GPCR CysLTR1/2 介导的信号通路在黑色素细胞增殖和衰老中的作用

IF 6.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Thomas Huber, Mizuho Horioka-Duplix, Yuanhuang Chen, Victoria R. Saca, Emilie Ceraudo, Yu Chen, Thomas P. Sakmar
{"title":"GPCR CysLTR1/2 介导的信号通路在黑色素细胞增殖和衰老中的作用","authors":"Thomas Huber,&nbsp;Mizuho Horioka-Duplix,&nbsp;Yuanhuang Chen,&nbsp;Victoria R. Saca,&nbsp;Emilie Ceraudo,&nbsp;Yu Chen,&nbsp;Thomas P. Sakmar","doi":"10.1126/scisignal.adp3967","DOIUrl":null,"url":null,"abstract":"<div >In contrast with sun exposure–induced melanoma, rarer melanocytic tumors and neoplasms with low mutational burden present opportunities to study isolated signaling mechanisms. These include uveal melanoma and blue nevi, which are often driven by mutations within the G protein–coupled signaling cascade downstream of cysteinyl leukotriene receptor 2. Here, we review how the same mutations within this pathway drive the growth of melanocytes in one tissue but can inhibit the growth of those in another, exemplifying the role of the tissue environment in the delicate balance between uncontrolled cell growth and senescence.</div>","PeriodicalId":21658,"journal":{"name":"Science Signaling","volume":"17 854","pages":""},"PeriodicalIF":6.7000,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The role of signaling pathways mediated by the GPCRs CysLTR1/2 in melanocyte proliferation and senescence\",\"authors\":\"Thomas Huber,&nbsp;Mizuho Horioka-Duplix,&nbsp;Yuanhuang Chen,&nbsp;Victoria R. Saca,&nbsp;Emilie Ceraudo,&nbsp;Yu Chen,&nbsp;Thomas P. Sakmar\",\"doi\":\"10.1126/scisignal.adp3967\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div >In contrast with sun exposure–induced melanoma, rarer melanocytic tumors and neoplasms with low mutational burden present opportunities to study isolated signaling mechanisms. These include uveal melanoma and blue nevi, which are often driven by mutations within the G protein–coupled signaling cascade downstream of cysteinyl leukotriene receptor 2. Here, we review how the same mutations within this pathway drive the growth of melanocytes in one tissue but can inhibit the growth of those in another, exemplifying the role of the tissue environment in the delicate balance between uncontrolled cell growth and senescence.</div>\",\"PeriodicalId\":21658,\"journal\":{\"name\":\"Science Signaling\",\"volume\":\"17 854\",\"pages\":\"\"},\"PeriodicalIF\":6.7000,\"publicationDate\":\"2024-09-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Science Signaling\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.science.org/doi/10.1126/scisignal.adp3967\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science Signaling","FirstCategoryId":"99","ListUrlMain":"https://www.science.org/doi/10.1126/scisignal.adp3967","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

与阳光照射诱导的黑色素瘤相比,较罕见的黑色素细胞肿瘤和突变负荷较低的肿瘤为研究孤立的信号转导机制提供了机会。这些肿瘤包括葡萄膜黑色素瘤和蓝痣,它们通常是由半胱氨酰白三烯受体2下游的G蛋白偶联信号级联中的突变驱动的。在这里,我们将回顾这一通路中的相同突变是如何在一个组织中驱动黑色素细胞生长,但在另一个组织中却能抑制黑色素细胞生长的,从而说明组织环境在细胞失控生长与衰老之间的微妙平衡中所起的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of signaling pathways mediated by the GPCRs CysLTR1/2 in melanocyte proliferation and senescence
In contrast with sun exposure–induced melanoma, rarer melanocytic tumors and neoplasms with low mutational burden present opportunities to study isolated signaling mechanisms. These include uveal melanoma and blue nevi, which are often driven by mutations within the G protein–coupled signaling cascade downstream of cysteinyl leukotriene receptor 2. Here, we review how the same mutations within this pathway drive the growth of melanocytes in one tissue but can inhibit the growth of those in another, exemplifying the role of the tissue environment in the delicate balance between uncontrolled cell growth and senescence.
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
Science Signaling
Science Signaling BIOCHEMISTRY & MOLECULAR BIOLOGY-CELL BIOLOGY
CiteScore
9.50
自引率
0.00%
发文量
148
审稿时长
3-8 weeks
期刊介绍: "Science Signaling" is a reputable, peer-reviewed journal dedicated to the exploration of cell communication mechanisms, offering a comprehensive view of the intricate processes that govern cellular regulation. This journal, published weekly online by the American Association for the Advancement of Science (AAAS), is a go-to resource for the latest research in cell signaling and its various facets. The journal's scope encompasses a broad range of topics, including the study of signaling networks, synthetic biology, systems biology, and the application of these findings in drug discovery. It also delves into the computational and modeling aspects of regulatory pathways, providing insights into how cells communicate and respond to their environment. In addition to publishing full-length articles that report on groundbreaking research, "Science Signaling" also features reviews that synthesize current knowledge in the field, focus articles that highlight specific areas of interest, and editor-written highlights that draw attention to particularly significant studies. This mix of content ensures that the journal serves as a valuable resource for both researchers and professionals looking to stay abreast of the latest advancements in cell communication science.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信