Authentication email has already been sent, please check your email box: and activate it as soon as possible.
You can login to My Profile and manage your email alerts.
If you haven’t received the email, please:
|
|
There are 6 papers published in subject: > since this site started. |
Results per page: |
Select Subject |
Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
1. ABCC3 Network Construction and Analysis of Human Lung adenocarcinoma compared with normal adjacent tissues by Integrative Biocomputation | |||
SHI Jitao,WANG Lin,HUANG Juxiang | |||
Biology 15 August 2018 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Single molecular functional network construction and analysis of disease is very useful to identify novel and potential targets for prognosis and therapy. This paper integrated an infer method based on linear programming and decomposition procedure with function analysis using Kappa statistics and fuzzy heuristic cluster (DAVID). We first identified the significant molecule ABCC3, then constructed ABCC3 up- and down-stream network by infer and further data-mined the main ABCC3 modules including transporter activity, splice variant, sequence variant, cell fraction, transmembrane, catalytic activity and ATP-binding from 25 lung adenocarcinoma and 25 human normal adjacent tissues in the same GEO Dataset GSE7670. Our infer ABCC3 network result showed the different gene rate of lung adenocarcinoma as 54% (26/48) compared with the control considering activation and inhibition relationship. The different active genes in lung adenocarcinoma include ASPM, GCNT3, SPP1, SRD5A1_2, CRABP2, HIST1H4J, MKI67, PYCR1 and the different inhibitory genes include BIRC5, COL1A1_2, GINS2, GREM1_2, HIST1H4J, HLXB9, MELK, MMP11, SPINK1, TOP2A_2, ASPM, COL3A1, HMGB3, HMMR, MMP12, SRD5A1_1, SRD5A1_2, TOX3_3. Our integrative analysis showed the positive results of ABCC3 transporter activity and cell fraction through the net numbers of activation minus inhibition compared with the control and predicted the increases of these modules in lung adenocarcinoma, whereas the negative results of ABCC3 ATP-binding, transmembrane, catalytic activity, splice variant and sequence variant, and deduced the decreases of these modules in lung adenocarcinoma. | |||
TO cite this article:SHI Jitao,WANG Lin,HUANG Juxiang. ABCC3 Network Construction and Analysis of Human Lung adenocarcinoma compared with normal adjacent tissues by Integrative Biocomputation[OL].[15 August 2018] http://en.paper.edu.cn/en_releasepaper/content/4745828 |
2. Transcriptome analysis of murine thymic epithelial cells reveals age-associated changes in microRNA expression | |||
Guo Zhibin,Chi Feng,Song Yan,Wei Tianli,Zhu Xike | |||
Biology 20 August 2013 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Age-related thymic involution is accompanied by a decrease in thymopoiesis and thus deficiency in T-cell-mediated immunity in the elderly. Many events involved in thymic involution have been discovered; however, it is unclear if they are causes or consequences of thymic involution. These events include the degeneration of T-cell progenitors as well as the deterioration of the thymic stroma, which is a characteristic of thymic epithelial cell loss due to increased apoptosis and decreased cell proliferation. MicroRNA (miRNA) is believed to play important roles in regulating cell death and proliferation in the aging network. The aim of this study is to profile the miRNA expression in thymic epithelial cells and delineate the change in the expression level along with thymic aging. By comparing the expression levels of various miRNAs in thymic epithelial cells and their changes in different age groups, this study provides first-hand information about the changes of miRNA expression in the thymic stroma with aging. | |||
TO cite this article:Guo Zhibin,Chi Feng,Song Yan, et al. Transcriptome analysis of murine thymic epithelial cells reveals age-associated changes in microRNA expression[OL].[20 August 2013] http://en.paper.edu.cn/en_releasepaper/content/4556213 |
3. Interactions between anti-ErbB2 antibody A21 and the ErbB2 extracellular domain provide a basis for improving A21 affinity | |||
Chang Liang ,Zhou Changhai ,Xu Man,Liu Jing | |||
Biology 01 February 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Anti-ErbB2 antibodies are well researched for the therapy of ErbB2-overexpressing tumors. The therapeutic potential and efficacy of these antibodies are closely related to their affinities to ErbB2. Previously we reported that an anti-ErbB2 antibody A21 targeting a conformational epitope comprising several loops in ErbB2 extracellular subdomain I and II could inhibit the proliferation of ErbB2-overexpressing cancer cells in vitro and in vivo. Here we found that another structureless and non-conserved loop in subdomain I of ErbB2 extracellular domain (ECD) was important for binding to A21, and then the antigen-contact sites on A21 were determined by site-directed mutation. The loop was constructed by molecular modeling, and a new model of A21-ErbB2 complex was generated by docking using the crystal structure of the scfv A21 and the model of ErbB2 ECD with the loop built. Based on the complex model, computational design for A21 affinity improvement was performed to enhance its affinity to ErbB2. Two mutants with about 1.7-fold improvement in affinity were obtained. Our study provided a rational molecular basis for affinity improvement and mechanism investigation of A21. | |||
