Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2014.00115
Yaoqian Pan, B. Pan, Xing-you Liu, Ruili Li, J. Yue
{"title":"Dicer and its miRNAs are necessary gene and regulatory factors for differentiation and proliferation of vascular smooth muscle cell","authors":"Yaoqian Pan, B. Pan, Xing-you Liu, Ruili Li, J. Yue","doi":"10.3724/SP.J.1206.2014.00115","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00115","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90933438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00206
Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li
MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.
{"title":"Establishment of Cardiomyocyte-specific miR-30b Transgenic Mice and Exploring The Function of miR-30b","authors":"Yuan-yuan Fan, B. Long, Fang Liu, Luyu Zhou, Kun Wang, Peifeng Li","doi":"10.3724/SP.J.1206.2013.00206","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00206","url":null,"abstract":"MicroRNAs(miRNAs) array results have shown that the expression of miR-30b is downregulated in heart tissues from patients with familial hypertrophic cardiomyopathy who were carriers of missense mutations in the MYH7,and also in a murine heart failure model,implying that miR-30b might play an important role in heart diseases.To study miR-30b in vivo function,we generated a transgenic mouse line overexpressing miR-30b under the control of the 5.5 kb promoter of α-myosin heavy chain(α-MHC).qRT-PCR results demonstrated that miR-30b was significantly increased in the heart tissues of miR-30b transgenic mice(P 0.05).miR-30b transgenic mice did not exhibit significant heart/body weight and left ventricular(LV)/body weight changes and abnormal myocardium structure.At present,little is known about how miR-30b regulates myocardial infarction.We constructed I/R models by the coronary artery ligation method and sham-operated mice were used as controls.Biochemical detection results and TTC-Evans blue results showed that after ischemia-reperfusion,these transgenic mice had lower releases of LDH,CK and cTn玉(P 0.05)and their hearts exhibited a smaller infarct size compared to those from control mice(P 0.05).Echocardiographic results indicated that cardiac function of transgenic mice was markedly improved compared to that of control mice.In conclusion,miR-30b has protective effect upon ischemic-reperfusion injury.And it may provide a new therapeutic approach for preventing and treating myocardial infarction.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85901467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2013.00396
Z. Yong, Zhou Ming, Xia-Yu Li, Zhang Wen-ling, Gong Zhao-Jian, Li Qian-jin, Xiao-Ling Li, Zeng Zhao-yang, Ma Jian, Shen Shou-rong, W. Fang, Xiong Wei
Secretion on the surface of human nasal mucosa contains many innate proteins,the key factors of which are SPLUNC1 and LPLUNC1,members of the palate,lung and nasal epithelium clone(PLUNC) family.These two proteins are highly expressed in nasopharyngeal epithelium with the relative specificity.Both of them have bacterial/permeability-increasing protein(BPI) domain which can bind to lipopolysaccharide(LPS) to inhibit or kill bacterial growth directly.They also have the immuno defense function to protect nasopharyngeal epithelium from Epstein-Barr virus(EBV) and some other pathogenic microorganism effectively.These proteins play a significant role in the process of chronic inflammation and carcinogenesis of nasopharyngeal epithelium by inhibiting the secretion of inflammatory factors,such as IL-6,through activating NF-κB and STAT3 signaling pathways.In addition,they also can suppress nasopharyngeal carcinoma(NPC) cell growth and induce cell apoptosis through MAPK and miR-141-PTEN-AKT signaling pathways when the PLUNC proteins are re-expressed in NPC cell lines.Further study about the mechanism of PLUNC protein family in pathogenesis of NPC has important significance for the prevention and treatment guidance of NPC.
