Mami Noda , Nobuto Ishizaka , Shigeru Yokoyama , Naoto Hoshi , Yasuhiro Kimura , Minako Hashii , Megumi Taketo , Alla Egorova , Rimma Knijnik , Kazuhiko Fukuda , Hitoshi Morikawa , David A. Brown , Haruhiro Higashida
{"title":"肌醇三磷酸/Ca2+作为缓激肽B2和毒蕈碱乙酰胆碱ml-m4受体在神经母细胞瘤来源的杂交细胞中的信使","authors":"Mami Noda , Nobuto Ishizaka , Shigeru Yokoyama , Naoto Hoshi , Yasuhiro Kimura , Minako Hashii , Megumi Taketo , Alla Egorova , Rimma Knijnik , Kazuhiko Fukuda , Hitoshi Morikawa , David A. Brown , Haruhiro Higashida","doi":"10.1016/0929-7855(96)00523-8","DOIUrl":null,"url":null,"abstract":"<div><p>Neuroblastoma × glioma hybrid NG108-15 and neuroblastoma × fibroblast hybrid NL308 cells possess endogenous bradykinin B<sub>2</sub> receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (ml and m3) activated phospholipase C and increased inositol trisphosphate/Ca<sup>2+</sup>, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.</p></div>","PeriodicalId":79347,"journal":{"name":"Journal of lipid mediators and cell signalling","volume":"14 1","pages":"Pages 175-185"},"PeriodicalIF":0.0000,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0929-7855(96)00523-8","citationCount":"16","resultStr":"{\"title\":\"Inositol trisphosphate/Ca2+ as messengers of bradykinin B2 and muscarinic acetylcholine ml-m4 receptors in neuroblastoma-derived hybrid cells\",\"authors\":\"Mami Noda , Nobuto Ishizaka , Shigeru Yokoyama , Naoto Hoshi , Yasuhiro Kimura , Minako Hashii , Megumi Taketo , Alla Egorova , Rimma Knijnik , Kazuhiko Fukuda , Hitoshi Morikawa , David A. Brown , Haruhiro Higashida\",\"doi\":\"10.1016/0929-7855(96)00523-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Neuroblastoma × glioma hybrid NG108-15 and neuroblastoma × fibroblast hybrid NL308 cells possess endogenous bradykinin B<sub>2</sub> receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (ml and m3) activated phospholipase C and increased inositol trisphosphate/Ca<sup>2+</sup>, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.</p></div>\",\"PeriodicalId\":79347,\"journal\":{\"name\":\"Journal of lipid mediators and cell signalling\",\"volume\":\"14 1\",\"pages\":\"Pages 175-185\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1996-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0929-7855(96)00523-8\",\"citationCount\":\"16\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of lipid mediators and cell signalling\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0929785596005238\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of lipid mediators and cell signalling","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0929785596005238","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Inositol trisphosphate/Ca2+ as messengers of bradykinin B2 and muscarinic acetylcholine ml-m4 receptors in neuroblastoma-derived hybrid cells
Neuroblastoma × glioma hybrid NG108-15 and neuroblastoma × fibroblast hybrid NL308 cells possess endogenous bradykinin B2 receptors and m4 muscarinic acetylcholine receptors (mAChRs), which couple to phospholipase C and adenylate cyclase, respectively. Four genetic subtypes of mAChRs differed in their effects when stimulated in NG108-15 and NL308 cells overexpressing mAChRs. Broadly speaking, the principal effects fell into two categories: the odd-numbered receptors (ml and m3) activated phospholipase C and increased inositol trisphosphate/Ca2+, as bradykinin did, whereas the even-numbered receptors (m2 and m4) inhibited adenylate cyclase via a pertussis toxin (PTx)-sensitive G-protein in NG108-15 cells. But all four types of NL308 cells overexpressing each m1, m2, m3 and m4 receptor activated phospholipase C, while keeping the PTx-sensitivity in m2/m4, but not in m1/m3 receptors. Coupling to ion channel effectors showed a comparable dichotomy in NG108-15 cells, while cross-activation occurred in NL308 cells.
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