海湾
化学
激酶
背景(考古学)
蛋白激酶B
磷脂酰肌醇
细胞毒性
PI3K/AKT/mTOR通路
酶
细胞生物学
生物化学
细胞凋亡
癌症研究
体外
生物
古生物学
土木工程
工程类
作者
Lars Wortmann,Nico Bräuer,Simon J. Holton,Horst Irlbacher,Jörg Weiske,Christian Lechner,Robin Meier,Jakob Karén,Catrine Sioberg,Vera Pütter,Clara D. Christ,Antonius ter Laak,Philip Lienau,Ralf Lesche,Barbara Nicke,Shing‐Hu Cheung,Marcus Bauser,Andrea Haegebarth,Franz von Nussbaum,Dominik Mumberg
标识
DOI:10.1021/acs.jmedchem.1c01245
摘要
PIP4K2A is an insufficiently studied type II lipid kinase that catalyzes the conversion of phosphatidylinositol-5-phosphate (PI5P) into phosphatidylinositol 4,5-bisphosphate (PI4,5P2). The involvement of PIP4K2A/B in cancer has been suggested, particularly in the context of p53 mutant/null tumors. PIP4K2A/B depletion has been shown to induce tumor growth inhibition, possibly due to hyperactivation of AKT and reactive oxygen species-mediated apoptosis. Herein, we report the identification of the novel potent and highly selective inhibitors BAY-091 and BAY-297 of the kinase PIP4K2A by high-throughput screening and subsequent structure-based optimization. Cellular target engagement of BAY-091 and BAY-297 was demonstrated using cellular thermal shift assay technology. However, inhibition of PIP4K2A with BAY-091 or BAY-297 did not translate into the hypothesized mode of action and antiproliferative activity in p53-deficient tumor cells. Therefore, BAY-091 and BAY-297 serve as valuable chemical probes to study PIP4K2A signaling and its involvement in pathophysiological conditions such as cancer.
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