李朝军
1.细胞分裂调控研究。2. 细胞应激的信号传递研究。3. HGF促进细胞离散的分子机制研究。
个性化签名
- 姓名:李朝军
- 目前身份:
- 担任导师情况:
- 学位:
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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:1.细胞分裂调控研究。2. 细胞应激的信号传递研究。3. HGF促进细胞离散的分子机制研究。
李朝军
个人经历:
1984年进入南京大学生物系动物专业学习,1988年于南京大学生物系攻读硕士学位,1991年南京大学生物系攻读博士研究生,1994年毕业获博士学位。1994年到2008年南京师范大学生命科学学院任特聘教授。2008年聘为南京大学医学院教授,博士生导师。曾任南京师范大学江苏省分子医学生物技术重点实验室主任,生命科学学院分子细胞生物学研究所所长。1996年到1998年于香港科技大学做博士后。1999年6月到2000年5月在美国耶鲁大学医学院做博士后。2001、2002及2004年到美国匹兹堡大学医学院做短期访问。
先后主持参加国家自然科学基金6项(目前主持国家自然科学基金1项),参加国家自然科学基金重点课题一项,主持科技部“十五”攻关重大项目开放课题一项,主持江苏省自然科学基金2项,教育部青年基金一项。已在国内外发表论文100余篇,34篇论文为SCI收录。
研究方向\兴趣:
1.细胞分裂调控研究:采用FRET方法研究蛋白质在活细胞内的空间和时间的相互作用,采用CALI方法在活细胞内实时淬灭蛋白质的活性研究其功能,使细胞成为一个“微试管”。目前研究细胞胞质分裂的启动和完成的时空调控。
2. 细胞应激的信号传递研究:研究细胞在低氧、血清饥饿、高糖等应激状态下MAPK-Egr-1-GGPPS信号通路的作用。我们发现,早期应激反应转录因子Egr-1可以通过激活GGPPS表达,影响Ras的异戊二烯化修饰,对胰岛素抵抗的形成起调控作用。
3. HGF促进细胞离散的分子机制研究:我们发现肝细胞生长因子HGF可以通过激活经典的Wnt信号途径,激活MMP7的表达,MMP7通过降解E-cadherin促进了细胞的离散。
科研项目:
1.国家重大科学研究计划“蛋白质整体功能的在体遗传操作新技术新方法研究”子项目:“利用小鼠DNA大片段定向敲除新技术新方法分析黑色素肿瘤抗原蛋白质家族整体功能” 2009-2013
2.国家重大科学研究计划 “心脏发育与血管发生过程中的信号调控机制研究”子项目“心脏发育的离子通道和应激信号通路的作用” 2007-20011
3.国家自然科学基金“EGR-1调控胰岛素诱发的PI3K/Akt和MAPK信号传递”2007-2009
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主页访问
1071
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关注数
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成果阅读
324
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成果数
6
李朝军, Haixiang Sun a, b, , Linjun Chen b, Guijun Yan b, Ruina Wang a, Zhenyu Diao b, Yali Hub, Chaojun Li a, c, *
Biochemical and Biophysical Research Communications 379 (2009) 16-21,-0001,():
-1年11月30日
Implantation is the first maternal-embryo crosstalk that only occurs during a finite period called the, implantation window'. HOXA10, a homeobox transcription factor, plays an important regulatory role during this period. However, the target genes of HOXA10 involved in implantation and decidualization have not been identified. Using a chromatin immunoprecipitation screen, we identified the p300/CBPassociated factor (p/CAF) as a direct HOXA10 target gene in vivo. Adenovirus-mediated overexpression and siRNA-specific knockdown of HOXA10 altered p/CAF promoter activity via interaction with the three consecutive TTAT element units in human endometrial cells. These results indicate that p/CAF is a novel HOXA10 target gene, and HOXA10 promotes human endometrial development, at least in part, through the regulation of p/CAF gene.
