Peptides from the amino terminal mdm-2-binding domain of p53, designed from conformational analysis, are selectively cytotoxic to transformed cells-Reference-Cited by-同舟云学术

登录注册会员服务联系我们

Peptides from the amino terminal mdm-2-binding domain of p53, designed from conformational analysis, are selectively cytotoxic to transformed cells

Published:2001-10-16 Issue:22 Volume:98 Page:12438-12443
ISSN:0027-8424
Container-title:Proceedings of the National Academy of Sciences
language:en
Short-container-title:Proceedings of the National Academy of Sciences

Author:

Kanovsky M.,Raffo A.,Drew L.,Rosal R.,Do T.,Friedman F. K.,Rubinstein P.,Visser J.,Robinson R.,Brandt-Rauf P. W.,Michl J.,Fine R. L.,Pincus M. R.

Publisher

Proceedings of the National Academy of Sciences

Subject

Multidisciplinary

Reference22 articles.

1. Biochemical properties and biological effects of p53

2. Mdm2 promotes the rapid degradation of p53

3. MEKK1/JNK signaling stabilizes and activates p53

Cited by 89 articles. 订阅此论文施引文献订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献

1. The role of ETFS amino acids on the stability and inhibition of p53-MDM2 complex of anticancer p53-derivatives peptides: Density functional theory and molecular docking studies;Journal of Molecular Graphics and Modelling;2023-07

2. Designed Multifunctional Peptides for Intracellular Targets;Antibiotics;2022-09-03

3. Poroptosis: A form of cell death depending on plasma membrane nanopores formation;iScience;2022-06

4. The role of cell‐penetrating peptides in potential anti‐cancer therapy;Clinical and Translational Medicine;2022-05

5. PNC-27, a Chimeric p53-Penetratin Peptide Binds to HDM-2 in a p53 Peptide-like Structure, Induces Selective Membrane-Pore Formation and Leads to Cancer Cell Lysis;Biomedicines;2022-04-20

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线，采集、加工和组织学术论文而形成的新型学术文献查询和分析系统，可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容，当前同舟云学术共收录了国内外主流学术期刊6万余种，收集的期刊论文及会议论文总量共计约1.5亿篇，并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询！咨询电话：010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号京ICP备18003416号-3