{"title":"The Effect and Mechanism of PLUNC Protein Family Against Inflammation and Carcinogenesis of Nasopharyngeal Carcinoma","authors":"Z. Yong, Zhou Ming, Xia-Yu Li, Zhang Wen-ling, Gong Zhao-Jian, Li Qian-jin, Xiao-Ling Li, Zeng Zhao-yang, Ma Jian, Shen Shou-rong, W. Fang, Xiong Wei","doi":"10.3724/SP.J.1206.2013.00396","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00396","url":null,"abstract":"Secretion on the surface of human nasal mucosa contains many innate proteins,the key factors of which are SPLUNC1 and LPLUNC1,members of the palate,lung and nasal epithelium clone(PLUNC) family.These two proteins are highly expressed in nasopharyngeal epithelium with the relative specificity.Both of them have bacterial/permeability-increasing protein(BPI) domain which can bind to lipopolysaccharide(LPS) to inhibit or kill bacterial growth directly.They also have the immuno defense function to protect nasopharyngeal epithelium from Epstein-Barr virus(EBV) and some other pathogenic microorganism effectively.These proteins play a significant role in the process of chronic inflammation and carcinogenesis of nasopharyngeal epithelium by inhibiting the secretion of inflammatory factors,such as IL-6,through activating NF-κB and STAT3 signaling pathways.In addition,they also can suppress nasopharyngeal carcinoma(NPC) cell growth and induce cell apoptosis through MAPK and miR-141-PTEN-AKT signaling pathways when the PLUNC proteins are re-expressed in NPC cell lines.Further study about the mechanism of PLUNC protein family in pathogenesis of NPC has important significance for the prevention and treatment guidance of NPC.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88866783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2014.00036
Jun-Ping Liu
Aging occurs with cell beginning to lose function in a variety of cell types. If it takes place in a given tissue or organ prematurely ahead of other tissues and organs,it causes pathological development of diseases. How to treat aging cells and associated molecules is a challenge in anti-aging research. It has been demonstrated recently that aging occurs under physiological conditions during embryonic development of mammals,and that to some life forms aging never occurs. Involved in diverse diseases,aging is difficult to be measured and does not have universal markers. It is thus essential to comprehend the types of cells that undergo aging in human diseases and thereby the underlying molecular mechanisms. This article discusses recent research advances including:(1) The concept,classification and relevant mechanisms of cell aging;(2) Physiological aging: Developmentally programmed senescence;(3) Tissue homeostasis and aging;(4) Cell replicative senescence and related diseases: telomeres and cancer prognosis,idiopathic pulmonary fibrosis,hypertension;(5) Non-replicative cell aging and related diseases: Parkinson disease and diabetes;(6) Species diversity in aging and longevity.
{"title":"Aging and related diseases: Research progress","authors":"Jun-Ping Liu","doi":"10.3724/SP.J.1206.2014.00036","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2014.00036","url":null,"abstract":"Aging occurs with cell beginning to lose function in a variety of cell types. If it takes place in a given tissue or organ prematurely ahead of other tissues and organs,it causes pathological development of diseases. How to treat aging cells and associated molecules is a challenge in anti-aging research. It has been demonstrated recently that aging occurs under physiological conditions during embryonic development of mammals,and that to some life forms aging never occurs. Involved in diverse diseases,aging is difficult to be measured and does not have universal markers. It is thus essential to comprehend the types of cells that undergo aging in human diseases and thereby the underlying molecular mechanisms. This article discusses recent research advances including:(1) The concept,classification and relevant mechanisms of cell aging;(2) Physiological aging: Developmentally programmed senescence;(3) Tissue homeostasis and aging;(4) Cell replicative senescence and related diseases: telomeres and cancer prognosis,idiopathic pulmonary fibrosis,hypertension;(5) Non-replicative cell aging and related diseases: Parkinson disease and diabetes;(6) Species diversity in aging and longevity.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86233138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-01-01DOI: 10.3724/SP.J.1206.2012.00613
Gong Zj, Ming Zhou, Peng Sp, J. Ma, Xiaoyan Li, Hongbin Huang, Hongbin Huang, Y. Li, Xiaoling Li, H. Bo, Zeng Zy, Strong, Gui-yuan Li, Xiang Jj, W. Xiong, F. Wei, Zhang Wl, Liao Qj, K. Tang, Song Yl
Recently, we sequenced the transcriptomes of a hepatocellular carcinoma biopsy and a normal liver tissue using the RNA-Sequencing(RNA-Seq) strategy based on the Next Generation Sequencing(NGS) technique, and identified several adjacent high RNA-Seq signal peaks on chromosome 11q13.1 in the hepatocellular carcinoma biopsy, while not in the normal control tissue. In this chromosome region, there is no characterized genes have been identified, implying that these RNA-Seq peaks may represent one or more novel genes. Further study was confirmed that these RNA-Seq peaks were transcribed by one novel gene. Through cloning the full length of this novel gene, we found that this novel gene transcribed many splicing isoforms, and the longest isoform is 3 562 bp. Then we deposited twelve representative RNA isoforms into the GenBank database of the National Center for Biotechnology Information(NCBI), and created the GenBank IDs from KC136297 to KC136308 for these isoforms. None significant open reading fragment(ORF) was found in any transcripts of this novel gene, implying that this gene may encodes long non-coding RNAs(lncRNAs). To further elucidate the potential transcriptional regulation mechanism of this lncRNA gene, we predicted the promoter from the upstream sequence of the lncRNA gene using bioinformatic tools, and found that there is one potential promoter in-719 to-469 bp from the transcript start site of the lncRNA gene, and there are seven Sp1, one STAT5 and one EGR1 transcription factor binding sites in the promoter region. The molecular mechanisms of the lncRNA gene in carcinogenesis and progression of hepatocellular carcinoma are worthful for further investigation.
