ReferenceID 3091

Tubulosine selectively inhibits JAK3 signalling by binding to the ATP-binding site of the kinase of JAK3

J Cell Mol Med

Gain- or loss-of-function mutations in Janus kinase 3 (JAK3) contribute to the pathogenesis of various haematopoietic malignancies and immune disorders, suggesting that aberrant JAK3 signalling is an attractive therapeut

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Reference Id
3091
Evidence Id
19681
Core Evidence Id
19681
Source Reference Id
6179
Herb2 Reference Id
HBREF006976
Subject Paper Key
HBIN047335_32558259
Pubmed Id
32558259
Doi
10.1111/jcmm.15362
Paper Title
Tubulosine selectively inhibits JAK3 signalling by binding to the ATP-binding site of the kinase of JAK3
Paper Abstract
Gain- or loss-of-function mutations in Janus kinase 3 (JAK3) contribute to the pathogenesis of various haematopoietic malignancies and immune disorders, suggesting that aberrant JAK3 signalling is an attractive therapeutic target to treat these disorders. In this study, we performed structure-based computational database screening using the 3D structure of the JAK3 kinase domain and the National Cancer Institute diversity set and identified tubulosine as a novel JAK3 inhibitor. Tubulosine directly blocked the catalytic activity of JAK3 by selective interacting with the JAK3 kinase domain. Consistently, tubulosine potently inhibited persistently activated and interleukin-2-dependent JAK3, and JAK3-mediated downstream targets. Importantly, it did not affect the activity of other JAK family members, particularly prolactin-induced JAK2/signal transducer and activator of transcription 5 and interferon alpha-induced JAK1-TYK2/STAT1. Tubulosine specifically decreased survival and proliferation of cancer cells, in which persistently active JAK3 is expressed, by inducing apoptotic and necrotic/autophagic cell death without affecting other oncogenic signalling. Collectively, tubulosine is a potential small-molecule compound that selectively inhibits JAK3 activity, suggesting that it may serve as a promising therapeutic candidate for treating disorders caused by aberrant activation of JAK3 signalling.
Journal
J Cell Mol Med
Publish Year
2020
Experiment Subject
Experiment Type
Others
Phenotype Related
Immune Disorders; Haematopoietic Malignancies; Cancer
Paper Title Cn
Paper Title En
Tubulosine selectively inhibits JAK3 signalling by binding to the ATP-binding site of the kinase of JAK3
Bilingual Status
semi_complete