李隽
目前主要开展肿瘤病理生理的基础研究,包括探索原癌基因 AEG-1 诱导肿瘤发生发展的分子机制及炎症信号通路 NF- k B 在肿瘤发生中的表观调节机制等。
个性化签名
- 姓名:李隽
- 目前身份:
- 担任导师情况:
- 学位:
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学术头衔:
教育部“新世纪优秀人才支持计划”入选者, 博士生导师
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学科领域:
病理学
- 研究兴趣:目前主要开展肿瘤病理生理的基础研究,包括探索原癌基因 AEG-1 诱导肿瘤发生发展的分子机制及炎症信号通路 NF- k B 在肿瘤发生中的表观调节机制等。
李隽 教授、博士
中山大学基础医学院生物化学教研室
教育背景:
李隽 , 男 , 中山大学 教授, 博士生导师。 1999 年获中国药科大学博士学位, 2000-2006 年先后在美国麻省新英格兰医疗中心及美国西北大学担任博士后及助理研究员,进行有关乳腺癌病理、其发病机制及中心体复制与肿瘤发生发展机制的研究。 2006 年 11 月,申请者作为中山大学“百人计划”引进人才回国。 2007 年入选教育部“新世纪优秀人才支持计划” 目前主要开展肿瘤病理生理的基础研究,包括探索原癌基因 AEG-1 诱导肿瘤发生发展的分子机制及炎症信号通路 NF- k B 在肿瘤发生中的表观调节机制等。 上述领域的工作 已在 JCI , Oncogene , Cancer res, Clin. Cancer Res 等 SCI 杂志上发表。
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【期刊论文】ORIGINAL ARTICLE DSS1 is required for the stability of BRCA2
李隽, J Li, C Zou, Y Bai, DE Wazer, V Band and Q Gao
Oncogene (2005), 1-9,-0001,():
-1年11月30日
DSS1 is an evolutionarily conserved acidic protein that binds to BRCA2. However, study of the function of DSS1 in mammalian cells has been hampered because endogenous DSS1 has not been detectable by Western blotting. Here, we developed a modified Western blotting protocol that detects endogenous DSS1 protein, and used it to study the function of DSS1 and its interaction with BRCA2 in mammalian cells. We found that essentially all BRCA2 in human cell lines is associated with DSS1. Importantly, we found that RNAi knockdown of DSS1 in human cell lines led to dramatic loss of BRCA2 protein, mainly due to its increased degradation. Furthermore, the stability of BRCA2 mutant devoid of the DSS1-binding domain is unaffected by the depletion of DSS1. Most notably, like BRCA2 depletion, DSS1 depletion also led to hypersensitivity to DNA damage. These results demonstrated that the stability of BRCA2 protein in mammalian cells depends on the presence of DSS1. Deletion or mutation of DSS1 or suppression of its expression by other mechanisms are therefore potential causative mechanisms for human breast and ovarian cancer. Such mechanisms may be relevant to sporadic as well as familiar breast cancer where BRCA1 and BRCA2 mutations are not present.
DSS1, BRCA2, DNA damage repair, tumor, suppressor gene, protein degradation, breast cancer
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