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Identification of variants associated with sporadic thoracic aortic dissection: a case--control study

《医学前沿（英文）》 2021年 第15卷 第3期   页码 438-447 doi: 10.1007/s11684-020-0826-1

摘要： Thoracic aortic dissection (TAD) without familial clustering or syndromic features is known as sporadic TAD (STAD). So far, the genetic basis of STAD remains unknown. Whole exome sequencing was performed in 223 STAD patients and 414 healthy controls from the Chinese Han population (N = 637). After population structure and genetic relationship and ancestry analyses, we used the optimal sequence kernel association test to identify the candidate genes or variants of STAD. We found that COL3A1 was significantly relevant to STAD (P = 7.35 × 10−6) after 10 000 times permutation test (P = 2.49 × 10−3). Moreover, another independent cohort, including 423 cases and 734 non-STAD subjects (N = 1157), replicated our results (P = 0.021). Further bioinformatics analysis showed that COL3A1 was highly expressed in dissected aortic tissues, and its expression was related to the extracellular matrix (ECM) pathway. Our study identified a profile of known heritable TAD genes in the Chinese STAD population and found that COL3A1 could increase the risk of STAD through the ECM pathway. We wanted to expand the knowledge of the genetic basis and pathology of STAD, which may further help in providing better genetic counseling to the patients.

关键词： sporadic thoracic aortic dissection     exome sequencing     gene COL3A1     case–control study     extracellular matrix    

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Novel variants in LAMA3 and COL7A1 and recurrent variant in KRT5 underlying epidermolysis bullosa in

《医学前沿（英文）》 2022年 第16卷 第5期   页码 808-814 doi: 10.1007/s11684-021-0878-x

摘要： Epidermolysis bullosa (EB) is a group of clinically and genetically heterogeneous diseases characterized by trauma-induced mucocutaneous fragility and blister formation. Here, we investigated five Chinese families with EB, and eight variants including a novel nonsense variant (c.47G>A, p.W16*) in LAMA3, a known recurrent variant (c.74C>T, p.P25L) in KRT5, 2 novel (c.2531T>A, p.V844E; c.6811_6814del, p.R2271fs) and 4 known (c.6187C>T, p.R2063W; c.7097G>A, p.G2366D; c.8569G>T, p.E2857*; c.3625_3635del, p.S1209fs) variants in COL7A1 were detected. Notably, this study identified a nonsense variant in LAMA3 that causes EB within the Chinese population and revealed that this variant resulted in a reduction in LAMA3 mRNA and protein expression levels by nonsense-mediated mRNA decay. Our study expands the mutation spectra of Chinese patients with EB.

关键词： epidermolysis bullosa     LAMA3     COL7A1     KRT5     Chinese families    

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Influence and related mechanism of Retn gene expression on glucose uptake in 3T3-L1 cells

LI Yahui, DONG Shiyuan, YU Chao, JIANG Yu, LI Huaixing, SUN Shuhan

《医学前沿（英文）》 2007年 第1卷 第3期   页码 269-273 doi: 10.1007/s11684-007-0051-1

摘要： The aim of this article was to investigate the influence and the related mechanism of the gene on glucose uptake and insulin resistance in 3T3-L1 cells. Radioimmunoassay was used to determine glucose uptake in 3T3-L1 cells with different gene expression levels, whether cells were stimulated by insulin or not. RT-PCR and real-time RT-PCR analysis were used to determine the mRNA levels of several glucose transport proteins in 3T3-L1 cells with different gene expression levels, including insulin receptor substrate-1(IRS-1), phosphatidylinositol 3-kinase (PI-3K), AKT-2, glucose transporter-4 (GLUT-4), p38 mitogen-activated protein kinase (p38MAPK) and glycogen synthase kinase-3b (GSK-3). The glucose uptake decreased with the increase in gene expression in 3T3-L1 cells, which was independent of whether the cells were stimulated by insulin or not. The mRNA expression of two signal proteins PI-3K and AKT-2 decreased and the other two signal proteins, GSK-3 and p38MAPK, increased with overexpression in 3T3-L1 cells. Resistin could induce insulin resistance in adipocytes, which might be related to the changes of some proteins in PI-3K and Ras pathways.

