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RECEPTOR-LIKE KINASE 902 Associates with and Phosphorylates BRASSINOSTEROID-SIGNALING KINASE1 to Regulate Plant Immunity 被引量:8
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作者 Yaofei Zhao Guangheng Wu +1 位作者 Hua Shi Dingzhong Tang 《Molecular Plant》 SCIE CAS CSCD 2019年第1期59-70,共12页
Plants employ receptor-like kinases (RLKs)and receptor-like proteins for rapid recognition of invading pathogens,and RLKs then transmit signals to receptor-like cytoplasmic kinases (RLCKs)to activate immune responses.... Plants employ receptor-like kinases (RLKs)and receptor-like proteins for rapid recognition of invading pathogens,and RLKs then transmit signals to receptor-like cytoplasmic kinases (RLCKs)to activate immune responses.RLKs are under fine regulation mediated by subcellular trafficking,which contributes to proper activation of plant immunity.In this study,we show that Arabidopsisthaliana RECEPTOR-LIKE KINASE 902 (RLK902)plays important roles in resistance to the bacterial pathogen Pseudomonas syringae, but not to the fungal powdery mildew pathogen Golovinomyces cichoracearum.RLK902 localizes at the plasma membrane and associates with ENHANCED DISEASE RESISTANCE 4 (EDR4),a protein involved in clathrin-mediated trafficking pathways.EDR4 and CLATHRIN HEAVY CHAIN 2 (CHC2)regulate the subcellular trafficking and accumulation of RLK902 protein.Furthermore,we found that RLKg02 directly associates with the RLCK BRASSINOSTEROID-SIGNALING KINASE1 (BSK1),a key component of plant immunity,but not with other members of the FLAGELLIN SENSING 2 immune complex.RLK902 phosphorylates BSK1,and its Ser-230 is a key phosphorylation site critical for RLK902-mediated defense signaling. Taken together,our data indicate that EDR4 regulates plant immunity by modulating the subcellular trafficking and protein accumulation of RLK902,and that RLK902 transmits immune signals by phosphorylating BSK1. 展开更多
关键词 RLK902 BSK1 edr4 SUBCELLULAR TRAFFICKING PHOSPHORYLATION plant immunity
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融合受体eDR4/iFas提高sTRAIL对HT-29细胞凋亡的敏感性
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作者 李招发 王从阳 +1 位作者 邓小英 惠二京 《中国临床药理学与治疗学》 CAS CSCD 2014年第9期966-972,共7页
目的:探讨sTRAIL联合融合受体eDR4/iFas对HT-29细胞的凋亡作用。方法:采用PCR方法分别扩增eDR4和iFas,通过重叠PCR将两者连接起来组成融合受体基因eDR4/iFas,将其克隆到带Survivin启动子的表达载体上,另外采用组成型启动子CAG调控sTRAI... 目的:探讨sTRAIL联合融合受体eDR4/iFas对HT-29细胞的凋亡作用。方法:采用PCR方法分别扩增eDR4和iFas,通过重叠PCR将两者连接起来组成融合受体基因eDR4/iFas,将其克隆到带Survivin启动子的表达载体上,另外采用组成型启动子CAG调控sTRAIL表达。体外转染结直肠癌细胞株HT-29和人胚肾细胞HEK293,MTT法检测两种细胞的存活率,RTPCR和Western Blot检测目的蛋白的表达,Hoechst染色进一步分析eDR4/iFas联合sTRAIL对HT-29细胞的凋亡效果。结果:在HT-29细胞中,sTRAIL组的细胞存活率为40.9%±18.7%,而eDR4/iFas+sTRAIL组的细胞存活率为21.6%±9.1%,两者间存在统计学差异(P<0.05)。结论:eDR4/iFas能提高sTRAIL对HT-29细胞凋亡的敏感性,而对正常细胞HEK293没有毒副作用。 展开更多
关键词 STRAIL 融合受体 edr4/iFas Sur-vivin启动子 结直肠癌细胞株HT-29
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