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核因子-κB 诱导激酶:免疫系统和癌症中的关键调节因子。

NF-κB inducing kinase: a key regulator in the immune system and in cancer.

机构信息

Department of Veterans Affairs Medical Center, Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

出版信息

Cytokine Growth Factor Rev. 2010 Aug;21(4):213-26. doi: 10.1016/j.cytogfr.2010.06.002. Epub 2010 Aug 3.

DOI:10.1016/j.cytogfr.2010.06.002
PMID:20685151
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2939163/
Abstract

NF-κB inducing kinase (NIK) is a kinase that activates the canonical and non-canonical NF-κB pathways to control transcriptional expression of certain proteins such as cytokines, chemokines and NF-κB signaling molecules. Many advances have been made in understanding the molecular mechanisms by which the stability of NIK is regulated to affect downstream signaling. Genetic mouse models suggest that NIK plays an essential role in the regulation of the immune system as well as in the bone microenvironment. Increasing evidence links NIK to the tumorigenesis of hematological cancers, such as multiple myeloma, and solid tumors, such as pancreatic carcinoma and melanoma. Understanding the mechanism by which NIK is de-regulated will potentially provide therapeutic options for certain diseases such as autoimmunity and cancer.

摘要

核因子-κB 诱导激酶(NIK)是一种激酶,可激活经典和非经典 NF-κB 途径,以控制某些蛋白质(如细胞因子、趋化因子和 NF-κB 信号分子)的转录表达。人们在理解 NIK 稳定性调节的分子机制以影响下游信号方面取得了许多进展。遗传小鼠模型表明,NIK 在免疫系统调节以及骨骼微环境中发挥着重要作用。越来越多的证据表明,NIK 与血液癌症(如多发性骨髓瘤)和实体瘤(如胰腺癌和黑色素瘤)的肿瘤发生有关。了解 NIK 失调的机制可能为某些疾病(如自身免疫和癌症)提供治疗选择。

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Tumor necrosis factor (TNF) signaling, but not TWEAK (TNF-like weak inducer of apoptosis)-triggered cIAP1 (cellular inhibitor of apoptosis protein 1) degradation, requires cIAP1 RING dimerization and E2 binding.肿瘤坏死因子(TNF)信号转导,但不是 TWEAK(TNF 样凋亡弱诱导剂)触发的 cIAP1(细胞凋亡抑制蛋白 1)降解,需要 cIAP1 RING 二聚体化和 E2 结合。
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