关键词： 3T3-L1     influence     resistance     receptor substrate-1     transport    

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APPLE SUMO E3 LIGASE MDSIZ1 NEGATIVELY REGULATES DROUGHT TOLERANCE

《农业科学与工程前沿（英文）》 2021年 第8卷 第2期

摘要：

Drought stress typically causes heavy losses in apple production and uncovering the mechanisms by which apple tolerates drought stress is important in apple breeding. MdSIZ1 is a SUMO (small ubiquitin-like modifier) E3 ligase that promotes SUMO binding to substrate proteins. Here, we demonstrate that MdSIZ1 in apple has a negative relationship with drought tolerance. MdSIZ1 RNAi transgenic apple trees had a higher survival rate after drought stress. During drought stress they had higher leaf water potential, reduced ion leakage, lower H2O2 and malondialdehyde contents, and higher catalase activity. In addition, MdSIZ1 RNAi transgenic plants had a higher net photosynthetic rate during the latter period of drought stress. Finally, the transgenic apple trees also altered expression levels of some microRNAs in response to drought stress. Taken together, these results indicate that apple MdSIZ1 negatively regulates drought stress by enhancing leaf water-holding capacity and antioxidant enzyme activity.

 

关键词： apple / drought tolerance / gene expression / MdSIZ1    

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APPLE SUMO E3 LIGASE MDSIZ1 NEGATIVELY REGULATES DROUGHT TOLERANCE

Baohua CHU, Jia SUN, Huan DANG, Ziqing MA, Shuang ZHAO, Qingmei GUAN, Xuewei LI

《农业科学与工程前沿（英文）》   页码 247-261 doi: 10.15302/J-FASE-2021388

摘要： Drought stress typically causes heavy losses in apple production and uncovering the mechanisms by which apple tolerates drought stress is important in apple breeding. MdSIZ1 is a SUMO (small ubiquitin-like modifier) E3 ligase that promotes SUMO binding to substrate proteins. Here, we demonstrate that in apple has a negative relationship with drought tolerance. RNAi transgenic apple trees had a higher survival rate after drought stress. During drought stress they had higher leaf water potential, reduced ion leakage, lower H O and malondialdehyde contents, and higher catalase activity. In addition, RNAi transgenic plants had a higher net photosynthetic rate during the latter period of drought stress. Finally, the transgenic apple trees also altered expression levels of some microRNAs in response to drought stress. Taken together, these results indicate that apple MdSIZ1 negatively regulates drought stress by enhancing leaf water-holding capacity and antioxidant enzyme activity.

关键词： apple     drought tolerance     gene expression     MdSIZ1    

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Bioinformatic exploration of MTA1-regulated gene networks in colon cancer

null

《医学前沿（英文）》 2016年 第10卷 第2期   页码 178-182 doi: 10.1007/s11684-016-0442-2

摘要：

Metastasis-associated gene 1 (MTA1) controls a series of biological processes in tumor progression. Tumor progression is a complex process regulated by a gene network. The global cancer gene regulatory network must be analyzed to determine the position of MTA1 in the molecular network and its cooperative genes by further exploring the biological functions of this gene. We used TCGA data sets and GeneCards database to screen MTA1-related genes. GO and KEGG pathway analyses were conducted with DAVID and gene network analysis via STRING and Cytoscape. Results showed that in the development of colon cancer, MTA1 is linked to certain signal pathways, such as Wnt/Notch/nucleotide excision repair pathways. The findings also suggested that MTA1 demonstrates the closest relationship in a coregulation process with the key molecules AKT1, EP300, CREBBP, SMARCA4, RHOA, and CAD. These results lead MTA1 exploration to an in-depth investigation in different directions, such as Wnt, Notch, and DNA repair.

关键词： metastasis-associated gene 1     colon cancer     bioinformatics    

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NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

《医学前沿（英文）》 2019年 第13卷 第6期   页码 646-657 doi: 10.1007/s11684-018-0643-y

摘要： gene is thought to be a tumor-suppressor gene. Our previous study found that overexpression of gene in PC3 cell line could slow down the tumor proliferation rate, associated with a mild decrease in expression. The decrease could increase the sensitivity of radiotherapy to tumors. Thus, we supposed to have an “enhanced firepower” effect by combining overexpressed gene therapy and I radiation therapy uptake by overexpressed hNIS protein. We found a weak endogenous expression of hNIS protein in PC3 cells and demonstrated that the low expression of hNIS protein in PC3 cells might be the reason for the low iodine uptake. By overexpressing in PC3, the radioactive iodine uptake ability was significantly increased. Results of and tumor proliferation experiments and F-fluorothymidine ( F-FLT) micro-positron emission tomography/computed tomography (micro-PET/CT) imaging showed that the combined gene therapy and I radiation therapy mediated by overexpressed hNIS protein had the best tumor proliferative inhibition effect. Immunohistochemistry showed an obvious decrease of expression and the lowest expression. These data suggest that via inhibition of expression, overexpressed might enhance the effect of radiation therapy of I uptake in overexpressed PC3 cells.