HOXA10, p/, CAF, Endometrium
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李朝军, Jun Yuan a, b, Guo-Xin Shi a, Yue Shao a, Gu Daia, Jun-Ning Wei a, Donald C. Changc, ∗, Chao-Jun Li a, ∗∗
The International Journal of Biochemistry & Cell Biology 40 (2008) 284-293,-0001,():
-1年11月30日
Calmodulin (CaM) is a major cytoplasmic calcium receptor that performs multiple functions including cell motility. To investigate the mechanism of the regulation of CaM on cell morphology and motility, first we checked the distribution of CaM in the living cells using GFP-CaM as an indicator. We found that GFP-CaM showed a fiber-like distribution pattern in the cytosol of living Potorous tridactylis kidney (PtK2) cells but not in living HeLa cells. The endogenous CaM in heavily permeabilized HeLa was also found to display a fiber-like distribution pattern. Further examination showed that the distribution pattern of GFP-CaM was same as that of stress fibers, but not microtubules. Co-immunoprecipitation also showed that CaM can interact with actin directly or indirectly. The microinjection of trp peptide, a specific inhibitor of CaM, attenuated the polymerization of stress fibers and induced the alteration of cell morphology. A wound-healing assay and a single cell tracking experiment showed that CaM in PtK2 cells could increase cell motility. The data we have got from living cells suggested that CaM affect cell morphology and motility through binding to stress fibers and regulate f-actin polymerization.
Calmodulin, Stress fiber, Actin, Morphology, Motility
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李朝军, Jie Chena, , Gu Daia, c, Yi-Qian Wanga, Sheng Wanga, Fei-Yan Pana, Bin Xuea, Dong-Hong Zhaoa, Chao-Jun Lia, b, *
FEBS Letters 580 (2006) 3624-3630,-0001,():
-1年11月30日
Ultraviolet (UV) irradiation can result in cell cycle arrest. The reactivation of Polo-like kinase 1 (Plk1) is necessary for cell cycle reentry. But the mechanism of how Plk1 regulates p53 in UV-induced mitotic arrest cells remained elusive. Here we find that UV treatment leads HEK293 cells to inverse changes of Plk1 and p53. Over-expression of Plk1 rescue UV-induced mitotic arrest cells by inhibiting p53 activation. Plk1 could also inhibit p53 phosphorylation at Ser15, thus facilitates its nuclear export and degradation. Further examination shows that Plk1, p53 and Cdc25C can form a large complex. Plk1 could bind to the sequence-specific DNA-binding domain of p53 and active Cdc25C by hyperphosphorylation. These results hypothesize that Plk1 and Cdc25C participate in recovery the mitotic arrest through binding to the different domain of p53. Cdc25C may first be actived by Plk1, and then its phosphatase activity makes p53 dephosphorylated at Ser15.
Polo-like kinase 1, p53, Cdc25C, UV, Mitosis arrest
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李朝军, Sheng-Zhou Zhang, , Fei-Yan Pan, Jian-Feng Xu, Jun Yuan, Shi-Ying Guo, Gu Dai, Bin Xue, Wei-Gan Shen, Chuan-Jun Wen, Dong-Hong Zhao, and Chao-Jun Li
Mol Cancer Ther 2005; 4(10). October 2005,-0001,():
-1年11月30日
c-Met is highly expressed and constitutively activated in various human tumors. We employed adenovirus-mediated RNA interference technique to knock down c-Met expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. Among the five hepatocellular carcinoma and one normal human liver cell lines we analyzed, c-Met was highly expressed and constitutively tyrosine phosphorylated in only MHCC97-L and HCCLM3 hepatocellular carcinoma cells. Knockdown of c-Met could inhibit MHCC97-L cells proliferation by arresting cells at G0-G1 phase. Soft agar colony formation assay indicated that the colony forming ability of MHCC97-L cells decreased by f70% after adenovirus AdH1-small interfering RNA (siRNA)/met infection. In vivo experiments showed that adenovirus AdH1-siRNA/met inhibited the tumorigenicity of MHCC97-L cells and significantly suppressed tumor growth when injected directly into tumors. These results suggest that knockdown of c-Met by adenovirus-delivered siRNA may be a potential therapeutic strategy for treatment of hepatocellular carcinoma in which c-Met is overexpressed.
