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细胞因子信号转导抑制蛋白(SOCS)和 JAK/STAT 通路:SOCS1 和 SOCS3 对 T 细胞炎症的调节。

Suppressors of cytokine signaling (SOCS) proteins and JAK/STAT pathways: regulation of T-cell inflammation by SOCS1 and SOCS3.

机构信息

Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

出版信息

Arterioscler Thromb Vasc Biol. 2011 May;31(5):980-5. doi: 10.1161/ATVBAHA.110.207464.

Abstract

Various cytokines are involved in the regulation of the immune system and inflammation. Dysregulation of cytokine signaling can cause a variety of diseases, including allergy, autoimmune diseases, inflammation, and cancer. Most cytokines use the so-called janus kinase/signal transducer and activator of transcription pathway, and this pathway is negatively regulated by suppressors of cytokine signaling (SOCS) proteins. SOCS proteins bind to janus kinase and to certain cytokine receptors and signaling molecules, thereby suppressing further signaling events. Studies have shown that SOCS proteins are key physiological regulators of inflammation. Recent studies have also demonstrated that SOCS1 and SOCS3 are important regulators of adaptive immunity.

摘要

各种细胞因子参与免疫系统和炎症的调节。细胞因子信号转导的失调可导致多种疾病,包括过敏、自身免疫性疾病、炎症和癌症。大多数细胞因子使用所谓的 Janus 激酶/信号转导和转录激活因子途径,该途径受细胞因子信号转导抑制剂 (SOCS) 蛋白的负调控。SOCS 蛋白与 Janus 激酶和某些细胞因子受体及信号分子结合,从而抑制进一步的信号事件。研究表明,SOCS 蛋白是炎症的关键生理调节剂。最近的研究还表明,SOCS1 和 SOCS3 是适应性免疫的重要调节剂。

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