关键词： androgen-independent prostate cancer     normal epithelial cell-specific 1/kallikrein 10     sodium/iodide symporter     radiation therapy     proliferation    

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Cloning of human XAF1 gene promoter and assay of its transcription activity in a variety of cell lines

Qiong CHEN, Qing YU, Yuhu SONG, Peiyuan Li, Ying CHANG, Zhijun WANG, Lifeng LIU, Wei WU, Jusheng LIN

《医学前沿（英文）》 2009年 第3卷 第2期   页码 148-152 doi: 10.1007/s11684-009-0032-7

摘要： To investigate the regulation of tumor suppressor XAF1 gene expression in digestive system cancers, we studied XAF1 gene promoter transcription activity and mRNA level in digestive system cancer cell lines (human hepatoma cell line HepG2, human colon cancer cell line LoVo, and human gastric cancer cell line AGS) and nontumor cell lines (human embryonic liver cell line L02 (L02 cells) and human embryonic kidney 293 cells [HEK293 cells]) as controls. 1395-bp-promoter fragment of XAF1 gene was amplified by polymerase chain reaction (PCR) and cloned into pGL3-basic vector and pEGFP-1 vector to assay its promoter transcription activity. The plasmids were transfected into a variety of cell lines by lipofectamine 2000. The promoter transcription activity was determined by dual-luciferase report assay, and enhanced green fluorescent protein (EGFP)-positive cells were detected by fluorescence microscope. The expression of XAF1 mRNA in HEK293 and L02 were significantly higher than that in any of the three digestive system cancer cell lines. The dual-luciferase reporter assay showed that the promoter transcription activity in digestive system tumor cell lines transfected with pGL3-XAF1p promoter was apparently lower than that of both HEK293 and L02 cells. Expression of green fluorescent protein (GFP) under the control of XAF1 promoter in the three digestive system cancer cell lines was lower than that of both HEK293 and L02 cells. The activities of pGL3-XAF1p in the three digestive system cancer cell lines after treatment with heat stress were significantly lower than those in the unstressed cells. The results suggested that remarkably down-regulated XAF1 mRNA expression in digestive system cancer cell lines may be due to loss of transcription activity of XAF1 promoter.

关键词： gene     X-linked inhibitor of apoptosis protein associated factor-1 (XAF1)     promoter     transcription regulation    

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Distinct gene expression pattern of mutations coordinated by target repression and promoter hypermethylation

《医学前沿（英文）》 2022年 第16卷 第4期   页码 627-636 doi: 10.1007/s11684-020-0815-4

摘要： Runt-related transcription factor 1 (RUNX1) is an essential regulator of normal hematopoiesis. Its dysfunction, caused by either fusions or mutations, is frequently reported in acute myeloid leukemia (AML). However, RUNX1 mutations have been largely under-explored compared with RUNX1 fusions mainly due to their elusive genetic characteristics. Here, based on 1741 patients with AML, we report a unique expression pattern associated with RUNX1 mutations in AML. This expression pattern was coordinated by target repression and promoter hypermethylation. We first reanalyzed a joint AML cohort that consisted of three public cohorts and found that RUNX1 mutations were mainly distributed in the Runt domain and almost mutually exclusive with NPM1 mutations. Then, based on RNA-seq data from The Cancer Genome Atlas AML cohort, we developed a 300-gene signature that significantly distinguished the patients with RUNX1 mutations from those with other AML subtypes. Furthermore, we explored the mechanisms underlying this signature from the transcriptional and epigenetic levels. Using chromatin immunoprecipitation sequencing data, we found that RUNX1 target genes tended to be repressed in patients with RUNX1 mutations. Through the integration of DNA methylation array data, we illustrated that hypermethylation on the promoter regions of RUNX1-regulated genes also contributed to dysregulation in RUNX1-mutated AML. This study revealed the distinct gene expression pattern of RUNX1 mutations and the underlying mechanisms in AML development.

