标题:beta-Arrestin 1 ' s Interaction with TC45 Attenuates Stat signaling by dephosphorylating Stat to inhibit antimicrobial peptide expression
作者:Sun, Jie-Jie; Yang, Hui-Ting; Niu, Guo-Juan; Feng, Xiao-Wu; Lan, Jiang-Feng; Zhao, Xiao-Fan; Wang, Jin-Xing
作者机构:[Sun, Jie-Jie; Yang, Hui-Ting; Niu, Guo-Juan; Feng, Xiao-Wu; Lan, Jiang-Feng; Zhao, Xiao-Fan; Wang, Jin-Xing] Shandong Univ, Shandong Prov Key Lab Ani 更多
通讯作者:Wang, JX
通讯作者地址:[Wang, JX]Shandong Univ, Shandong Prov Key Lab Anim Cells & Dev Biol, Sch Life Sci, Jinan 250100, Shandong, Peoples R China.
来源:SCIENTIFIC REPORTS
出版年:2016
卷:6
DOI:10.1038/srep35808
摘要:Impaired phosphatase activity leads to the persistent activation of signal transducers and activators of transcription (Stat). In mammals, Stat family members are often phosphorylated or dephosphorylated by the same enzymes. To date, only one Stat similar to mammalian Stat5a/b has been found in crustaceans and there have been few studies in Stat signal regulation in crustaceans. Here, we report that beta-arrestin1 interacts with TC45 (45-kDa form of T cell protein tyrosine phosphatase) in the nucleus to attenuate Stat signaling by promoting dephosphorylation of Stat. Initially, we showed that Stat translocates into the nucleus to induce antimicrobial peptide (AMP) expression after bacterial infection. beta Arr1 enters the nucleus of hemocytes and recruits TC45 to form the beta arr1-TC45-Stat complex, which dephosphorylates Stat efficiently. The interaction of TC45 with Stat decreased and Stat phosphorylation increased in beta arr1-silenced shrimp (Marsupenaeus japonicus) after challenge with Vibrio anguillarum. beta Arr1 directly interacts with Stat in nucleus and accelerates Stat dephosphorylation by recruiting TC45 after V. anguillarum challenge. Further study showed that beta arr1 and TC45 also affect AMP expression, which is regulated by Stat. Therefore, beta arr1 and TC45 are involved in the anti-V. anguillarum immune response by regulating Stat activity negatively to decrease AMP expression in shrimp.
收录类别:SCIE
WOS核心被引频次:1
资源类型:期刊论文
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