c-Met is a transmembrane tyrosine kinase receptor for hepatocyte growth factor/, scatter factor encoded by the c-met proto-oncogene (, 1-3), ., It is composed of a 50 kDa
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【期刊论文】Calmodulin regulates the post-anaphase reposition of centrioles during ytokinesis
李朝军, Yue Yue YU, Gu DAI, Fei Yan PAN, Jie CHEN, Chao Jun LI*
Cell Research, 15(7): 548-552, July 2005,-0001,():
-1年11月30日
A transient postanaphase repositioning of the centriole is found to control the completion of cytokinesis. Using a green fluorescent protein-calmodulin fusion protein as a living cell probe, we have previously found that calmodulin is associated with the initiation and progression of cytokinesis. In this study, we further studied the effect of calmodulin on the repositioning of the centriole and subsequent cell cycle progression. When activity of calmodulin is inhibited, the regression of the centriole from the intercellular bridge to the cell center is blocked, and thus the completion of cell division is repressed and two daughter cells are linked by longer cell bridge in perturbed cells. W7 treatment during cytokinesis also results in unfinished cytokinesis and stopped G1 phase. These results suggest that calmodulin activity is required for centriole repositioning and can affect the completion of cytokinesis and cell cycle progression.
CaM,, centriole reposition,, cytokinesis,, W7.,
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李朝军, Wen Ning*†, Chao-Jun Li*†‡, Naftali Kaminski*, Carol A. Feghali-Bostwick*, Sean M. Alber§, Yuanpu P. Di¶, Sherrie L. Otterbein*, Ruiping Song*, Shizu Hayashi, Zhihong Zhou*, David J. Pinsky**, Simon C. Watkins§, Joseph M. Pilewski*, Frank C. Sciurba*, David G. Peters*, James C. Hogg, and Augustine M. K. Choi*††
PNAS, October 12, 2004, vol. 101, no.41, 14895-14900,-0001,():
-1年11月30日
To better understand the molecular basis of chronic obstructive pulmonary disease (COPD), weused serial analysis of gene expression (SAGE) and microarray analysis to compare the gene expression patterns of lung tissues from COPD and control smokers. A total of 59, 343 tags corresponding to 26,502 transcripts were sequenced in SAGE analyses. A total of 327 genes were differentially expressed (1.5-fold up-or down-regulated). Microarray analysis using the same RNA source detected 261 transcripts that were differentially expressed to a significant degree between GOLD-2 and GOLD-0 smokers. We confirmed the altered expression of a select number of genes by using real-time quantitative RT-PCR. These genes encode for transcription factors (EGR1 and FOS), growth factors or related proteins (CTGF, CYR61, CX3CL1, TGFB1, and PDGFRA), and extracellular matrix protein (COL1A1). Immunofluorescence studies on the same lung specimens localized the expression of Egr-1, CTGF, and Cyr61 to alveolar epithelial cells, airway epithelial cells, and stromal and inflammatory cells of GOLD-2 smokers. Cigarette smoke extract induced Egr-1 protein expression and increased Egr-1 DNA-binding activity in human lung fibroblast cells. Cytomix (tumor necrosis factor, IL-1, and IFN-) treatment showed that the activity of matrix metalloproteinase-2 (MMP-2) was increased in lung fibroblasts from EGR1 control (/) mice but not detected in that of EGR1 null (/) mice, whereas MMP-9 was regulated by EGR1 in a reverse manner. Our study represents the first comprehensive analysis of gene expression on GOLD-2 versus GOLD-0 smokers and reveals previously unreported candidate genes that may serve as potential molecular targets in COPD.
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