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Sprouty family of proteins regulates organogenesis and carcinogenesis through the signaling caused by RET tyrosine kinase

Sprouty family of proteins regulates organogenesis and carcinogenesis through the signaling caused by RET tyrosine kinase
Sprouty 蛋白家族通过 RET 酪氨酸激酶引起的信号调节器官发生和癌变
批准号:
18590367
负责人:
ICHIHARA Masatoshi
金额:
$2.65万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2006
资助国家:
日本
项目状态:
已结题
起止时间:
2006 至 2007

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中文摘要
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英文摘要
The Sprouty family of proteins includes important regulators of downstream signaling initiated by receptor tyrosine kinases. In the present study, we investigated the role of Sprouty proteins in intracellular signaling via RET tyrosine kinase. Expression of Sprouty family proteins in HEK293T cells transfected with RET and GFRα1 genes significantly reduced sustained activation of ERK, whereas their expression had no remarkable influence on the activation of p38, Akt and JNK. Since expression of Sprouty2 was efficiently induced by GDNF in TGW human neuroblastoma cells expressing RET and GFRα1, we further investigated the role of Sprouty2 in growth and differentiation of TGW cells. Expression of wild-type Sprouty2 (WT-SPRY2) decreased the growth of TGW cells. In contrast, expression of a dominant negative form of Sprouty2 (MT-SPRY2, with a mutated tyrosine residue) enhanced cell proliferation. In addition, expression of WT-SPRY2 reduced GDNF-dependent neurite outgrowth of TGW cells, where … More as expression of MT-SPRY2 enhanced it. Taken together, our results suggest that Sprouty2 regulates GDNF-dependent proliferation and differentiation of TGW neuroblastoma cells mediated by RET tyrosine kinase. These results have been reported in Cancer Science (Cancer Sci 98: 815-821, 2007). We next generated double knocli-out and knock-in mice between mutant RET (Y1062F) and Sprouty2 and observed their phenotype especially in the enteric nervous system and the kidney. Sprouty2-defficient mice demonstrated increased number of enteric neurons and achalasia-like dilution of esophagus, whereas Sprouty2 deficiency did not affect nephrogenesis even though high expression of Sprouty2 in the kidney. In contrast, mice with homozygous mutant RET demonstrated the decreased number of enteric neurons and small kidneys accompanying histological change. Interesting, Sprouty2 deficiency partially rescued the abnormal phenotype both in the enteric nervous system and nephrogenesis in homozygous RET mutant mice. These results suggest that Sprouty2 actually modulates the downstream signaling of RET tyrosine kinase and regulates mouse organogenesis in vivo. Less
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RET受容体型チロシンキナーゼのシグナル伝達系におけるSproutyファミリータンパク質の機能解析
Sprouty家族蛋白在RET受体酪氨酸激酶信号转导系统中的功能分析
DOI: --
发表时间: 2006
期刊:
影响因子: --
作者: [Fujii H, Ikura Y, et. al., Suzuki C, Jiang P, Suzuki C, Jiang P, Murakami M, Ishida M, Ishida M, Sato T, Hasegawa M, Dambara A, Murakami M, Ishida M, Ichihara M, Sato T, Hasegawa M, Dambara A, Suzuki C, Ichihara M, Uchida M, Murakumo Y, Uchida M, Murakumo Y, Murakumo Y, Uchida M, Ishida M, 花房 朋, Hanafusa T, 時々輪 真由美, Jijiwa M, 石田 麻紀, 加藤 琢哉, Ishida M, Katoh T, 石田 麻紀]
通讯作者: 石田 麻紀
DOI: 10.1093/nar/gkm699
发表时间: 2007
期刊: NUCLEIC ACIDS RESEARCH
影响因子: 14.9
作者: [Ichihara, Masatoshi, Murakumo, Yoshiki, Masuda, Akio, Matsuura, Toru, Asai, Naoya, Jijiwa, Mayumi, Ishida, Maki, Shinmi, Jun, Yatsuya, Hiroshi, Qiao, Shanlou, Takahashi, Masahide, Ohno, Kinji]
通讯作者: Ohno, Kinji
Functional analysis of Sprouty protein in signaling mediated by RET tyrosine kinase
Sprouty 蛋白在 RET 酪氨酸激酶介导的信号传导中的功能分析
DOI: --
发表时间: 2006
期刊:
影响因子: --
作者: [Fujii H, Ikura Y, et. al., Suzuki C, Jiang P, Suzuki C, Jiang P, Murakami M, Ishida M, Ishida M, Sato T, Hasegawa M, Dambara A, Murakami M, Ishida M, Ichihara M, Sato T, Hasegawa M, Dambara A, Suzuki C, Ichihara M, Uchida M, Murakumo Y, Uchida M, Murakumo Y, Murakumo Y, Uchida M, Ishida M, 花房 朋, Hanafusa T, 時々輪 真由美, Jijiwa M, 石田 麻紀, 加藤 琢哉, Ishida M]
通讯作者: Ishida M
損傷乗り越え合成に関わるREV7タンパク質の結合特異性についての解析
参与损伤克服合成的 REV7 蛋白的结合特异性分析
DOI: --
发表时间: 2007
期刊:
影响因子: --
作者: [Fujii H, Ikura Y, et. al., Suzuki C, Jiang P, Suzuki C, Jiang P, Murakami M, Ishida M, Ishida M, Sato T, Hasegawa M, Dambara A, Murakami M, Ishida M, Ichihara M, Sato T, Hasegawa M, Dambara A, Suzuki C, Ichihara M, Uchida M, Murakumo Y, Uchida M, Murakumo Y, Murakumo Y, Uchida M, Ishida M, 花房 朋]
通讯作者: 花房 朋
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