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1. Heat shock treatment regulates the expression of NFKBIA (IκBα) in a post-transcriptional manner | |||
Mei Zhuzhong,Li Tao,Wang Ni,Chen Xinyu,Ou Xiaoli,Jiang Yong | |||
Basic Medicine 08 January 2014 | |||
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Abstract:IκBα, encoded by NFKBIA, is the prototype inhibitor of transcription factor NF-κB. Notably, the transcription of NFKBIA is directly regulated by NF-κB. In contrast, the contribution of post-transcriptional regulation in the expression of NFKBIA remains obscure. To elucidate the post-transcriptional regulation of NFKBIA, we first aligned the 3?-UTR from several different species (human, mouse, rat, dog and cow). The alignment results revealed that the 3?-UTR sequences were highly conserved among these analyzed species. Dual luciferase assay analysis showed that 3?-UTR of mouse NFKBIA downregulated the expression of associated luciferase gene. Heat shock treatment stabilized NFKBIA mRNA and promote the expression of luciferase gene associated with mouse NFKBIA 3?-UTR. Biotin-labeled RNA pulldown assay followed mass spectrometry analysis identified specific binding proteins to the 3?-UTR of mouse NFKBIA mRNA. Half of them were identified as ribosomal proteins of 40S and 60S ribosome subunits. | |||
TO cite this article:Mei Zhuzhong,Li Tao,Wang Ni, et al. Heat shock treatment regulates the expression of NFKBIA (IκBα) in a post-transcriptional manner[OL].[ 8 January 2014] http://en.paper.edu.cn/en_releasepaper/content/4581250 |
2. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling | |||
ZHAO Jing,CHI Yingkai,LIU Haijing,ZOU Yongxin,CUI Suping,JIANG Ping,WANG Huali,ZHANG Hong,MAO Jingzhuo,HOU Lin,ZHANG Bo | |||
Basic Medicine 11 January 2012 | |||
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Abstract:Centrosome amplification, a characteristic of cancer cells, has been believed a driving force for genetic instability in the development of cancer and received extensively exploration in recent years. In our previous work, we have demonstrated that TEIF(transcriptional elements-interacting factor)distributes at the centrosome and regulates its status in physiological condition, DNA damage response or carcinogenesis. Here, we further expand our knowledge of TEIF to the downstream effector of EGF/PI3K/Akt signaling. The addition of EGF or transfection of active Akt stimulated TEIF expression, resulting in an increase of centrosome splitting and amplification, while the inhibitors of either PI3K or Akt attenuated the changes in TEIF and its associated centrosome status. A consensus motif for Akt phosphorylation (RHRVLT) was revealed in TEIF domain of localizing at the centrosome and identified as the site for phosphorylation of TEIF both in vitro and in vivo experiments, indicating TEIF as a direct substrate to Akt1. Furthermore, in a collection of aggressive breast cancers a positive correlation between the expression of TEIF and centrosome amplification was clarified and also closely concerned to the over-expression of CerbB2 (a member of EGFR family) and the level of phosphorylated Akt (pAkt) in cancer tissues. These findings not only could link EGF/PI3K/Akt oncogenic signaling with centrosome amplification, but also could provide more choices in the development of specific inhibitors for anti-cancer therapeutic agents targeting to EGF/PI3K/Akt signaling. | |||
TO cite this article:ZHAO Jing,CHI Yingkai,LIU Haijing, et al. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling[OL].[11 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4461460 |
3. The distribution of human papillomavirus genotypes in uterine cervical lesions in Yanbian of Northern China | |||
Zhao Yiwei ,Lin Hai ,Wu Qunying ,Han Songying ,Zhang Meihua,Lin Zhenhua | |||
Basic Medicine 09 October 2007 | |||
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Abstract:Purposes: To investigate the distribution of human papillomavirus (HPV) genotypes in uterine cervical lesions in Yanbian of Northern China. Materials and Methods: Paraffin embedded blocks of 62 cases of squamous cell carcinomas (SCC), 28 cases of adenocarcinomas, and 143 cases of CIN (CIN-1: 45; CIN-2: 46; CIN-3: 52) were selected from Dept. of Pathology, Yanbian University Hospital and Yanbian Women’s Hospital in the period of 2000-2005. DNA was extracted by using High Pure PCR Template Preparation Kit from all above blocks. And HPV genotypes were detected by using oligonucleotide microarray (HPV DNA-chip). Results: All the 20 cases of normal cervical epithelia are negative for HPV by both TaKaRa PCR and DNA-chip methods. The positive rate of high-risk HPV is 28.9% in CIN-1, 41.3% in CIN-2, 44.2% in CIN-3, 85.5% in SCC, and 82.1% in adenocarcinoma by TaKaRa PCR method. Similarly, it is 26.7% in CIN-1, 41.3% in CIN-2, 40.4% in CIN-3, 82.3% in SCC, and 78.6% in adenocarcinoma by HPV DNA-chip. HPV 16 is the major type in all CIN and SCC cervical lesions. However, in cervical adenocarcinoma, HPV 18 is the most common type (59.1% in HPV positive cases), and HPV 16 is the second type, but still show a high percentage (31.8% in HPV positive cases). There is small number of multi-types HPV detected in CIN-3, SCC, and adenocarcinoma, but none in CIN-1/2. Meanwhile, there is no significant difference on the HPV screening between TaKaRa PCR and HPV DNA-chip methods (p<0.05). Conclusions: HPV 16 is the type most frequently involved in the development of SCC of the cervix, whereas both HPV 18 and 16 play a prominent role in the development of adenocarcinoma of the cervix in Yanbian of Northern China. Both TaKaRa PCR and HPV DNA-chip methods are sensitive for HPV detection, and can be used for the screening of HPV infection status and genotyping in uterine cervical lesions, and maybe helpful for the prediction of the development and progress of CIN-2/3. | |||
TO cite this article:Zhao Yiwei ,Lin Hai ,Wu Qunying , et al. The distribution of human papillomavirus genotypes in uterine cervical lesions in Yanbian of Northern China[OL].[ 9 October 2007] http://en.paper.edu.cn/en_releasepaper/content/15558 |
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