TO cite this article:Chang Liang ,Zhou Changhai ,Xu Man, et al. Interactions between anti-ErbB2 antibody A21 and the ErbB2 extracellular domain provide a basis for improving A21 affinity [OL].[ 1 February 2010] http://en.paper.edu.cn/en_releasepaper/content/39758 |
4. Toxoplasma gondii Profilin Induces Cytokine-mediated Acute Liver Injury through Kupffer Cells and NK Cells in D-Galactosamine-sensitized Mice | |||
Jiang Qun ,Wei Haiming ,Sun Rui ,Tian Zhigang | |||
Biology 01 February 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Accumulating evidence suggests that parasites is inflammatorily active in liver, but the molecular mechanism(s) through which parasites modulates the hepatic innate immune system has not been clearly elucidated. In this study, we found that Toxoplasma gondii profilin, a ligand of toll-like receptor 11 (TLR11), induced the fulminant hepatitis in D-GalN-sensitized mice. The levels of inflammatory cytokine TNFα, IFN-γ and IL-12 in the serum were significantly increased following administration of profilin and D-GalN. Neutralization of these cytokine completely abolished profilin/GalN-induced liver injury. Profilin/GalN treatment could induce recruitment and activation of Kupffer cells and NK cells in liver. TNFα and IFN-γ were produced by Kupffer cells and NK cells, respectively, in profilin/GalN treated mice. Moreover, depletion of Kuppfer cells or NK cells could protect mice from profilin/GalN-induced liver injury, suggesting that these innate immune cells were the major sources of those inflammatory cytokines. This is the first report to show TLR11-induced liver injury, which is helpful to study the liver diseases with parasite infection. | |||
TO cite this article:Jiang Qun ,Wei Haiming ,Sun Rui , et al. Toxoplasma gondii Profilin Induces Cytokine-mediated Acute Liver Injury through Kupffer Cells and NK Cells in D-Galactosamine-sensitized Mice[OL].[ 1 February 2010] http://en.paper.edu.cn/en_releasepaper/content/39741 |
5. Study of IL-12 Cytokine Therapy for OVA-Induced Asthma Model Mice | |||
Xuewei Qu,Fengqi Li,Zhigang Tian,Haiming Wei | |||
Biology 28 January 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Asthma is the disease of allergic hypersensitivity with airway hyperresponsiveness and airway inflammation. Recent studies have shown that IL-12 has a good role in the treatment of asthma, but the mechanisms are not clearly. Therefore, we construct the OVA-induced mouse asthma to studying the mechanisms of IL-12 treatment. Here we demonstrate that IL-12 treatment ameliorated the pathology of OVA-induced asthma. The roles of IL-12 were to inhibit the increase of NKT cells and promote the increase of NK cells. Furthermore, IL-12 treatment promoted the activation of NK cells and enhanced the expression of IFN-γ in lung NK cells. Our results provide the mechanisms of IL-12 cytokine therapy for OVA-induced asthma model mice. | |||
TO cite this article:Xuewei Qu,Fengqi Li,Zhigang Tian, et al. Study of IL-12 Cytokine Therapy for OVA-Induced Asthma Model Mice[OL].[28 January 2010] http://en.paper.edu.cn/en_releasepaper/content/39596 |
6. Molecular cloning, characterization and expression analysis of an Interleukin-2 enhancer binding factor 2 homologue from Tetraodon nigroviridis | |||
Xiang Lixin ,Shao Jianzhong | |||
Biology 09 November 2006 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Interleukin-2 enhancer binding factor 2 (ILF2) was reported to regulate transcription of interleukin-2 (IL-2), a central cytokine in the regulation of T-cell responses. This property of ILF2 was well characterized in human and mammals, but little is known in bony fish. In this paper, an ILF2 homologue was cloned and well characterized from Tetraodon nigroviridi for the further investigation of the function of ILF2 in bony fish. The full-length Tetraodon ILF2 cDNA was 1380 bp in size and contained an open reading frame (ORF) of 1164 bp that translates into a 387 amino-acid peptide with a molecular weight of 42.9 kDa, a 5’ untranslated region (UTR) of 57 bp, and a 3’ UTR of 159 bp containing a poly A tail. The deduced peptide of Tetraodon ILF2 shared an overall identity of 58%~93% with other known ILF2 sequences, and contained two N-glycosylation sites, two N-myristoylation sites, one RGD cell attachment sequence, six protein kinase C phosphorylation sites, one amino-terminal RGG-rich single-stranded RNA-binding domain, and a DZF zinc-finger nucleic acid binding domain, most of which were highly conserved through species compared. Constitutive expression of Tetraodon ILF2 was observed in all tissues examined, including gill, gut, head kidney, spleen, liver, brain and heart. The highest expression was detected in heart, followed by liver, head kidney and brain. Stimulation with LPS did not significantly alter the expression of Tetraodon ILF2. Gene organization analysis showed that the Tetraodon ILF2 gene have fifteen exons, one more than other known ILF2 genes in human and mouse. Genes up- and down-stream from the Tetraodon ILF2 were Rpa12, Peroxin-11b, Smad4, Snapap and Txnip homologue, which were different from that in human and mouse. | |||
TO cite this article:Xiang Lixin ,Shao Jianzhong. Molecular cloning, characterization and expression analysis of an Interleukin-2 enhancer binding factor 2 homologue from Tetraodon nigroviridis[OL].[ 9 November 2006] http://en.paper.edu.cn/en_releasepaper/content/9393 |
Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
Results per page: |
About Sciencepaper Online | Privacy Policy | Terms & Conditions | Contact Us
© 2003-2012 Sciencepaper Online. unless otherwise stated