, A N Eberle

{"title":"Homologous regulation of the MSH receptor in melanoma cells.","authors":"W Siegrist, A N Eberle","doi":"10.3109/10799899309073659","DOIUrl":"https://doi.org/10.3109/10799899309073659","url":null,"abstract":"We have examined the mechanism of homologous regulation of MSH receptor binding and receptor-mediated adenylate cyclase activation in three human and two mouse melanoma cell lines. Pretreatment with alpha-MSH resulted in a time- and dose-dependent up-regulation of MSH receptors in human D10 and 205 melanoma cells whereas in human HBL and in mouse B16-F1 and Cloudman S91 cells alpha-MSH induced receptor down-regulation. Up-regulation of receptors was maximal after a 24-h incubation period and an alpha-MSH concentration of 100 nM (EC50 = 2.4 nM). The increase in alpha-MSH binding was independent of adenylate cyclase activation and protein synthesis and appeared to be caused by recruitment of spare receptors. The structural requirements of the peptide for triggering this process differed from those found in receptor-binding analyses. Receptor down-regulation was maximal after 12 h and hence more rapid than up-regulation. In B16-F1 cells, 10 nM alpha-MSH caused the disappearance of 85-90% of the MSH receptors, the EC50 of 0.23 nM lying exactly between that for alpha-MSH-induced melanogenesis (0.027 nM) and the dissociation constant of receptor binding (1.31 nM). Down-regulation in B16-F1 cells appears to be the consequence of receptor internalization following MSH binding and seems to be initiated during an early step in MSH signalling, preceding the activation of adenylate cyclase and the cAMP signal. Receptor up- and down-regulation were not accompanied by an alteration in affinity to alpha-MSH, as demonstrated by Scatchard analysis of the binding curves.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 1-4","pages":"263-81"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309073659","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19368606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 20

Cloning of several genes coding for retinoic acid nuclear receptors in the mouse embryonal carcinoma cell line PCC7-MZ1. 小鼠胚胎癌细胞PCC7-MZ1维甲酸核受体编码基因的克隆。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073687

R Heiermann, M Rentrop, E Lang, A Maelicke

{"title":"Cloning of several genes coding for retinoic acid nuclear receptors in the mouse embryonal carcinoma cell line PCC7-MZ1.","authors":"R Heiermann, M Rentrop, E Lang, A Maelicke","doi":"10.3109/10799899309073687","DOIUrl":"https://doi.org/10.3109/10799899309073687","url":null,"abstract":"Mouse embryonal carcinoma cell line PCC7-Mz1 can be induced by retinoic acid (RA) to differentiate into several well defined phenotypes of neuroectodermal origin (Lang, E. et al. (1989) J. Cell. Biol. 109, 2481-2493). Several subclones of the cell line (clonal variants) differ from each other in their developmental potential. To test whether these differences in cellular fate are due to somatic mutations in specific genes of these cells, we have cloned full length cDNAs coding for the alpha 1 and beta 2 isoforms, and partial length cDNAs coding for the alpha 2, beta 1 and beta 3 isoforms of the retinoic acid nuclear receptor (RAR). The cloned cDNAs did not differ in sequence from those of normal mouse cells. Using as probe the beta 2-RAR promoter region from mouse liver, we also checked for restriction fragment length polymorphism in the promoter regions of RA-inducible and RA-resistant cell variants. No alterations in this region of RAR genes was found in the clonal variants tested. The different patterns of derivatives produced by the variants upon exposure to RA therefore cannot be caused by somatic mutations in RAR genes of the tumor cell lines.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 1-4","pages":"693-709"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309073687","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19369028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 11

Cordil reversibly inhibits the Na,K-ATPase from outside of the cell membrane. Role of K-dependent dephosphorylation. Cordil从细胞膜外可逆地抑制Na, k - atp酶。k依赖性去磷酸化的作用。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309063265

