IRBIT regulates CaMKII alpha activity and contributes to catecholamine homeostasis through tyrosine hydroxylase phosphorylation

Kawaai Katsuhiro; Mizutani Akihiro; Shoji HirotakaOgawa NaokoEbisui EtsukoKuroda YukikoWakana ShigeharuMiyakawa TsuyoshiHisatsune ChihiroMikoshiba Katsuhiko

首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >IRBIT regulates CaMKII alpha activity and contributes to catecholamine homeostasis through tyrosine hydroxylase phosphorylation

【24h】

IRBIT regulates CaMKII alpha activity and contributes to catecholamine homeostasis through tyrosine hydroxylase phosphorylation

机译：IRBIT regulates CaMKII alpha activity and contributes to catecholamine homeostasis through tyrosine hydroxylase phosphorylation

获取原文

获取原文并翻译 | 示例

掌桥外文数据库（机构版） >>

开具论文收录证明 >>

文献代查 >>

页面导航

摘要
著录项
相关主题

摘要

Inositol 1,4,5-trisphosphate receptor (IP3R) binding protein released with IP3 (IRBIT) contributes to various physiological events (electrolyte transport and fluid secretion, mRNA polyadenylation, and the maintenance of genomic integrity) through its interaction with multiple targets. However, little is known about the physiological role of IRBIT in the brain. Here we identified calcium calmodulin-dependent kinase II alpha (CaMKII alpha) as an IRBIT-interacting molecule in the central nervous system. IRBIT binds to and suppresses CaMKIIa kinase activity by inhibiting the binding of calmodulin to CaMKIIa. In addition, we show that mice lacking IRBIT present with elevated catecholamine levels, increased locomotor activity, and social abnormalities. The level of tyrosine hydroxylase (TH) phosphorylation by CaMKII alpha, which affects TH activity, was significantly increased in the ventral tegmental area of IRBIT-deficient mice. We concluded that IRBIT suppresses CaMKII alpha activity and contributes to catecholamine homeostasis through TH phosphorylation.

著录项

来源
《Proceedings of the National Academy of Sciences of the United States of America》 |2015年第17期|5515-5520|共6页
作者
Kawaai Katsuhiro; Mizutani Akihiro; Shoji HirotakaOgawa NaokoEbisui EtsukoKuroda YukikoWakana ShigeharuMiyakawa TsuyoshiHisatsune ChihiroMikoshiba Katsuhiko;
展开▼
作者单位

Showa Pharmaceut Univ, Dept Pharmacotherapeut, Machida, Tokyo 1948543, Japan;

Fujita Hlth Univ, Inst Comprehens Med Sci, Div Syst Med Sci, Toyoake, Aichi 4701192, Japan;

RIKEN, Brain Sci Inst, Lab Dev Neurobiol, Wako, Saitama 3510198, JapanKeio Univ, Sch Med, Lab Cell & Tissue Biol, Tokyo 1608582, JapanRIKEN, BioResource Ctr, Technol & Dev Team Mouse Phenotype Anal, Tsukuba, Ibaraki 3050074, Japan;

展开▼
收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
IRBIT; CaMKII alpha; catecholamine; hyperactivity;

IRBIT regulates CaMKII alpha activity and contributes to catecholamine homeostasis through tyrosine hydroxylase phosphorylation

摘要

著录项

相关主题

期刊订阅