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- 저자 : ( Tai Ping Shi ) (검색결과 4 건)
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Human HS1BP3 induces cell apoptosis and activates AP-1
( Tai Ping Shi ),( Jie Shi Xie ),( Ying Xiong ),( Wei Wei Deng ),( Jin Hai Guo ),( Feng Wang ),( Da Long Ma ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.6
In the present study, we characterized the function of HS1-binding protein 3 (HS1BP3), which is mutated in essential tremor and may be involved in lymphocyte activation. We found that HS1BP3 localized to the mitochondria and endoplasmic reticulum partially. Overexpression of HS1BP3 induced apoptosis in HEK293T and HeLa cell lines. When these cell lines were transfected with HS1BP3, they exhibited nuclear DNA condensation, externalization of phosphatidylserine (PS), and cleavage of poly ADP ribose polymerase (PARP). Furthermore, suppression of HS1BP3 or HS1 expression attenuates HS1BP3 induced apoptosis. In addition, HS1BP3 enhanced activator protein 1 (AP-1)-mediated transcription in a dose-dependent manner. Therefore, we conclude that HS1BP3 regulates apoptosis via HS1 and stimulates AP-1-mediated transcription. [BMB reports 2011; 44(6): 381-386]
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( Ping Zhang Wang ),( Ying Xiong ),( Chuan Ma ),( Tai Ping Shi ),( Da Long Ma ) 생화학분자생물학회 (구 한국생화학분자생물학회) 2010 BMB Reports Vol.43 No.11
The c-Jun NH2-terminal kinase (JNK) signaling pathway participates in many physiological functions. In the current study we reported the cloning and characterization of five novel JNK2 transcript variants, which were designated as JNK2 α3, JNK2 α4, JNK2 β3, JNK2 γ1 and JNK2 γ2, respectively. Among them, JNK2 α4 and JNK2 γ2 are potential non-coding RNA because they contain pre-mature stop codons. Both JNK2α3 and JNK2β3 contain an intact kinase domain, and both encode a protein product of 46 kDa, the same as those of JNK2α1 and JNK2β1. JNK2γ1 contains a disrupted kinase domain and it showed a disable function. When over-expressed in mammalian cells, JNK2α3 showed higher activity on AP-1 than that of JNK2β3 and JNK2γ1. Furthermore, JNK2α3 and JNK2β3 showed different levels of substrate phosphorylation, although they both could promote the proliferation of 293T cells. Our results further demonstrate that JNK2 isoforms preferentially target different substrates and may regulate the expression of various target genes. [BMB reports 2010; 43(11): 738-743]
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Dynamic analysis for gene expression profiles of endothelial colony forming cells under hypoxia
De-Cai Yu,Wen-Du Feng,Xian-Biao Shi,hi-Yong Wang,Wei Ge,Chun-Ping Jiang,Xi-Tai Sun,Yi-Tao Ding 한국유전학회 2013 Genes & Genomics Vol.35 No.4
Previous studies have shown that endothelial colony forming cells (ECFCs) play an important role in the neovascularization of tumors. Hypoxia is emphasized as an important promoter of angiogenesis. However, little is known about genome-wide transcriptional regulation of ECFCs under hypoxic conditions. In this study, gene expression profiles in ECFCswere evaluated under hypoxic conditions for 3, 6, 12, 24,and 48 h, using Affymetrix U133 plus 2.0 chip microarray. 1,103 hypoxia-regulated genes were filtered, with 379(0.693 %) genes up-regulated and 724 (1.32 %) genes downregulated. Most of the up-regulated genes were involved in apoptosis, cell proliferation, or metabolic processes, while most of the down-regulated genes were involved in cell adherence,cell cycle,DNAandmRNAmetabolic processes,multi-cellular organism development, protein metabolic processes, response to stress, signal transduction, or transport. This expression profile is ECFC-specific, because it is significantly different from those of endothelial cells and smooth muscle cells under hypoxic conditions. Moreover, hypoxia-regulated apoptosis in ECFCs is mainly related with the mitochondrial pathway (p53-BAX-Caspase-9) and the death receptor pathway (FASCaspase-8-Caspase-3). MAPK pathway is activated in ECFCs under hypoxic conditions. The differentially expressed genes of ECFCs were identified under hypoxic conditions, and related with cell apoptosis, cell cycle and MAPK pathways, shedding light on the mechanism of angiogenesis.
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In Vitro Biological Characterization of DCUN1D5 in DNA Damage Response
Guo, Wei,Li, Guo-Jun,Xu, Hong-Bo,Xie, Jie-Shi,Shi, Tai-Ping,Zhang, Sheng-Zhong,Chen, Xiao-Hong,Huang, Zhi-Gang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8
Background: Novel prognostic biomarkers or therapeutic molecular targets for laryngeal squamous cell carcinoma (LSCC) are an urgent priority. We here sought to identify multiple novel LSCC-associated genes. Methods: Using high-density microarray expression profiling, we identified multiple genes that were significantly altered between human LSCCs and paired normal tissues. Potential oncogenic functions of one such gene, DCUN1D5, were further characterized in vitro. Results: Our results demonstrated that DCUN1D5 was highly expressed in LSCCs. Overexpression of DCUN1D5 in vitro resulted in 2.7-fold increased cellular migration, 67.5% increased invasive capacity, and 2.6-fold increased proliferation. Endogenous DCUN1D5 expression was decreased in a time-dependent manner after genotoxic stress, and silencing of DCUN1D5 by siRNA decreased the number of cells in the S phase by 10.2% and increased apoptosis by 11.7%. Conclusion: Our data suggest that DCUN1D5 in vitro might have vital roles in DNA damage response, but further studies are warranted to assess its significance in vivo.
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