J M Maixent, A Gerbi, I Berrebi-Bertrand, P E Correa, G Genain, A Baggioni

{"title":"Cordil reversibly inhibits the Na,K-ATPase from outside of the cell membrane. Role of K-dependent dephosphorylation.","authors":"J M Maixent, A Gerbi, I Berrebi-Bertrand, P E Correa, G Genain, A Baggioni","doi":"10.3109/10799899309063265","DOIUrl":"https://doi.org/10.3109/10799899309063265","url":null,"abstract":"Cordil-LND796 is a new cardiotonic glycoside under development. In rat brain microsomes where three isoforms of the Na,K-ATPase with differential affinities for cardiac glycosides have been identified, Cordil had higher affinity for the alpha 3 (IC50 = 0.02 microM) than for the alpha 2 (IC50 = 0.6 microM) and the alpha 1 (IC50 = 30 microM) isozymes. Cordil is potentially a selective inhibitor for both alpha 2 and alpha 3 Na,K-ATPase isoforms. Using inside out vesicles we have shown that Cordil binds to and inhibits Na,K-ATPase at an extracellular site. The dissociation kinetic rates (k-1) from the ATPase and the phosphatase activity (K-dependent dephosphorylation) of the Na,K-ATPase were similar for Cordil. Despite these similarities to ouabain comparison of the kinetics of the Na,K-ATPase inhibition by ouabain and Cordil revealed marked differences in their association rates (k+1 = 0.7 l mol-1 min-1 and k+1 = 6 x 10(-3) l mol-1 min-1 respectively) and their dissociation rates (k-1 = 1.3 +/- 0.2 x 10(-4) s-1 and k-1 = 69 +/- 7 x 10(-4) s-1 respectively). Both binding association and dissociation rates were enhanced for Cordil. These data are compatible with a stabilizing effect of Cordil on the E2P conformational state of Na,K-ATPase.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 7","pages":"1083-92"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309063265","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19380539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Solubilization and characterization of the A2-adenosine receptor. a2 -腺苷受体的增溶和表征。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073703

C Nanoff, G L Stiles

{"title":"Solubilization and characterization of the A2-adenosine receptor.","authors":"C Nanoff, G L Stiles","doi":"10.3109/10799899309073703","DOIUrl":"https://doi.org/10.3109/10799899309073703","url":null,"abstract":"Binding of [3H]CGS 21680, an agonist radioligand selective for A2-adenosine receptors (A2AR), to membranes and solubilized preparations from bovine brain striatum revealed labelling of a single high affinity binding state. In membranes, guanine nucleotides per se were ineffective in modulating agonist binding whereas cations, Na+ and Mg++, had distinct effects. The addition of NaCl (200 mM) as well as the Mg(++)-free preparation of membranes led to a significant decrease in binding affinity and the number of binding sites. Moreover, the presence of Na+ was required for the demonstration of a guanine nucleotide effect, i.e. a decrease in maximal binding. Following solubilization, agonist-A2AR interactions were sensitive to guanine nucleotides even in the absence of Na+; guanine nucleotides and Na+ had additive effects in reducing the number of binding sites. Moreover, the effect of GTP was reversible, i.e. binding returned to control levels upon removal of the nucleotide. This suggests the A2AR and its G protein (presumably Gs) are solubilized as a functional unit and may not dissociate even in the presence of GTP following solubilization. We, therefore, believe that a \"tight\" association exists between receptor and G protein (Gs), and that guanine nucleotides and sodium act at different sites on the R-G complex. Drawing an analogy with similar observations on the avian beta-adrenergic receptor (Hertel et al, J. Biol. Chem. 265:17988-94, 1990; Parker & Ross, J. Biol. Chem. 266:9987-96, 1991) we postulate that the regulatory features of the A2AR can be attributed to a distinct receptor domain that interacts with cellular regulatory elements.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 6","pages":"961-73"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309073703","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19492644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 36

