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Two novel gene-specific markers at the Pik locus facilitate the application of rice blast resistant alleles in breeding 被引量:3
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作者 TIAN Da-gang CHEN Zi-qiang +6 位作者 LIN Yan CHEN Zai-jie LUO Jia-mi JI Ping-sheng YANG Li-ming WANG Zong-hua WANG Feng 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2021年第6期1554-1562,共9页
Blast,a disease caused by Magnaporthe oryzae,is a major constraint for rice production worldwide.Introgression of durable blast resistance genes into high-yielding rice cultivars has been considered a priority to cont... Blast,a disease caused by Magnaporthe oryzae,is a major constraint for rice production worldwide.Introgression of durable blast resistance genes into high-yielding rice cultivars has been considered a priority to control the disease.The blast resistance Pik locus,located on chromosome 11,contains at least six important resistance genes,but these genes have not been widely employed in resistance breeding since existing markers hardly satisfy current breeding needs due to their limited scope of application.In this study,two PCR-based markers,Pikp-Del and Pi1-In,were developed to target the specific In Del(insertion/deletion)of the Pik-p and Pi-1 genes,respectively.The two markers precisely distinguished Pik-p,Pi-1,and the K-type alleles at the Pik locus,which is a necessary element for functional genes from rice varieties.Results also revealed that only several old varieties contain the two genes,of which nearly half carry the K-type alleles.Therefore,these identified varieties can serve as new gene sources for developing blast resistant rice.The two newly developed markers will be highly useful for the use of Pik-p,Pi-1 and other resistance genes at the Pik locus in markerassisted selection(MAS)breeding programs. 展开更多
关键词 rice blast disease molecular marker pik-p pi-1 K-type alleles
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p53通过调控p55PIK抑制肝细胞癌SMMC-7721细胞的增殖 被引量:3
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作者 傅寅佳 杨熹 +4 位作者 曹小年 来森艳 王桂华 胡俊波 李襄 《华中科技大学学报(医学版)》 CAS CSCD 北大核心 2015年第3期247-250,共4页
目的探讨p55PIK对肝癌SMMC-7721细胞增殖能力的影响,及p55PIK上游可能的调控机制。方法以肝癌SMMC-7721细胞为研究对象,通过脂质体转染p55PIK特异性小干扰RNA(siRNA)si-p55构建p55PIK低表达的实验模型。通过CCK8检测p55PIK对肝癌SMMC-7... 目的探讨p55PIK对肝癌SMMC-7721细胞增殖能力的影响,及p55PIK上游可能的调控机制。方法以肝癌SMMC-7721细胞为研究对象,通过脂质体转染p55PIK特异性小干扰RNA(siRNA)si-p55构建p55PIK低表达的实验模型。通过CCK8检测p55PIK对肝癌SMMC-7721细胞增殖能力的影响。通过流式细胞术检测p55PIK对细胞周期进程的影响。转染针对p53的小干扰RNA(siRNA)si-p53低表达p53,采用Western blot检测p53对p55PIK表达的影响,并通过CCK8法检测p53对p55PIK在肝癌细胞增殖调控中的作用。结果低表达p55PIK可导致肝癌SMMC-7721细胞的增殖能力降低[转染后96h,si-NC组、si-p55组的A值分别为(1.325±0.050)、(1.183±0.019)],细胞周期G0/G1期阻滞[si-NC组:(39.07±2.02)%;si-p55组:(49.66±1.05)%]。低表达p53可在肝癌SMMC-7721细胞中上调p55PIK的表达。p55PIK可部分拮抗p53对肝癌SMMC-7721细胞增殖的抑制作用。结论p53可部分通过调控p55PIK抑制肝癌SMMC-7721细胞的增殖。 展开更多
关键词 肝癌 p55pik p53 细胞增殖
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