Saving β cell function in the NIK of time.
Saving β cell function in the NIK of time.
复制标题
保存β细胞功能在NIK的时间。
DOI：
10.1084/jem.2128insight2
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发表时间：
2015
期刊：
影响因子：
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通讯作者：
Rane,SushilG
中科院分区：
文献类型：
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作者：
Tarbell,KristinV;Rane,SushilG
2型糖尿病是一种胰岛素抵抗性疾病，B细胞功能对维持正常水平的胰岛素产生很重要。经典NF-kB信号通路已被充分研究，但对胰岛功能障碍背景下的非经典NF-kB通路知之甚少。在这个问题上，Malle等证明了非经典NF-κ B诱导激酶（NIK）是饮食诱导肥胖症中B细胞功能的负调节因子。在经典的NF-κ B通路中，IKK激活导致IkBa降解和p50的核转位。相反，在非经典的NF-κ B通路中，p100被加工成p52，其与RelB复合用于核定位和转录调节。NIK激活p100加工，是这种非经典NF-kB通路的中心调节因子。
Type 2 diabetes is a disease of insulin resistance, and b cell function is important for maintaining normal levels of insulin production. The canonical NF-kB signaling pathway has been well studied, but little is known about the noncanonical NF-kB pathway in the context of pancreatic islet dysfunction. In this issue, Malle et al. demonstrate that the noncanonical NF-kB–inducing kinase (NIK) is a negative regulator of b cell function in diet-induced obesity. In the canonical NF-kB pathway, IKK activation leads to IkBa degradation and nuclear translocation of p50. In contrast, in the noncanonical NF-kB pathway, p100 is processed into p52 that complexes with RelB for nuclear localization and transcription regulation. NIK activates p100 processing and is a central regulator of this noncanonical NF-kB pathway.