Amino acid residues within the sequence region alpha 55-74 of Torpedo nicotinic acetylcholine receptor interacting with antibodies to the main immunogenic region and with snake alpha-neurotoxins. 鱼雷烟碱乙酰胆碱受体α 55-74序列区氨基酸残基与主要免疫原区抗体和蛇α神经毒素相互作用。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073705

J L Wahlsten, J M Lindstrom, B M Conti-Tronconi

{"title":"Amino acid residues within the sequence region alpha 55-74 of Torpedo nicotinic acetylcholine receptor interacting with antibodies to the main immunogenic region and with snake alpha-neurotoxins.","authors":"J L Wahlsten, J M Lindstrom, B M Conti-Tronconi","doi":"10.3109/10799899309073705","DOIUrl":"https://doi.org/10.3109/10799899309073705","url":null,"abstract":"The sequence region 55-74 of the alpha-subunit of the acetylcholine receptor (AChR) from Torpedo californica electroplax comprises the amino-terminal end of a sequence segment--residues alpha 67-76--forming the main immunogenic region (MIR), which is most frequently recognized by anti-AChR autoantibodies in myasthenia gravis. The synthetic sequence alpha 55-74 of Torpedo AChR binds alpha-bungarotoxin (alpha BTX), suggesting that amino acid residues within this sequence region may contribute to formation of an alpha BTX binding site. Using single-residue substituted synthetic analogues of the sequence alpha 55-74 of Torpedo AChR, in which each residue was sequentially substituted by either glycine or alanine, we sought identification of the amino acids involved in interaction with alpha-neurotoxins and with three different anti-MIR monoclonal antibodies (mAbs 6, 22, and 198). Substitution of Arg55, Arg57, Trp60, Arg64, Leu65, Arg66, Trp67, or Asn68 strongly inhibited alpha-toxin binding, whereas substitutions of Ile61, Val63, Pro69, Ala70, Asp71, or Tyr72 had marginal effects. Substitutions within the region alpha 68-72 significantly diminished binding of anti-MIR mAbs, although residue preferences differed among mAbs. Further, substituting Trp60 substantially reduced binding of mAb 198, and moderately affected binding of mAb 6, and substitution of Asp62 slightly but consistently affected binding of mAbs 6 and 22.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 6","pages":"989-1008"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309073705","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19492645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Regulation of dopamine receptors by bupropion: comparison with antidepressants and CNS stimulants. 安非他酮对多巴胺受体的调节:与抗抑郁药和中枢神经系统兴奋剂的比较。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073665

A Vassout, A Bruinink, J Krauss, P Waldmeier, S Bischoff

引用次数: 24

CD4:p56lck association studied in vivo using antibody-induced capping and double indirect immunofluorescence microscopy. 利用抗体诱导封顶和双间接免疫荧光显微镜研究体内CD4:p56lck关联。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073688

M Gassmann, K E Amrein, P Burn

引用次数: 11

A model for the effect of estrogen antagonists on cooperative estradiol binding. 雌激素拮抗剂对雌二醇协同结合影响的模型。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309063264

