Transmembrane Signaling

跨膜信号传导

基本信息

批准号：
01045035
负责人：
EBASHI Setsuro
金额：
$ 5.44万
依托单位：
Okazaki National Research Institutes (National Institute for Physiological Sciences)
依托单位国家：
日本
项目类别：
Grant-in-Aid for international Scientific Research
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1991
项目状态：
已结题

项目摘要

This project aimed at elucidation of signal transduction pathway from membrane receptors to physiological cellular responses.1. First Year (1989) : We studied signal transduction pathway in muscle cells.(1) Involvement of lyotonin in contraction of smooth muscles was studied.(2) Involvement of inositol metabolites in Ca transients in skeletal muscles was studied.(3) Fura-2 visualization of Ca transients in bull-frog skeletal muscles was done.The threshold for caffeine stimulation for Ca release was measured to be 1-2 mM.2. Second Year (1990) : We studied exocrine glands and anti-channel drugs.(1) In colonic goblet cells, okadaic acid blocked the late part of the secretory and Ca responses induced by muscarinic stimulation. Thus, phosphorylation of muscarinic receptors mediates desensitization of these cellular responses.(2) Exocytotic responses in salivary gland of tupai were clearly detected by DIC microscopy. Water secretion was visualized as periodical movements of the apical membra … More ne of acinar cells. Muscarinic stimulants and ATP were effective but BETA stimulants were not in inducing secretory responses in the sublingual gland.(3) Toosendainine was found to suppress the Ca channel activity in NG108 cells.(4) A neurotoxin that specifically blocks the Na channel in insects was purified from the scorpion venom.3. Third Year (1991) : Stimulation-secretion coupling in tupai salivary gland and glutamate responses in retinal horizontal cells were studied.(1) Either various activators of protein kinase C nor K-depolarization were not effective in inducing secretory response in the salivary gland. These suggested that transmembrane signaling in salivary gland is mediated by a 2nd messenger system other than A-kinase and C-kinase systems.(2) Kinate-induced currents were studied in horizontal cells. Dopamine modulated the kinate current in a dose-dependent manner. Haroperidol suppressed the effect of dopamine on the kinate current. These modulatory effects are thought to arise from alteration of cGMP messenger system. Less

该项目旨在阐明从膜受体到物理细胞反应的信号转导途径1。第一年（1989年）：我们研究了肌肉细胞中的信号转导途径。（1）lyotonin参与光滑肌肉的收缩。测量为1-2毫米2。第二年（1990年）：我们研究了外分泌网格和抗通道药物。（1）在结肠杯状细胞中，冈田酸阻止了毒蕈碱刺激引起的秘密和Ca反应的晚期。通过DIC显微镜清楚地检测到了毒蕈碱受体的磷酸化介导这些细胞反应的脱敏。（2）TIC显微镜清楚地检测到了Tupai唾液腺中的胞吐反应。水分被认为是顶膜的周期运动……更多的腺泡细胞运动。毒蕈碱刺激剂和ATP是有效的，但β刺激剂并未在舌下腺体中引起的秘密反应。（3）Toosendaine被发现抑制NG108细胞中的CA通道活性。（4）一种神经毒素，一种神经毒素，该神经毒素特异性地阻断了从昆虫中净化NA的NA，从Scorpion Venom.3。第三年（1991）：研究了残留水平细胞中Tupai唾液腺和谷氨酸反应的刺激 - 分泌耦合。（1）要么在唾液腺中诱导的秘密反应，要么在蛋白激酶C或K-Depolarisis的各种激活剂中无效。这些表明，唾液腺中的跨膜信号传导是由A-激酶和C-激酶系统以外的第二个Messenger系统介导的。（2）在水平细胞中研究了Kinate诱导的电流。多巴胺以剂量依赖性方式调节了kinate电流。 Haroperidol抑制了多巴胺对Kinate电流的影响。这些调节作用被认为是由CGMP Messenger系统的改变产生的。较少的