Bau是neurabin - 1的一种剪接形式,与肿瘤抑制因子Bin1相互作用,抑制恶性细胞转化。

J Duhadaway, F Rowe, K Elliott, N C Mao, G C Prendergast
{"title":"Bau是neurabin - 1的一种剪接形式,与肿瘤抑制因子Bin1相互作用,抑制恶性细胞转化。","authors":"J Duhadaway,&nbsp;F Rowe,&nbsp;K Elliott,&nbsp;N C Mao,&nbsp;G C Prendergast","doi":"10.3109/15419069909034394","DOIUrl":null,"url":null,"abstract":"<p><p>Bin1 is a nucleocytoplasmic adaptor protein and tumor suppressor. A novel protein termed Bau was identified through its ability to interact with a region of Bin1 required to inhibit malignant cell transformation by certain oncogenes. Bau is a splice form of Neurabin-I, one of two related F-actin-binding proteins that are proposed to link cadherin-based cell-cell adhesion sites with the growth regulatory kinase p70S6K. Bau lacks actin- and p70S6K-binding domains found in Neurabin-I but includes coiled-coil domains that are part of its central domain as well as additional sequences not found in Neurabin-I. Interaction with Bin1 requires the presence of the U3 region which is alternately spliced in muscle cells. Bau localizes to the nucleus and cytosol. Like Bin1, Bau can suppress oncogene-mediated transformation and inhibit tumor cell growth. We suggest that Bau may link Bin1 to the Neurabin-I/p70S6K system in muscle and other cells, perhaps providing a mechanism to influence adhesion-dependent signals which affect cell fate.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"7 2","pages":"99-110"},"PeriodicalIF":0.0000,"publicationDate":"1999-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069909034394","citationCount":"5","resultStr":"{\"title\":\"Bau, a splice form of Neurabin-I that interacts with the tumor suppressor Bin1, inhibits malignant cell transformation.\",\"authors\":\"J Duhadaway,&nbsp;F Rowe,&nbsp;K Elliott,&nbsp;N C Mao,&nbsp;G C Prendergast\",\"doi\":\"10.3109/15419069909034394\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Bin1 is a nucleocytoplasmic adaptor protein and tumor suppressor. A novel protein termed Bau was identified through its ability to interact with a region of Bin1 required to inhibit malignant cell transformation by certain oncogenes. Bau is a splice form of Neurabin-I, one of two related F-actin-binding proteins that are proposed to link cadherin-based cell-cell adhesion sites with the growth regulatory kinase p70S6K. Bau lacks actin- and p70S6K-binding domains found in Neurabin-I but includes coiled-coil domains that are part of its central domain as well as additional sequences not found in Neurabin-I. Interaction with Bin1 requires the presence of the U3 region which is alternately spliced in muscle cells. Bau localizes to the nucleus and cytosol. Like Bin1, Bau can suppress oncogene-mediated transformation and inhibit tumor cell growth. We suggest that Bau may link Bin1 to the Neurabin-I/p70S6K system in muscle and other cells, perhaps providing a mechanism to influence adhesion-dependent signals which affect cell fate.</p>\",\"PeriodicalId\":79325,\"journal\":{\"name\":\"Cell adhesion and communication\",\"volume\":\"7 2\",\"pages\":\"99-110\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1999-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3109/15419069909034394\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell adhesion and communication\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3109/15419069909034394\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell adhesion and communication","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/15419069909034394","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5

摘要

Bin1是一种核细胞质接头蛋白和肿瘤抑制蛋白。一种名为Bau的新蛋白通过其与Bin1区域相互作用的能力被鉴定出来,该区域是抑制某些癌基因的恶性细胞转化所必需的。Bau是neurabin - 1的一种剪接形式,neurabin - 1是两种相关的f -actin结合蛋白之一,被提出将钙粘蛋白为基础的细胞-细胞粘附位点与生长调节激酶p70S6K连接起来。Bau缺乏在Neurabin-I中发现的actin-和p70s6k结合结构域,但包括作为其中心结构域一部分的卷曲结构域以及在Neurabin-I中未发现的其他序列。与Bin1的相互作用需要在肌肉细胞中交替剪接的U3区域的存在。Bau定位于细胞核和细胞质。与Bin1一样,Bau可以抑制癌基因介导的转化,抑制肿瘤细胞的生长。我们认为Bau可能将Bin1与肌肉和其他细胞中的Neurabin-I/p70S6K系统联系起来,可能提供一种机制来影响影响细胞命运的粘附依赖性信号。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Bau, a splice form of Neurabin-I that interacts with the tumor suppressor Bin1, inhibits malignant cell transformation.

Bin1 is a nucleocytoplasmic adaptor protein and tumor suppressor. A novel protein termed Bau was identified through its ability to interact with a region of Bin1 required to inhibit malignant cell transformation by certain oncogenes. Bau is a splice form of Neurabin-I, one of two related F-actin-binding proteins that are proposed to link cadherin-based cell-cell adhesion sites with the growth regulatory kinase p70S6K. Bau lacks actin- and p70S6K-binding domains found in Neurabin-I but includes coiled-coil domains that are part of its central domain as well as additional sequences not found in Neurabin-I. Interaction with Bin1 requires the presence of the U3 region which is alternately spliced in muscle cells. Bau localizes to the nucleus and cytosol. Like Bin1, Bau can suppress oncogene-mediated transformation and inhibit tumor cell growth. We suggest that Bau may link Bin1 to the Neurabin-I/p70S6K system in muscle and other cells, perhaps providing a mechanism to influence adhesion-dependent signals which affect cell fate.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Expression of MacMARCKS restores cell adhesion to ICAM-1-coated surface. Quantitative determination of gap junction intercellular communication by scrape loading and image analysis. Expression of a soluble functional form of the integrin alpha4beta1 in mammalian cells. Tumor-derived mutated E-cadherin influences beta-catenin localization and increases susceptibility to actin cytoskeletal changes induced by pervanadate. Rac is essential in the transformation of endothelial cells by polyoma middle T.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1