کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2129885 | 1401567 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
LRRC14 attenuates Toll-like receptor-mediated NF-κB signaling through disruption of IKK complex
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Activation of NF-κB signaling plays pivotal roles in innate immune responses against pathogens. It requires strict control to avert inflammatory diseases. However, the mechanisms underlying this tight regulation are not completely understood. Here, we identified LRRC14, a novel member of LRR (leucine-rich repeat) protein family, as a negative regulator in TLR signaling. Expression of LRRC14 resulted in decreased activation of NF-κB, whereas knockdown of LRRC14 enhanced NF-κB activation as well as the production of inflammatory cytokines. Mechanistically, LRRC14 bound to HLH domain of IKKβ to block its interaction with NEMO and thereby inhibiting the phosphorylation of IKKβ and NF-κB activation. In addition, our data showed that TLR signaling led to lower expression of LRRC14. Together, LRRC14 may function as a checkpoint to prevent overzealous inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 347, Issue 1, 10 September 2016, Pages 65-73
Journal: Experimental Cell Research - Volume 347, Issue 1, 10 September 2016, Pages 65-73
نویسندگان
Chenglei Wu, Yexin Yang, Jiayu Ou, Liang Zhu, Wei Zhao, Jun Cui,