{"title":"Cloning and Functional Characterization of a Novel Long Non-coding RNA Gene Associated With Hepatocellular Carcinoma","authors":"Gong Zj, Ming Zhou, Peng Sp, J. Ma, Xiaoyan Li, Hongbin Huang, Hongbin Huang, Y. Li, Xiaoling Li, H. Bo, Zeng Zy, Strong, Gui-yuan Li, Xiang Jj, W. Xiong, F. Wei, Zhang Wl, Liao Qj, K. Tang, Song Yl","doi":"10.3724/SP.J.1206.2012.00613","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2012.00613","url":null,"abstract":"Recently, we sequenced the transcriptomes of a hepatocellular carcinoma biopsy and a normal liver tissue using the RNA-Sequencing(RNA-Seq) strategy based on the Next Generation Sequencing(NGS) technique, and identified several adjacent high RNA-Seq signal peaks on chromosome 11q13.1 in the hepatocellular carcinoma biopsy, while not in the normal control tissue. In this chromosome region, there is no characterized genes have been identified, implying that these RNA-Seq peaks may represent one or more novel genes. Further study was confirmed that these RNA-Seq peaks were transcribed by one novel gene. Through cloning the full length of this novel gene, we found that this novel gene transcribed many splicing isoforms, and the longest isoform is 3 562 bp. Then we deposited twelve representative RNA isoforms into the GenBank database of the National Center for Biotechnology Information(NCBI), and created the GenBank IDs from KC136297 to KC136308 for these isoforms. None significant open reading fragment(ORF) was found in any transcripts of this novel gene, implying that this gene may encodes long non-coding RNAs(lncRNAs). To further elucidate the potential transcriptional regulation mechanism of this lncRNA gene, we predicted the promoter from the upstream sequence of the lncRNA gene using bioinformatic tools, and found that there is one potential promoter in-719 to-469 bp from the transcript start site of the lncRNA gene, and there are seven Sp1, one STAT5 and one EGR1 transcription factor binding sites in the promoter region. The molecular mechanisms of the lncRNA gene in carcinogenesis and progression of hepatocellular carcinoma are worthful for further investigation.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78171140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-07-01DOI: 10.3724/SP.J.1206.2013.00079
Junye Miao, Jing Lu, Ziang Zhang, Zhiqian Tong, R. He
A certain concentration of formaldehyde can cause protein misfolding, cell death and biological dysfunction. Though it has been reported that formaldehyde has cytotoxicity, how formaldehyde affects cell cycle of neural cells and the molecular mechanism still needs to be clarified. In this study, neuroblastoma cell line SH-SY5Y was utilized to incubate with formaldehyde and the effect of formaldehyde on cell cycle was in formaldehyde concentration-dependent manner. No significant changes in cell cycle could be detected when[FA] ≤0.1 mmol/L (cells were incubated for 48 h), while the percentages of cells in S phase and G2/M phase were markedly increased with the elevation of formaldehyde concentration (0.1 mmol/L < [FA] ≤ 0.2 mmol/L). In the medium with 0.3 mmol/L formaldehyde, 46.28% of cells were in S phase while only 16.05% of them were in G2/M phase, that is, cell proliferation was obviously inhibited under the conditions. When cells were synchronized at G2/M phase, formaldehyde (0.1∼0.3 mmol/L) could markedly increase the number of cells in S phase, though, to some extent, the number of cells in G2/M phase decreased. When cells were synchronized at S phase, 0.1 mmol/L formaldehyde could decrease the number of cells in G2/M phase, while 0.3 mmol/L formaldehyde could markedly decrease the number of cells in G2/M phase and significantly increase that in S phase. In the presence of formaldehyde, primary neurons of SD rat exhibited similar changes in cell cycle as that in SH-SY5 Y cells. Furthermore, early and late apoptosis was markedly observed when 0.1 mmol/L ≤ [FA] ≤0.2 mmol/L, while DNA were obviously damaged and most cells were apoptosis and some of them underwent necrosis when [FA] ≤ 0.3 mmol/L. In sum, formaldehyde at a low concentration (0.1 mmol/L≤ [FA] ≤0.2 mmol/L) mainly suppresses DNA synthesis in S phase via hypermethylation of global DNA, while formaldehyde at a higher concentration ([FA] ≥ 0.3 mmol/L) causes DNA damage, both of them lead to the aberrant effects on cell cycle.
