于晓光
主要从事前列腺癌转移相关分子机制、寻找治疗前列腺癌的药物或辅助治疗药物以及与中国科学院动物所合作研究胚胎植入的分子机理等方面的研究工作。
个性化签名
- 姓名:于晓光
- 目前身份:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
生物化学
- 研究兴趣:主要从事前列腺癌转移相关分子机制、寻找治疗前列腺癌的药物或辅助治疗药物以及与中国科学院动物所合作研究胚胎植入的分子机理等方面的研究工作。
于晓光 女 1963年生,现任哈尔滨医科大学基础医学学院生物化学与分子生物学教研室副主任,医学博士,教授,博士生导师;中国生物化学与分子生物学会理事,黑龙江省生物化学与分子生物学会副理事长;国家自然基金一审评审专家,教育部博士点基金评审专家,中国高校科技进步奖评审专家,黑龙江省自然基金、黑龙江省海外学人基金、黑龙江省教育厅等基金的评审专家;《中国药理学通报》、《吉林大学学报》(理学版)、《生命科学研究》、《哈尔滨医科大学学报》审稿专家。 1987.7毕业于吉林大学分子生物学系生物化学专业,同年分配到哈尔滨医科大学生物化学与分子生物学教研室任助教,1993.9晋升为讲师,1999.晋升为副教授,2002.9拔尖晋升为教授至今;期间1989.9 ~ 1992.7在哈尔滨医科大学攻读硕士学位,1997.9 ~ 2000.7攻读博士学位,1998.5 ~ 2000.5作为客座研究员到中国科学院动物研究所生殖生物学国家重点实验室从事胚胎植入机理的研究工作;2008.3~2009.3作为访问学者到美国Purdue University 生物系主要从事骨生长和发育生物学领域的研究工作。近5年来,作为项目负责人主要从事前列腺癌转移相关分子机制、寻找治疗前列腺癌的药物或辅助治疗药物以及与中国科学院动物所合作研究胚胎植入的分子机理等方面的研究工作。目前作为课题负责人主持两项国家自然科学基金 (2008.1-2010.12)、(2010.1-2012.12)和中国科学院动物所国家重点开放实验室基金 (2007.5-2009.5)、黑龙江省自然科学基金 (2008.1-2010.12)、黑龙江省教育厅资助课题 (2008.1-2010.12)、黑龙江省卫生厅资助课题(2007.1-2009.12)、哈尔滨市创新人才优秀学科带头人专项基金项目(2008.1-2010.12)等多项科研课题;目前科研经费近80万元,以通讯作者发表科研论文30余篇,其中SCI收录5篇;获中国高校科技进步二等奖一项,黑龙江省科技进步二等奖一项,黑龙江省高校科技进步一等奖一项;目前共培养硕士研究生近20名,已毕业12名,博士研究生5名,已毕业1名。 于晓光教授曾获黑龙江省“优秀教师”、哈尔滨医科大学“优秀教师”、哈尔滨医科大学“教学标兵”、哈尔滨医科大学“巾帼文明示范岗先进个人”的光荣称号和哈尔滨医科大学“课堂教学”一等奖。
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1923
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0
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成果阅读
154
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成果数
3
于晓光, YU Xiaoguang , , LI Qinglei , WANG Hongmei , LUO Wenxiang , SHAO Longjiang , NI Jiang & ZHU Cheng
Chinese Science Bulletin, 2002, 47(12)1011~1014,-0001,():
-1年11月30日
The expression and regulation of metalloproteinases-2,-9(MMP-2,-9) and their tissue inhibitors TIMP-1,-2,-3mRNA were studied in this experiment. In the PMSGhCG primed pseudopregnant rat, MMP-2,-9mRNA levels were the highest at Day 1, decreased from Day 4, and reached the minimal level at Day 8, then increased at Day 14; no significant changes were observed in TIMP-2 mRNA expression from Day 1 to Day 14; TIMP-3 mRNA expression was the lowest at Day 1, increased from Day 4, reached the maximal level at Day 8, and persisted to Day 14. TNF-a could significantly increase the expression of MMP-2,-9 and TIMP-1 mRNA in the in vitro perfused pseudopregnant CL, and decrease the expression of TIMP-3 mRNA, but had no effect on TIMP-2 mRNA expression. The results indicate that MMP-2,-9and TIMP-1,-2,-3 might be involved in the regulation of CL function and maintenance of CL structure via their coordinated gene expression. TNF-a could inhibit luteal regression via increasing MMP-2,-9andTIMP-1 mRNA in the in vitro perfused pseudopregnant ovary.
matrix metalloproteinases,, tissue inhibitors of metalloproteinases,, mRNA,, corpusluteum,, ovary perfusion.,
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于晓光, 刘洋, 林平, 刘鑫
《生命的化学》,2005,25(4):292~294,-0001,():
-1年11月30日
α肿瘤坏死因子转换酶(tumor necrosis factor-αconverting enzyme,TACE)是ADAM蛋白质家族的成员之一,又称ADAM17。TACE是锚定于细胞膜的细胞表面的蛋白质,是一种多结构域的Ⅰ型跨膜蛋白,具有显著的金属蛋白酶水解活性,对TNF-α前体有水解作用。TACE 的胞内区富含脯氨酸,并包含一个潜在的磷酸化位点KKLDKQYESL,该位点具有和SH3区域相结合的潜能;很可能具有信号转导的功能,或对亚细胞定位有重要作用。
TACE, ADAM, 跨膜蛋白, 结构域, 信号转导
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【期刊论文】Expression and location of Smad2, 4 mRNAs during and after liver fibrogenesis of rats
于晓光, Yang Liu, Li-Feng Wang, Hai-Feng Zou, Xiao-Yan Song, Hua-Feng Xu, Ping Lin, Hai-Hong Zheng, Xiao-Guang Yu
World J Gastroenterol, 2006, 12(10)1577~1582,-0001,():
-1年11月30日
AIM; To investigate the location alteration of Smad2 and Smad4 mRNAs in the liver during and after fibrogenesis in rats. METHODS; Eighty male Wistar rats weighing approximately 200g each were used. The rat models of experimental hepatic fibrosis were established by injection with carbon tetrachloride(CCl4), normal rats and rats were injected with olive oil and served as control groups. In situ hybridization(ISH)was used to detect the Smad2 and Smad4 mRNA in liver. RESULTS; In situ hybridization showed Smad2 and Smad4 mRNA expressions in the cytoplasm of hepatic stellate cells(HSC), fibroblasts and myofibroblasts around the central vein and hepatic sinus during and after fibrogenesis. Expression of Smad2, 4 mRNA was higher than that in normal and control rats. CONCLUSION; In the process of and after hepatic fibrosis formation, HSC, fibroblasts and myofibroblasts are the major cells that express Smad2 and Smad4. The more serious the hepatic fibrosis is in the injured liver, the higher the level of Smad2 and Smad4 gene expression is during and after fibrogenesis respectively.
Smad2, Smad4, mRNA, Liver fibrogenesis
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