R N Porrelli, P J Munson, D Rodbard

{"title":"A model for the effect of estrogen antagonists on cooperative estradiol binding.","authors":"R N Porrelli, P J Munson, D Rodbard","doi":"10.3109/10799899309063264","DOIUrl":"https://doi.org/10.3109/10799899309063264","url":null,"abstract":"Partial agonists such as estriol and estrone have been reported to diminish or even eliminate the upward convexity of the Scatchard plot of the binding of labeled estradiol to estrogen receptor. This has been interpreted as agonist interference with the receptor dimerization induced by estradiol. In order to investigate how a partial agonist or antagonist might interfere with dimerization we have developed a theoretical mass-action law model, where soluble receptors can dimerize and bind to two different ligands. Special attention was devoted to manifestations of positive cooperativity to determine whether they could be modified by competition with a second ligand. This was done using a computer program that evaluated a large set of combinations of affinity constants in an effort to explore all possible situations. The model could reproduce the effect of a second ligand on the cooperative binding of estradiol to the estrogen receptor but only if the second ligand was anticooperative, which is not the case of estriol, estrone and tamoxifen. Furthermore, even when the Scatchard plot was linear, the model still required dimerization of the receptor in most of the cases, showing that the addition of an antagonist may eliminate the upward curvature of the Scatchard without truly eliminating dimerization or cooperativity. We conclude that the effect of a second ligand on the binding of labeled estradiol to estrogen receptor is not necessarily due to interference with dimerization and/or cooperativity. The inability of this model to fully explain the published data for estriol, estrone, clomiphene, and tamoxifen suggests that a more complex mechanism is involved.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 7","pages":"1055-81"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309063264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19351612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dopaminergic activity measured in D1- and D2-transfected fibroblasts by silicon-microphysiometry. 用硅微物理测量法测定D1和d2转染成纤维细胞的多巴胺能活性。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073679

C Bouvier, J A Salon, R A Johnson, O Civelli

引用次数: 14

Evidence for inverse regulation of high and low affinity binding sites for (-)125iodocyanopindolol in human mononuclear leucocytes during epinephrine infusion. 肾上腺素输注过程中人单核白细胞(-)125iodocyanopindolol高亲和力和低亲和力结合位点反向调节的证据。

Journal of receptor research Pub Date : 1993-01-01 DOI: 10.3109/10799899309073666

T Anhäupl, B Liebl, E Trunk, K Träger, H Ensinger, M Georgieff

{"title":"Evidence for inverse regulation of high and low affinity binding sites for (-)125iodocyanopindolol in human mononuclear leucocytes during epinephrine infusion.","authors":"T Anhäupl, B Liebl, E Trunk, K Träger, H Ensinger, M Georgieff","doi":"10.3109/10799899309073666","DOIUrl":"https://doi.org/10.3109/10799899309073666","url":null,"abstract":"As we have shown earlier (-)125Iodocyanopindolol (125ICYP) binding to beta-adrenoceptors (beta-AR) in human mononuclear leucocytes (MNL) yields evidence for the existence of high affinity (Bhiaff) and low affinity (Bloaff) binding sites. We studied the regulation of these 2 classes of binding sites during 240 min of (-)-epinephrine (EPI) infusion (0.1 microgram/kg/min) (n = 8) in male healthy volunteers. Saturation experiments were performed on MNL membranes with 125ICYP over a large concentration range (1-550 pmol/l). Binding parameters were calculated by computer analysis assuming 2 classes of binding sites. We found a preinfusion value of 830 +/- 50 [sites/cell] (KD = 1.5 +/- 0.2 pmol/l) of Bhiaff binding sites and 5210 +/- 510 [sites/cell] (KD = 420 +/- 80 pmol/l) of Bloaff. During EPI infusion we observed biphasic modulation of the Bhiaff and an inverse modulation of the Bloaff. After 40 min of EPI Bhiaff increased to 1970 +/- 280 [sites/cell] (KD = 4.2 +/- 0.8 pmol/l), whereas Bloaff decreased to 2720 +/- 280 [sites/cell] (KD = 140 +/- 70 pmol/l); despite constant plasma epinephrine concentration (PEC) after 240 min of EPI Bhiaff changed to 1310 +/- 240 [sites/cell] (KD = 2.8 +/- 1.0 pmol/l) vs. 4370 +/- 760 [sites/cell] (KD = 190 +/- 100 pmol/l) Bloaff. These results suggest an interdependent inverse modulation of the 2 classes of binding sites for 125ICYP on MNL during EPI infusion.","PeriodicalId":16948,"journal":{"name":"Journal of receptor research","volume":"13 1-4","pages":"355-67"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10799899309073666","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19369685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8