{"title":"The effect of formaldehyde on cell cycle is in a concentration-dependent manner","authors":"Junye Miao, Jing Lu, Ziang Zhang, Zhiqian Tong, R. He","doi":"10.3724/SP.J.1206.2013.00079","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2013.00079","url":null,"abstract":"A certain concentration of formaldehyde can cause protein misfolding, cell death and biological dysfunction. Though it has been reported that formaldehyde has cytotoxicity, how formaldehyde affects cell cycle of neural cells and the molecular mechanism still needs to be clarified. In this study, neuroblastoma cell line SH-SY5Y was utilized to incubate with formaldehyde and the effect of formaldehyde on cell cycle was in formaldehyde concentration-dependent manner. No significant changes in cell cycle could be detected when[FA] ≤0.1 mmol/L (cells were incubated for 48 h), while the percentages of cells in S phase and G2/M phase were markedly increased with the elevation of formaldehyde concentration (0.1 mmol/L < [FA] ≤ 0.2 mmol/L). In the medium with 0.3 mmol/L formaldehyde, 46.28% of cells were in S phase while only 16.05% of them were in G2/M phase, that is, cell proliferation was obviously inhibited under the conditions. When cells were synchronized at G2/M phase, formaldehyde (0.1∼0.3 mmol/L) could markedly increase the number of cells in S phase, though, to some extent, the number of cells in G2/M phase decreased. When cells were synchronized at S phase, 0.1 mmol/L formaldehyde could decrease the number of cells in G2/M phase, while 0.3 mmol/L formaldehyde could markedly decrease the number of cells in G2/M phase and significantly increase that in S phase. In the presence of formaldehyde, primary neurons of SD rat exhibited similar changes in cell cycle as that in SH-SY5 Y cells. Furthermore, early and late apoptosis was markedly observed when 0.1 mmol/L ≤ [FA] ≤0.2 mmol/L, while DNA were obviously damaged and most cells were apoptosis and some of them underwent necrosis when [FA] ≤ 0.3 mmol/L. In sum, formaldehyde at a low concentration (0.1 mmol/L≤ [FA] ≤0.2 mmol/L) mainly suppresses DNA synthesis in S phase via hypermethylation of global DNA, while formaldehyde at a higher concentration ([FA] ≥ 0.3 mmol/L) causes DNA damage, both of them lead to the aberrant effects on cell cycle.","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2013-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82881623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-08DOI: 10.3724/SP.J.1206.2012.00140
Xiao-Yan Liu, Qian Lu, Wu-jun Chen, Chao-ke Tang
{"title":"New Research Advances in Genetics Associated With High-density Lipoprotein Cholesterol*: New Research Advances in Genetics Associated With High-density Lipoprotein Cholesterol*","authors":"Xiao-Yan Liu, Qian Lu, Wu-jun Chen, Chao-ke Tang","doi":"10.3724/SP.J.1206.2012.00140","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2012.00140","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2013-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76753661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-08DOI: 10.3724/SP.J.1206.2012.00124
Wenping Luo, Dong-mei Tan, Genling Yang, Junjie Lu, Hai Zhao, Yi Tan
{"title":"Effects of GABA Signal on Mouse Placenta Establishment in Early-Middle Phase*: Effects of GABA Signal on Mouse Placenta Establishment in Early-Middle Phase*","authors":"Wenping Luo, Dong-mei Tan, Genling Yang, Junjie Lu, Hai Zhao, Yi Tan","doi":"10.3724/SP.J.1206.2012.00124","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2012.00124","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2013-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85315524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-08DOI: 10.3724/SP.J.1206.2012.00202
Fu-xiang Zhu, Ze-long Liu, Jing Miao, Hui-ge Qu, Xiao-yan Chi
{"title":"Intein-Fused Lucine Zippers Increase Plasma Coagulation Activity by Improving Protein Trans -Splicing in Dual-Vector Factor VIII Gene Delivered Mice*: Intein-Fused Lucine Zippers Increase Plasma Coagulation Activity by Improving Protein Trans -Splicing in Dual-Vector Factor VIII Gene Delivered Mice*","authors":"Fu-xiang Zhu, Ze-long Liu, Jing Miao, Hui-ge Qu, Xiao-yan Chi","doi":"10.3724/SP.J.1206.2012.00202","DOIUrl":"https://doi.org/10.3724/SP.J.1206.2012.00202","url":null,"abstract":"","PeriodicalId":20655,"journal":{"name":"生物化学与生物物理进展","volume":null,"pages":null},"PeriodicalIF":0.3,"publicationDate":"2013-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81562294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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