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Your search keyword '"Kaniskan, H. Ümit"' showing total 9 results
Start Over Author "Kaniskan, H. Ümit" Journal journal of the american chemical society
9 results on '"Kaniskan, H. Ümit"'

1. Structurally Specific Z-DNA Proteolysis Targeting Chimera Enables Targeted Degradation of Adenosine Deaminase Acting on RNA 1

Author

Wang, Zhen, primary, Zhang, Dingpeng, additional, Qiu, Xing, additional, Inuzuka, Hiroyuki, additional, Xiong, Yan, additional, Liu, Jing, additional, Chen, Li, additional, Chen, He, additional, Xie, Ling, additional, Kaniskan, H. Ümit, additional, Chen, Xian, additional, Jin, Jian, additional, and Wei, Wenyi, additional

Published
2024
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5. Harnessing the E3 Ligase KEAP1 for Targeted Protein Degradation

Author

Wei, Jieli, primary, Meng, Fanye, additional, Park, Kwang-Su, additional, Yim, Hyerin, additional, Velez, Julia, additional, Kumar, Prashasti, additional, Wang, Li, additional, Xie, Ling, additional, Chen, He, additional, Shen, Yudao, additional, Teichman, Emily, additional, Li, Dongxu, additional, Wang, Gang Greg, additional, Chen, Xian, additional, Kaniskan, H. Ümit, additional, and Jin, Jian, additional

Published
2021
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9. Acetylation Targeting Chimera Enables Acetylation of the Tumor Suppressor p53

Author

Kabir, Md, Sun, Ning, Hu, Xiaoping, Martin, Tiphaine C., Yi, Jingjie, Zhong, Yue, Xiong, Yan, Kaniskan, H. Ümit, Gu, Wei, Parsons, Ramon, and Jin, Jian

Abstract

With advances in chemically induced proximity technologies, heterobifunctional modalities such as proteolysis targeting chimeras (PROTACs) have been successfully advanced to clinics for treating cancer. However, pharmacologic activation of tumor-suppressor proteins for cancer treatment remains a major challenge. Here, we present a novel Acetylation Targeting Chimera (AceTAC) strategy to acetylate the p53 tumor suppressor protein. We discovered and characterized the first p53Y220C AceTAC, MS78, which recruits histone acetyltransferase p300/CBP to acetylate the p53Y220C mutant. MS78 effectively acetylated p53Y220C lysine 382 (K382) in a concentration-, time-, and p300-dependent manner and suppressed proliferation and clonogenicity of cancer cells harboring the p53Y220C mutation with little toxicity in cancer cells with wild-type p53. RNA-seq studies revealed novel p53Y220C-dependent upregulation of TRAIL apoptotic genes and downregulation of DNA damage response pathways upon acetylation induced by MS78. Altogether, the AceTAC strategy could provide a generalizable platform for targeting proteins, such as tumor suppressors, via acetylation.

Published
2023
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