The Mechanism of CIRP in Regulation of STAT3 Phosphorylation and Bag-1/S Expression Upon UVB Radiation.
The Mechanism of CIRP in Regulation of STAT3 Phosphorylation and Bag-1/S Expression Upon UVB Radiation.
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DOI：
10.1111/php.12981
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发表时间：
2018-11
影响因子：
3.3
通讯作者：
Tong L
中科院分区：
文献类型：
--
作者：
Sun W;Liao Y;Yi Q;Wu S;Tang L;Tong L
冷诱导RNA结合蛋白（Cold-inducible RNA binding protein，CIRP）是一种应激诱导蛋白，可被低温、低氧、紫外线等多种细胞应激激活。我们之前的研究表明UVB（3 mJ/cm 2）诱导CIRP表达，其通过激活STAT 3-Bag-1/S信号级联促进角质形成细胞生长、存活并最终转化。然而，CIRP调节p-STAT 3活化和Bag-1/S表达的机制尚未完全阐明。在这项研究中，我们证明，反复暴露于UVB（3 mJ/cm 2）或CIRP的过表达可能会导致HaCaT细胞中Janus激酶（JAK）家族蛋白（JAK 2和JAK 3）的磷酸化水平升高。JAK的磷酸化增加与细胞中STAT 3（p-STAT 3）的磷酸化增加相关;使用JAK抑制剂I抑制JAK导致在有或没有UVB暴露的HaCaT和CIRP稳定转染的HaCaT细胞中STAT 3磷酸化和Bag-1/S表达减少。此外，我们的数据表明，使用BAY 11 -7085抑制CIRP的下游因子NF-κB也可以降低p-STAT 3。这些结果提示CIRP通过激活JAK和NF-κB信号通路介导STAT 3-Bag-1/S信号级联反应的激活。冷诱导RNA结合蛋白（CIRP）是一种可被紫外线激活的逆境诱导蛋白。在这项研究中，我们证明，反复暴露于UVB（3 mJ/cm 2）或CIRP的过度表达可能会导致HaCaT细胞中JAK家族蛋白的磷酸化水平升高。JAK的磷酸化增加与细胞中STAT 3（p-STAT 3）的磷酸化增加相关。此外，抑制NF-κB也可降低p-STAT 3。这些结果提示CIRP通过激活JAK和NF-κB信号通路介导STAT 3-Bag-1/S信号级联反应的激活。
Cold-inducible RNA binding protein (CIRP) is a stress-inducible protein, which could be activated by various cellular stresses, such as hypothermia, hypoxia and UV irradiation. Our previous study indicated that UVB (3 mJ/cm2) induces CIRP expression, which promotes keratinocytes growth, survival and eventually transformation via activation of STAT3-Bag-1/S signaling cascade. However, the mechanism(s) of CIRP in regulating p-STAT3 activation and Bag-1/S expression have not been fully elucidated. In this study, we demonstrate that repeated exposure of UVB (3 mJ/cm2) or overexpression of CIRP could lead to an elevation of the phosphorylation of Janus kinase (JAK) family proteins (JAK2 and JAK3) in HaCaT cells. The increased phosphorylation of the JAKs correlates to an increased phosphorylation of STAT3 (p-STAT3) in the cells; inhibiting JAKs using JAK inhibitor I lead to a reduction of STAT3 phosphorylation and Bag-1/S expression in the HaCaT and CIRP stably transfected HaCaT cells with or without UVB exposure. Furthermore, our data indicated that inhibiting the downstream factor of CIRP, NF-κB, using BAY11–7085 could also decrease the p-STAT3. These results lead us to propose that CIRP mediates the activation of STAT3-Bag-1/S signaling cascade via activating the JAKs and NF-κB signaling pathways. Cold-inducible RNA binding protein (CIRP) is a stress-inducible protein, which could be activated by UV irradiation. In this study, we demonstrate that repeated exposure of UVB (3 mJ/cm2) or overexpression of CIRP could lead to an elevation of the phosphorylation of JAK family proteins in HaCaT cells. The increased phosphorylation of the JAKs correlates to an increased phosphorylation of STAT3 (p-STAT3) in the cells. In addition, inhibiting NF-κB could also decrease p-STAT3. These results lead us to propose that CIRP mediates the activation of STAT3-Bag-1/S signaling cascade via activating the JAKs and NF-κB signaling pathways.
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影响因子：
3.7
作者：
Iotzova-Weiss G;Freiberger SN;Johansen P;Kamarachev J;Guenova E;Dziunycz PJ;Roux GA;Neu J;Hofbauer GFL
通讯作者：
Hofbauer GFL
影响因子：
5.7
作者：
Sakurai T;Yada N;Watanabe T;Arizumi T;Hagiwara S;Ueshima K;Nishida N;Fujita J;Kudo M
通讯作者：
Kudo M
富含甘氨酸的RNA结合蛋白，介导了对哺乳动物细胞生长的冷诱导抑制。
影响因子：
7.8
作者：
Nishiyama, H;Itoh, K;Kaneko, Y;Kishishita, M;Yoshida, O;Fujita, J
通讯作者：
Fujita, J
垂体腺瘤中可冷诱导的RNA结合蛋白（CIRP）的表达及其与肿瘤复发的关系。
DOI：
10.12659/msm.893128
发表时间：
2015-05-02
期刊：
Medical science monitor : international medical journal of experimental and clinical research
影响因子：
--
作者：
Wang M;Zhang H;Heng X;Pang Q;Sun A
通讯作者：
Sun A
影响因子：
6.5
作者：
Mempel, M;Voelcker, V;Ollert, M
通讯作者：
Ollert, M