关键词： RUNX1     gene mutation     acute myeloid leukemia     transcriptional repression     DNA methylation    

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Identification of an E3 ligase-encoding gene

Yanfei Zhang, Xinchun Zhao, Yongchun Zhou, Min Wang, Guangbiao Zhou

《医学前沿（英文）》 2020年 第14卷 第3期   页码 318-326 doi: 10.1007/s11684-019-0708-6

摘要： In order to unveil ubiquitin pathway genes (UPGs) that are essential for non-small cell lung cancer (NSCLC) cell proliferation, we recently conducted a siRNA screening experiment to knockdown the expression of 696 UPGs found in the human genome in A549 and H1975 NSCLC cells. We found that silencing of one of the candidates, that encodes an E3 ubiquitin ligase essential for the repair of DNA interstrand cross-links in response to DNA damage, led to dramatic inhibition of NSCLC cell proliferation with significant -scores. Knockdown of suppressed colony forming activity of NSCLC cells. We further evaluated the significance of in NSCLCs and found that this gene was more elevated in tumor samples than in paired normal lung tissues and was inversely associated with the clinical outcome of patients with NSCLC. Moreover, expression was significantly higher in smokers than in non-smokers. These results show for the first time that is required for NSCLC cell proliferation and may have an important role in lung carcinogenesis.

关键词： RFWD3     NSCLC     prognosis     tobacco smoke    

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Antitumor immunity of human SART3 gene vaccine against mouse tumor

HE Yu, YANG Shuhua, LIU Yong, LI Tao

《医学前沿（英文）》 2008年 第2卷 第1期   页码 51-57 doi: 10.1007/s11684-008-0010-5

摘要： To determine whether squamous cell carcinoma antigen recognized by human T cell 3 (SART3) gene can induce antitumor immunity against tumor cells which express the gene, we constructed mouse tumor cells expressing human SART3 (LM8-SART3) and carried out experiments . After subcutaneous injection with SART3 gene vaccine, cytotoxic T lymphocyte (CTL) activity was measured using Cell Counting Kit-8. As for the part, C3H mice were divided into several groups. One group was challenged with tumor cells after immunity. Another group was treated with the vaccine after tumor implantation. It was found that human SART3 DNA vaccine can elicit a specific CTL reaction from the mouse splenocytes. After vaccination, tumor occurrence and tumor growth speed was reduced. The vaccine also shows activity in tumor treatment. We conclude that the human SART3 DNA vaccine can induce antitumor ability against tumor cells expressing human SART3 (LM8-SART3) which may provide new possibilities in antitumor therapy.

关键词： antitumor therapy     occurrence     implantation     DNA vaccine     SART3 DNA    

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Adenovirus-mediated tissue inhibitor of metalloproteinase-3 gene transfection inhibits rabbit intervertebral

Xudong YU MM, Zengwu SHAO MD, Liming XIONG MD, Weiwei XU MM, Hezhong WANG MM, Huifa XU MM,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 415-420 doi: 10.1007/s11684-009-0072-z

摘要： The aim of this study was to investigate the inhibitory effects of recombinant adenovirus vector carrying tissue inhibitor of metalloproteinase-3 (RAdTIMP-3) against degeneration of rabbit intervertebral disc. Thirty Japanese white rabbits of 4 months old were randomly divided into 5 groups. Mild or moderate rabbit lumbar disc degeneration model was constructed with the controllable axial loading device by imposing 98N pressure at the discs for 2 weeks. Various doses of virus were injected into the degenerated discs as follows: 20μL of normal saline in group 1; 20μL of RAd66 (an empty adenovirus vector, 1.0×10OPU/mL) in group 2; and 20, 10, and 5μL of RAdTIMP-3 (1.0×10OPU/mL) in groups 3, 4, and 5, respectively. Two weeks after the injection, the discs were collected for investigations, including assessment of degeneration degrees according to the Thompson’s grading system, reverse-transcription polymerase chain reaction (RT-PCR) assay for TIMP-3 gene, Safranin O-Fast green staining, and immunohistochemical staining for TIMP-3 and type II collagen. According to Thompson’s criteria, the degeneration of groups 3, 4, and 5, especially group 3, was alleviated as compared with groups 1 and 2. RT-PCR revealed that the expression of TIMP-3 in groups 3, 4, and 5, especially in group 3, was significantly enhanced as compared with group 1 (<0.01). Both Safranin O-Fast green staining and type II collagen staining demonstrated better reserved integrity of disc matrix in groups 3, 4, and 5 than in groups 1 and 2. TIMP-3 staining exhibited an obvious increase of positive-staining rate in groups 3, 4, and 5 as compared with group 1. The positive-staining rate in group 3 (79.42%±1.35%) was about 3times that of group 1 (25.47%±5.46%, <0.01). RAdTIMP-3 can effectively protect the matrix of rabbit intervertebral disc against overloading-induced degeneration in a dose-dependent manner, resulting in the alleviation of disc degeneration.

