徐振陆牛海霞李定柴蔚然张琳刘俊岭△.多肽LSARLAF 直接引发整合素活化及信号传导的研究[J].,2012,12(6):1009-1012 |
多肽LSARLAF 直接引发整合素活化及信号传导的研究 |
Peptide LSARLAF Directly Stimulate αIIbβ3 Activationand Outside-in Signaling |
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DOI: |
中文关键词: 多肽LSARLAF 整合素IIb 3 信号传导 |
英文关键词: LSARLAF Integrin αIIbβ3 |
基金项目:国家自然科学基金(81030039 to J. L.) (81000204 to D. L.),上海浦江计划(09PJ1406800 to J. L) |
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中文摘要: |
目的:研究LSA 引起信号传递以及PLC 2 诱导的血小板聚集和分泌的作用。方法:通过酶联免疫吸附配体- 受体结合及血
小板聚集和分泌实验,研究LSA 诱导血小板活化的作用及参与的信号分子。结果:LSA 引起了整合素IIb 3 上LIBS 表位表达明显
增加,PLC 2 可能以一种酪氨酸活化依赖性的方式参与了这种信号传递。结论:LSA 引起的信号传递是由β3 介导的,并且LSA 可
引起不依赖于聚集的活化剂的分泌,而这些活化剂能引发聚集依赖性IIb 3 信号传递。 |
英文摘要: |
Objective: To investigate the LSA-mediated signal transduction and to investigate PLC 2-induced platelet aggregation
and secretion. Methods: LSA-induced platelet activation and signaling molecules involved were studied by enzyme-linked
immunosorbent assay ligand - receptor binding and platelet aggregation and secretion experiments. Results:αIIbβ3 on the LIBS epitope
expression increased significantly by LSA. PLC 2 tyrosine activation may be involved in this signaling. Conclusion: LSA-mediated signal
transduction was mediated by the β3. LSA could cause activator secretion which was not depend on the aggregation, and it could lead to
aggregation activator-dependentαIIbβ3 signaling. |
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