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1.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

2.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

3.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

4.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

5.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

6.
c-Jun N-terminal kinases (JNK) is one of the important members of mitogen activated protein kinase family. JNK pathway participates in the apoptosis of pancreatic beta ceil. Beta cell apoptosis can be induced by IL-1β,TNF-α/IFN-γ,and inhibited by exendin-4, L-isoform of JNK inhibitor. New target may be provided through regulating JNK signal pathway.  相似文献   

7.
尽管对2型糖尿病时胰岛β细胞功能受损及凋亡的具体机制目前尚不清楚,但研究发现糖尿病时诱导或加重的内质网应激及氧化应激可导致胰岛β细胞功能损伤,尤其是c-Jun氨基端激酶通路作为两者的共同通路在其中发挥着重要作用.  相似文献   

8.
c-Jun氨基末端激酶信号转导途径与胰岛β细胞凋亡   总被引:1,自引:0,他引:1  
甲状腺激素受体 (TR)为配体依赖性转录因子。未结合T3 的TR与辅阻遏因子等形成复合物 ,此复合物通过使局部的组蛋白去乙酰化而使局部染色质变得紧密 ,进而抑制靶基因的基础转录。结合了T3 的TR与辅阻遏因子解离 ,转录恢复到基础水平。随后辅激活因子与结合了T3 的TR形成复合物 ,此复合物通过使组蛋白乙酰化而使局部染色质变得松弛 ,进而激活靶基因的转录。辅激活因子复合物还能使RNA聚合酶稳定 ,从而促进转录  相似文献   

9.
c-Jun氨基末端激酶信号转导途径与胰岛β细胞凋亡   总被引:1,自引:0,他引:1  
心脏是醛固酮作用的重要靶器官之一 ,而心脏本身也具有合成与分泌醛固酮的能力 ,后者以自分泌或(和 )旁分泌的形式调节心肌细胞的功能。心脏的心肌细胞、纤维细胞和血管内皮细胞包含的特异性盐皮质激素受体 ,在醛固酮介导的心血管系统病理生理变化中发挥重要作用。  相似文献   

10.
目前非酒精性脂肪性肝病(NAFLD)的发病率日益增加,但其发病机制至今仍不清楚.c-Jiln氨基末端激酶是进化上保守的富含丝氨酸/苏氨酸的蛋白激酶家族成员之一,它与多种疾病的发病机制有关.近年来研究发现,c-Jun氨基末端激酶在NAFLD发病机制中具有重要作用,尤其是两种不同亚型在其中的独特作用更加引人关注.  相似文献   

11.
促甲状腺素受体抗体检测的临床意义   总被引:1,自引:0,他引:1  
促甲状腺素受体抗体 (TRAb)与多种自身免疫性甲状腺疾病的发病密切相关 ,是临床诊断这些疾病的重要指标。TRAb在功能上可分为甲状腺刺激性抗体 (TSAb)和甲状腺刺激阻断性抗体(TSBAb) ,可与促甲状腺素受体分子上不同位点结合产生不同生物学效应。其中TSAb可引起Graves病 (GD)患者甲状腺功能亢进和弥漫性甲状腺肿的发生 ,而TSBAb则可导致自身免疫性甲状腺功能减退症 (甲减 )患者甲减的发生。本文将对TRAb检测在GD鉴别诊断、辅助制定GD治疗方案、抗甲状腺药物疗效及预测复发、筛查自身免疫性甲减等方面的临床价值作一全面综述。  相似文献   

12.
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