关键词： tissue inhibitor of metalloproteinase-3     intervertebral disc     rabbit     gene therapy    

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Haploinsufficiency of Lipin3 leads to hypertriglyceridemia and obesity by disrupting the expression andhypertriglyceridemia and obesity by disrupting the expression and nucleocytoplasmic localization of Lipin1

《医学前沿（英文）》 doi: 10.1007/s11684-023-1003-0

摘要： Lipin proteins including Lipin 1–3 act as transcriptional co-activators and phosphatidic acid phosphohydrolase enzymes, which play crucial roles in lipid metabolism. However, little is known about the function of Lipin3 in triglyceride (TG) metabolism. Here, we identified a novel mutation (NM_001301860: p.1835A>T/p.D612V) of Lipin3 in a large family with hypertriglyceridemia (HTG) and obesity through whole-exome sequencing and Sanger sequencing. Functional studies revealed that the novel variant altered the half-life and stability of the Lipin3 protein. Hence, we generated Lipin3 heterozygous knockout (Lipin3-heKO) mice and cultured primary hepatocytes to explore the pathophysiological roles of Lipin3 in TG metabolism. We found that Lipin3-heKO mice exhibited obvious obesity, HTG, and non-alcoholic fatty liver disorder. Mechanistic study demonstrated that the haploinsufficiency of Lipin3 in primary hepatocytes may induce the overexpression and abnormal distribution of Lipin1 in cytosol and nucleoplasm. The increased expression of Lipin1 in cytosol may contribute to TG anabolism, and the decreased Lipin1 in nucleoplasm can reduce PGC1α, further leading to mitochondrial dysfunction and reduced TG catabolism. Our study suggested that Lipin3 was a novel disease-causing gene inducing obesity and HTG. We also established a relationship between Lipin3 and mitochondrial dysfunction.

关键词： Lipin3     Lipin1     hypertriglyceridemia     obesity     mitochondrial dysfunction    

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Gene therapy for hemophilia B mice with scAAV8-LP1-hFIX

null

《医学前沿（英文）》 2016年 第10卷 第2期   页码 212-218 doi: 10.1007/s11684-016-0438-y

摘要：

Hemophilia B is a hemorrhagic disease caused by the deficiency of clotting factor IX (FIX). Gene therapy might be the ultimate strategy for the disease. However, two main problems that should be solved in gene therapy for hemophilia B are immunity and safety. Self-complementary adeno-associated virus serotype 8 (scAAV8), a non-human primate AAV featuring low immunogenicity and high transfection efficiency in liver cells, might be a potential vector for hemophilia B gene therapy. A strong liver-specific promoter-1 (LP1) was inserted and mutant human FIX Arg338Ala was introduced into plasmid scAAV8-LP1 to develop an optimized AAV8 vector that expresses human clotting factor FIX (hFIX). The efficiency of scAAV8-LP1-hFIX administered through normal systemic injection or hydrodynamic injection was compared. A high expression was achieved using hydrodynamic injection, and the peak hFIX expression levels in the 5×1011 and 1×1011 virus genome (vg) cohorts were 31.94% and 25.02% of normal level, respectively, at 60 days post-injection. From the perspective of long-term (200 days) expression, both injection methods presented promising results with the concentration value maintained above 4% of normal plasma. The results were further verified by enzyme-linked immunosorbent assay and activated partial thromboplastin time. Our study provides a potential gene therapy method for hemophilia B.

