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白细胞介素-9和信号转导及转录激活因子在血液系统恶性肿瘤中的作用(综述)

Role of IL-9 and STATs in hematological malignancies (Review).

作者信息

Chen Na, Wang Xin

机构信息

Department of Hematology, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.

Department of Hematology, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China ; Department of Diagnostics, Shandong University School of Medicine, Jinan, Shandong 250012, P.R. China.

出版信息

Oncol Lett. 2014 Mar;7(3):602-610. doi: 10.3892/ol.2013.1761. Epub 2013 Dec 16.

DOI:10.3892/ol.2013.1761
PMID:24520283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3919939/
Abstract

Although interleukin-9 (IL-9) exhibits pleiotropic functions in the immune system, it remains a well-known cytokine in hematological malignancies. Previous cell culture and animal model studies have revealed that the Janus kinase-signal transducer and activator of transcription signaling pathway, which may be activated by a number of cytokines including IL-9, is critical in hematological malignancies. The current review summarizes the characterization of the biological activities of IL-9, highlights the clearly defined roles of the cytokine, and outlines questions with regard to the functions of IL-9 that require further exploration and their downstream signaling proteins, signal transducers and activators of transcription.

摘要

尽管白细胞介素-9(IL-9)在免疫系统中具有多效性功能,但它在血液系统恶性肿瘤中仍是一种广为人知的细胞因子。先前的细胞培养和动物模型研究表明,Janus激酶-信号转导子和转录激活子信号通路可能被包括IL-9在内的多种细胞因子激活,该通路在血液系统恶性肿瘤中至关重要。本综述总结了IL-9的生物学活性特征,强调了该细胞因子明确的作用,并概述了关于IL-9功能仍需进一步探索的问题及其下游信号蛋白——信号转导子和转录激活子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf31/3919939/69026a869907/OL-07-03-0602-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf31/3919939/3b1da7cef26c/OL-07-03-0602-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf31/3919939/69026a869907/OL-07-03-0602-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf31/3919939/3b1da7cef26c/OL-07-03-0602-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf31/3919939/69026a869907/OL-07-03-0602-g01.jpg

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