Endocytosis of Cationized Ferritin in Marginal Cells of the Stria Vascularis Is Regulated by Protein Kinase, Protein Phosphatase, and MEK/ERK and PI3-K Signaling Pathways.

Kakigi A; Okada T; Takeda TTakeda SNishioka RTaguchi DNishimura MYamasoba T

首页> 外文期刊>Otology and neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology >Endocytosis of Cationized Ferritin in Marginal Cells of the Stria Vascularis Is Regulated by Protein Kinase, Protein Phosphatase, and MEK/ERK and PI3-K Signaling Pathways.

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Endocytosis of Cationized Ferritin in Marginal Cells of the Stria Vascularis Is Regulated by Protein Kinase, Protein Phosphatase, and MEK/ERK and PI3-K Signaling Pathways.

机译：蛋白激酶，蛋白质磷酸酶以及MEK/ERK和PI3-K信号传导途径调节肌纤维血管边缘细胞中阳离子铁蛋白的内吞作用。

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HYPOTHESIS: : The endocytosis of cationized ferritin (CF) via a clathrin-mediated pathway is regulated by a signaling network. BACKGROUND: : Marginal cells showed the active endocytosis of CF via a clathrin-mediated pathway. The internalization of receptors through the clathrin-mediated pathway is an important regulatory event in signal transduction. Numerous kinases are involved in endocytosis, and each endocytic route is subjected to high-order regulation by cellular signaling mechanisms. METHODS: : CF was infused into the cochlear duct with phorbol 12-myristate 13 acetate, okadaic acid, staurosporin, phenylarsine oxide, PD98059, SB20580 and wortmannin. Endocytic activity was measured at 30 minutes post-infusion by transmission electron microscopy. RESULTS: : The endocytosis of CF was stimulated by a protein kinase C activator (phorbol 12-myristate 13 acetate) and a protein kinase A activator (8-bromoadenosine-3', 5'-cyclic monophosphate). It was inhibited by protein phosphatase inhibitors (okadaic acid and phenylarsine oxide), mitogen-activated protein kinase/extracellular signal-related kinase inhibitors (PD98059 and SB20580), and a phosphatidylinositol 3-kinase inhibitor (wortmannin). CONCLUSION: : Our previous study showed the endocytosis of microperoxidase to be strongly dependent on protein kinase C, protein phosphatase, extracellular signal-related kinase, and phosphatidylinositol 3-kinase signaling networks but not on protein kinase A and mitogen-activated protein kinase signaling networks. The present study indicated that the signaling cascade regulating CF's internalization differed from the cascade for microperoxidase's endocytosis.

机译：假设：：通过网格蛋白介导的途径通过信号网络调节阳离子铁蛋白（CF）的内吞作用。背景：：边缘细胞通过网格蛋白介导的途径显示CF的活性内吞作用。通过网格蛋白介导的途径对受体的内在化是信号转导的重要调节事件。许多激酶参与内吞作用，每个内吞途径都通过细胞信号传导机制进行高阶调控。方法：： CF用佛波尔12-渴望的13醋酸盐，冈田酸，星孢菌素，氧化苯胺，PD98059，SB20580和Wortmannin注入人工耳蜗。通过透射电子显微镜在输注后30分钟测量内吞活性。结果：： CF的内吞作用是由蛋白激酶C活化剂（佛罗里杆菌12-溶酯13乙酸）和蛋白激酶A活化剂（8-溴腺苷-3'，5'-循环单磷酸）刺激的。蛋白质磷酸酶抑制剂（冈田酸和氧化苯烷），有丝分裂原激活的蛋白激酶/细胞外信号相关激酶抑制剂（PD98059和SB20580）抑制它。结论：：我们先前的研究表明，微孔过氧化物酶的内吞作用非常依赖于蛋白激酶C，蛋白质磷酸酶，细胞外信号相关激酶和磷脂酰辛基辛醇3-激酶信号网络，但不依赖于蛋白质激酶A和蛋白质激酶A的磷脂酰肌醇蛋白质酶信号酶网络。。本研究表明，调节CF内部化的信号级联反应与微孔过氧化物酶内吞作用的级联反应不同。

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《Otology and neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology》 |2011年第5期|856-862|共7页
作者
Kakigi A; Okada T; Takeda TTakeda SNishioka RTaguchi DNishimura MYamasoba T;
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*Department of Otolaryngology, Faculty of Medicine, University of Tokyo, Tokyo;

Departments of daggerOtolaryngology, and double daggerAnatomy, Kochi Medical School, Kochi;

section signDivision of Otolaryngology, Head and Neck Surgery, Tottori University F;

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正文语种英语
中图分类耳鼻咽喉科学;
关键词
Endocytosis; Stria Vascularis; protein kinase C activatorpolycationic ferritinPhosphoprotein PhosphatasesCONTAINMENT FAILUREProtein Kinasessignalling networkmicroperoxidaseCochlear DuctProtein Kinase Aoxophenylarsine;

机译：内吞作用;肌血管;蛋白激酶C活化蛋白溶解性铁蛋白磷酸蛋白磷酸蛋白磷酸蛋白磷酸蛋白失败衰竭蛋白kinasessignalling notchAsessignaling Networkmicroperoperoxiadasecochlear ductprotein ductprotein ductprotein ductprotein ductprotein ductprotein激酶激酶激酶激酶激酶激酶;

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Endocytosis of Cationized Ferritin in Marginal Cells of the Stria Vascularis Is Regulated by Protein Kinase, Protein Phosphatase, and MEK/ERK and PI3-K Signaling Pathways.

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