桥接(联网)
自身免疫
激酶
贾纳斯激酶
杰纳斯
细胞生物学
医学
生物
免疫学
免疫系统
纳米技术
计算机科学
材料科学
计算机网络
作者
Yazi Wei,Tiantai Zhang
标识
DOI:10.53941/ijddp.2024.100007
摘要
Review Janus Kinases and Autoimmunity: Bridging Pathways to Therapy Yazi Wei 1, and Tiantai Zhang 1,* State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China * Correspondence: ttzhang@imm.ac.cn Received: 7 February 2024; Revised: 1 March 2024; Accepted: 1 March 2024; Published: 5 June 2024 Abstract: Janus kinase (JAK) is a family of intracellular non-receptor tyrosine kinases with four members (JAK1, JAK2, JAK3, and Tyk2). The JAK-STAT (signal transducer and activator of transcription) pathway is an evolutionary conserved mechanism of transmembrane signal transduction relaying over 50 cytokines signals to regulate the proliferation, immune response, inflammation, and malignancy. The dysfunction of JAK-STAT signaling pathway is directly associated with the pathogenesis of inflammatory and autoimmune disorders, as well as tumor progression. Studies have shown that targeting the JAK family with small-molecule inhibitors can treat inflammatory and autoimmune diseases and myeloproliferative neoplasms. In this review, we discuss the current understanding of the JAK-STAT signaling and approved JAK inhibitors.
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