关键词： hemophilia B     AAV8     hFIX     gene therapy    

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Association of miRNA-122-binding site polymorphism at the interleukin-1 α gene and its interaction with

null

《医学前沿（英文）》 2014年 第8卷 第2期   页码 217-226 doi: 10.1007/s11684-014-0326-2

摘要：

This study was designed to investigate the contribution of miRNA-122-binding site polymorphism at the IL-1A gene and its multiplicative interactions with hepatitis B virus (HBV) mutations in the risk of hepatocellular carcinoma (HCC). A total of 1021 healthy controls, 302 HBV surface antigen (HBsAg) seroclearance subjects, and 2011 HBsAg-positive subjects (including 1021 HCC patients) were enrolled in this study. Quantitative PCR was used to genotype rs3783553. HBV mutations were determined by direct sequencing. Multivariate logistic regression analyses were performed to test the associations of rs3783553, mutations, and their interactions with the risk of HCC. No significant association was found between rs3783553 and the risk of HCC among healthy controls, HBsAg seroclearance subjects, HBsAg-positive subjects without HCC, and all controls. Additionally, rs3783553 was not significantly associated with chronic HBV infection, liver cirrhosis, HBV e antigen seroconversion, abnormal alanine aminotransferase, and high viral load (>104 copies/ml). However, the TTCA insertion allele of rs3783553 was significantly associated with an increased frequency of HBV C7A mutation compared with homozygous TTCA deletion carriers [(del/ins+ ins/ins) vs. del/del, adjusted odds ratio (OR)=1.48, 95% confidence interval (CI)=1.09-2.02, P=0.013]. Multiplicative interaction of rs3783553 with HBV preS deletion significantly reduced the risk of HCC in males, with an adjusted OR of 0.64 (95% CI=0.42-0.98; P=0.041) after age and HBV genotype were adjusted. Although rs3783553 did not significantly affect genetic susceptibility to HBV-related HCC, its variant allele may predispose the host to selecting HBV C7A mutation during evolution and significantly reduce the risk of HCC caused by HBV preS deletion. This study provides an insight into the complex host-virus interaction in HBV-induced hepatocarcinogenesis and is helpful in determining HBsAg-positive subjects who are likely to develop HCC.

关键词： hepatocellular carcinoma (HCC)     interaction     miRNA-122-binding site     IL-1A     rs3783553     hepatitis B virus (HBV) mutations    

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标题 作者 时间 类型 操作

Identification of variants associated with sporadic thoracic aortic dissection: a case--control study

期刊论文

Novel variants in LAMA3 and COL7A1 and recurrent variant in KRT5 underlying epidermolysis bullosa in

期刊论文

Influence and related mechanism of Retn gene expression on glucose uptake in 3T3-L1 cells

LI Yahui, DONG Shiyuan, YU Chao, JIANG Yu, LI Huaixing, SUN Shuhan

期刊论文

APPLE SUMO E3 LIGASE MDSIZ1 NEGATIVELY REGULATES DROUGHT TOLERANCE

期刊论文

APPLE SUMO E3 LIGASE MDSIZ1 NEGATIVELY REGULATES DROUGHT TOLERANCE

Baohua CHU, Jia SUN, Huan DANG, Ziqing MA, Shuang ZHAO, Qingmei GUAN, Xuewei LI

期刊论文

Bioinformatic exploration of MTA1-regulated gene networks in colon cancer

null

期刊论文

NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation

Jiajia Hu, Wenbin Shen, Qian Qu, Xiaochun Fei, Ying Miao, Xinyun Huang, Jiajun Liu, Yingli Wu, Biao Li

期刊论文

Cloning of human XAF1 gene promoter and assay of its transcription activity in a variety of cell lines

Qiong CHEN, Qing YU, Yuhu SONG, Peiyuan Li, Ying CHANG, Zhijun WANG, Lifeng LIU, Wei WU, Jusheng LIN

期刊论文

Distinct gene expression pattern of mutations coordinated by target repression and promoter hypermethylation

期刊论文

Identification of an E3 ligase-encoding gene

Yanfei Zhang, Xinchun Zhao, Yongchun Zhou, Min Wang, Guangbiao Zhou

期刊论文

Antitumor immunity of human SART3 gene vaccine against mouse tumor

HE Yu, YANG Shuhua, LIU Yong, LI Tao

期刊论文

Adenovirus-mediated tissue inhibitor of metalloproteinase-3 gene transfection inhibits rabbit intervertebral

Xudong YU MM, Zengwu SHAO MD, Liming XIONG MD, Weiwei XU MM, Hezhong WANG MM, Huifa XU MM,

期刊论文

Haploinsufficiency of Lipin3 leads to hypertriglyceridemia and obesity by disrupting the expression andhypertriglyceridemia and obesity by disrupting the expression and nucleocytoplasmic localization of Lipin1

期刊论文

Gene therapy for hemophilia B mice with scAAV8-LP1-hFIX

null

期刊论文

Association of miRNA-122-binding site polymorphism at the interleukin-1 α gene and its interaction with

null

期刊论文