MG132型
IκB激酶
αBκ
孤雌内酯
蛋白酶体抑制剂
NFKB1型
磷酸化
硼替佐米
信号转导
癌症研究
转录因子
化学
激酶
细胞生物学
NF-κB
细胞凋亡
蛋白酶体
生物
生物化学
免疫学
多发性骨髓瘤
基因
作者
Sajjad Molavi Pordanjani,Seyed Jalal Hosseinimehr
标识
DOI:10.2174/0929867323666160824162718
摘要
It is well documented that ionizing radiation (IR) activates the transcription factor (NF-κB) which is a trigger for resistance cancer cells to treatment. It is involved in activation of pro-survival signaling pathways and resulting in cancer development and progression. In unstimulated condition, NF-κB is sequestered in cytoplasm but after the cell exposure to IR, proteasomal degradation of IκB flowing phosphorylation via IKK, leads to aberrantly NF-κB activation and nuclear translocation. Therefore, interruption in IκB degradation, proteasome action, IKK phosphorylation and NF-κB nuclear translocation provide robust strategies for inhibiting adverse effect of IR induced NF-κB. In spite of uncompleted elucidation of NF-κB molecular mechanisms, different NF-κB inhibitors have been used in order to inhibiting the IR induced NF-κB. The aim of this review is to highlight the role of IR induced-NF-κB inhibitors such as MG132, bortezomib, curcumin, DHMEQ, naringin, sorafenib, genistein and parthenolide in suppression of IR induced NF-κB adverse effects. Moreover, their chemical, structural characteristics and molecular mechanisms will be discussed.
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