CDK调节因子-细胞周期进展或凋亡-正常细胞和癌细胞的情况。

3区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Nilmani, Maria D'costa, Anusha Bothe, Soumik Das, S Udhaya Kumar, R Gnanasambandan, C George Priya Doss
{"title":"CDK调节因子-细胞周期进展或凋亡-正常细胞和癌细胞的情况。","authors":"Nilmani,&nbsp;Maria D'costa,&nbsp;Anusha Bothe,&nbsp;Soumik Das,&nbsp;S Udhaya Kumar,&nbsp;R Gnanasambandan,&nbsp;C George Priya Doss","doi":"10.1016/bs.apcsb.2022.11.008","DOIUrl":null,"url":null,"abstract":"<p><p>Serine/threonine kinases called cyclin-dependent kinases (CDKs) interact with cyclins and CDK inhibitors (CKIs) to control the catalytic activity. CDKs are essential controllers of RNA transcription and cell cycle advancement. The ubiquitous overactivity of the cell cycle CDKs is caused by a number of genetic and epigenetic processes in human cancer, and their suppression can result in both cell cycle arrest and apoptosis. This review focused on CDKs, describing their kinase activity, their role in phosphorylation inhibition, and CDK inhibitory proteins (CIP/KIP, INK 4, RPIC). We next compared the role of different CDKs, mainly p21, p27, p57, p16, p15, p18, and p19, in the cell cycle and apoptosis in cancer cells with respect to normal cells. The current work also draws attention to the use of CDKIs as therapeutics, overcoming the pharmacokinetic barriers of pan-CDK inhibitors, analyze new chemical classes that are effective at attacking the CDKs that control the cell cycle (cdk4/6 or cdk2). It also discusses CDKI's drawbacks and its combination therapy against cancer patients. These findings collectively demonstrate the complexity of cancer cell cycles and the need for targeted therapeutic intervention. In order to slow the progression of the disease or enhance clinical outcomes, new medicines may be discovered by researching the relationship between cell death and cell proliferation.</p>","PeriodicalId":7376,"journal":{"name":"Advances in protein chemistry and structural biology","volume":"135 ","pages":"125-177"},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":"{\"title\":\"CDK regulators-Cell cycle progression or apoptosis-Scenarios in normal cells and cancerous cells.\",\"authors\":\"Nilmani,&nbsp;Maria D'costa,&nbsp;Anusha Bothe,&nbsp;Soumik Das,&nbsp;S Udhaya Kumar,&nbsp;R Gnanasambandan,&nbsp;C George Priya Doss\",\"doi\":\"10.1016/bs.apcsb.2022.11.008\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Serine/threonine kinases called cyclin-dependent kinases (CDKs) interact with cyclins and CDK inhibitors (CKIs) to control the catalytic activity. CDKs are essential controllers of RNA transcription and cell cycle advancement. The ubiquitous overactivity of the cell cycle CDKs is caused by a number of genetic and epigenetic processes in human cancer, and their suppression can result in both cell cycle arrest and apoptosis. This review focused on CDKs, describing their kinase activity, their role in phosphorylation inhibition, and CDK inhibitory proteins (CIP/KIP, INK 4, RPIC). We next compared the role of different CDKs, mainly p21, p27, p57, p16, p15, p18, and p19, in the cell cycle and apoptosis in cancer cells with respect to normal cells. The current work also draws attention to the use of CDKIs as therapeutics, overcoming the pharmacokinetic barriers of pan-CDK inhibitors, analyze new chemical classes that are effective at attacking the CDKs that control the cell cycle (cdk4/6 or cdk2). It also discusses CDKI's drawbacks and its combination therapy against cancer patients. These findings collectively demonstrate the complexity of cancer cell cycles and the need for targeted therapeutic intervention. In order to slow the progression of the disease or enhance clinical outcomes, new medicines may be discovered by researching the relationship between cell death and cell proliferation.</p>\",\"PeriodicalId\":7376,\"journal\":{\"name\":\"Advances in protein chemistry and structural biology\",\"volume\":\"135 \",\"pages\":\"125-177\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in protein chemistry and structural biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/bs.apcsb.2022.11.008\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in protein chemistry and structural biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/bs.apcsb.2022.11.008","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 3

摘要

被称为细胞周期蛋白依赖激酶(CDKs)的丝氨酸/苏氨酸激酶与细胞周期蛋白和CDK抑制剂(CKIs)相互作用以控制催化活性。CDKs是RNA转录和细胞周期推进的重要控制者。细胞周期CDKs的普遍过度活性是由人类癌症中的许多遗传和表观遗传过程引起的,其抑制可导致细胞周期阻滞和细胞凋亡。本文综述了CDK的激酶活性、磷酸化抑制作用以及CDK抑制蛋白(CIP/KIP、ink4、RPIC)。接下来,我们比较了不同CDKs(主要是p21、p27、p57、p16、p15、p18和p19)与正常细胞在癌细胞周期和凋亡中的作用。目前的工作也引起了对CDKIs作为治疗药物的关注,克服了泛cdk抑制剂的药代动力学障碍,分析了有效攻击控制细胞周期的cdk (cdk4/6或cdk2)的新化学类。并讨论了CDKI的缺点及其对癌症患者的联合治疗。这些发现共同证明了癌细胞周期的复杂性和靶向治疗干预的必要性。通过研究细胞死亡与细胞增殖之间的关系,可能会发现新的药物,以减缓疾病的进展或提高临床疗效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CDK regulators-Cell cycle progression or apoptosis-Scenarios in normal cells and cancerous cells.

Serine/threonine kinases called cyclin-dependent kinases (CDKs) interact with cyclins and CDK inhibitors (CKIs) to control the catalytic activity. CDKs are essential controllers of RNA transcription and cell cycle advancement. The ubiquitous overactivity of the cell cycle CDKs is caused by a number of genetic and epigenetic processes in human cancer, and their suppression can result in both cell cycle arrest and apoptosis. This review focused on CDKs, describing their kinase activity, their role in phosphorylation inhibition, and CDK inhibitory proteins (CIP/KIP, INK 4, RPIC). We next compared the role of different CDKs, mainly p21, p27, p57, p16, p15, p18, and p19, in the cell cycle and apoptosis in cancer cells with respect to normal cells. The current work also draws attention to the use of CDKIs as therapeutics, overcoming the pharmacokinetic barriers of pan-CDK inhibitors, analyze new chemical classes that are effective at attacking the CDKs that control the cell cycle (cdk4/6 or cdk2). It also discusses CDKI's drawbacks and its combination therapy against cancer patients. These findings collectively demonstrate the complexity of cancer cell cycles and the need for targeted therapeutic intervention. In order to slow the progression of the disease or enhance clinical outcomes, new medicines may be discovered by researching the relationship between cell death and cell proliferation.

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
Advances in protein chemistry and structural biology
Advances in protein chemistry and structural biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
7.40
自引率
0.00%
发文量
66
审稿时长
>12 weeks
期刊介绍: Published continuously since 1944, The Advances in Protein Chemistry and Structural Biology series has been the essential resource for protein chemists. Each volume brings forth new information about protocols and analysis of proteins. Each thematically organized volume is guest edited by leading experts in a broad range of protein-related topics.
×
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