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1. DDX3Y Computational Catalytic Network Construction and Analysis between Left Brain of Chimpanzee and Human | |||
LIU Xiaoxiao,HUANG Juxiang,WANG Lin | |||
Biology 07 November 2018 | |||
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Abstract:DDX3Y computational catalytic network construction and analysis of human left brain is very useful to identify novel markers and potential targets for the understanding of brain mechanism. By integration of gene regulatory network infer (GRNInfer) and the database for annotation, visualization and integrated discovery (DAVID 2010 version) we identified and constructed significant molecule DDX3Y catalytic network from 15 chimpanzee and 14 human left brain samples in the same GEO Dataset GDS2678. Our result verified DDX3Y catalytic module only in the downstream of chimpanzee left brain (AGL, PDIA2, PPID, RBBP6 activation; ENOSF1, GSTM3, RECQL, RPP14 inhibition) and downstream (DDX19A, ENPP2, RPP14, SPTLC1activation; AGL, ENOSF1, GSTM3, RECQL, HERC2P2, HERC2P3, PCSK6, PDE8A, PDIA2, PPID, RBBP6 inhibition), whereas in the upstream of human left brain (GSTM3, HSD17B6, PCSK6 activation; EGFR, ENOSF1 inhibition) and downstream (AGL, DDX19A, EGFR, HSD17B6 activation; ABCC10, ENPP2, GSTM3, HERC2P3, PCSK6, PDE8A, PDIA2, PPID, RECQL, SPTLC1 inhibition). Importantly, we datamined that DDX3Y catalytic cluster of human left brain is involved in nervous system development, ubl conjugation, response to chemical stimulus, neurogenesis, cell development and cognition, regulation of apoptosis, anatomical structure development, ATPase activity, coupled, endoplasmic reticulum, polysaccharide binding, pyrophosphatase activity, cellular localization, transport and calcium ion binding (only in human left brain terms) without Isomerase and zinc ion binding (only in chimpanzee left brain terms), the condition is vital to central nervous system development and cognition of human left brain. Our result demonstrated that common terms in both chimpanzee and human left brain include phosphoprotein, hydrolase, organelle, metabolic process, nucleic acid binding, metal-binding, acetylation, DNA binding, Golgi apparatus, identical protein binding, homeostatic process, signal transducer activity, membrane, developmental process, glycoprotein, cytoskeletal protein binding, regulation of cellular process and biosynthetic process, and these terms are more relative to development and cognition, therefore we deduced the stronger DDX3Y catalytic network in human left brain consistent with our number computation. It would be necessary of the stronger DDX3Y catalytic function to development and cognition of human left brain. | |||
TO cite this article:LIU Xiaoxiao,HUANG Juxiang,WANG Lin. DDX3Y Computational Catalytic Network Construction and Analysis between Left Brain of Chimpanzee and Human[OL].[ 7 November 2018] http://en.paper.edu.cn/en_releasepaper/content/4746419 |
2. 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 | |||
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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 |
3. C-terminus of MUC16 interacts with β-catenin to activate Wnt signaling pathway, tumorigenesis and metastasis | |||
Liu Qi,Yang Yun,Ma Huanhuan,Li Xiaotong,Li Qinxi | |||
Biology 26 May 2016 | |||
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Abstract:MUC16/CA125 has been identified as a prominent cancer biomarker, especially for epithelial ovarian cancers, in clinical test for over three decades. Due to its huge mass, limited knowledge of MUC16 was acquired previously. By utilizing a well characterized self-made MUC16 monoclonal antibody, we identified the endogenous interaction between a C-terminal fragment of MUC16 (MUC16C) and β-catenin for the first time, and further elucidated that trans-activation domain of β-catenin is required for this interaction. Such interaction could activate the Wnt/β-catenin signaling pathway by facilitating cytosol-nucleus transportation of β-catenin, consequently induce cell proliferation and migration, eventually lead to tumorigenesis and metastasis in nude mice. Consistently, knockdown of MUC16 significantly weakened the capabilities of cells for proliferation and migration. Based on our discovery, we suggest that MUC16 appears as an attractive target for the development of effective anticancer drugs. | |||
TO cite this article:Liu Qi,Yang Yun,Ma Huanhuan, et al. C-terminus of MUC16 interacts with β-catenin to activate Wnt signaling pathway, tumorigenesis and metastasis[OL].[26 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4692324 |
4. Caldesmon Phosphorylation Plays a Key Role in Tumor Metastasis | |||
JIANG Qifeng,XIONG Xingliang | |||
Biology 18 May 2016 | |||
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Abstract:In this paper, we have performed transwell migration assays and contractility measurements by traction microscopy using human breast cancer cell lines MDA MB-231 and MCF-7, transfected with wild-type or mutated CaD. We found that cells expressing the A1234 mutant of CaD exhibited most robust contractile activity, the effect being more profound in MDA-MB231 cells than in MCF-7 cells, whereas the same mutant resulted in most severely hampered migration in both types of cells. These mutant cells also exhibited enhanced stress fibers and delayed trypsin-induced detachment from substratum. Taken together, phosphorylation of CaD appears to have an opposite effect on cell migration and contractility. Cells with extensive and dynamic CaD phosphorylation favor motile activities. Unphosphorylated CaD facilitates stable actin filaments, which is needed to support cell contractility, but could stifle cell movement if irreversible. The observed difference between the two tumor cell lines may thus reflect their different intrinsic kinase activities. The metastatic MDA-MB231 cells have higher levels of CaD and more active kinases than the non-metastatic MCF-7 cells. An elevated amount of phosphorylated CaD contributes to cell migration and invasion. Our findings not only shed light on the mechanism by which CaD regulates cell motility, but also provide new insights into the nature of metastasis of cancer cells. | |||
TO cite this article:JIANG Qifeng,XIONG Xingliang. Caldesmon Phosphorylation Plays a Key Role in Tumor Metastasis[OL].[18 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4689102 |
5. E3 Activity of MDM2 is not required for MDM2 to Inhibits Axin-induced p53 Activation | |||
He Ying,Lian Guili,Ma Huanhuan,Lin Shuyong,Li Qinxi | |||
Biology 11 May 2016 | |||
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Abstract:MDM2 plays a crucial role in negatively regulating the functions of tumor suppressor p53. Here we show that MDM2 can inhibit Axin-stimulated p53-dependent apoptosis by suppressing p53 phosphorylation at Ser 46 and apoptosis-related p53 transactivational activity. Interestingly, the ubiquitin E3 ligase activity of MDM2 is not required for this inhibitory effect. Mechanically, either wildtype Mdm2 or its E3-dead mutant, disrupts the Axin-based HIPK2/p53 complex formation by blocking the binding of p53 and HIPK2 to Axin. Mdm2Δp53, a deletion mutant that lacks p53 binding domain fails to exert the inhibitory effect, demonstrating that the interaction of Mdm2 and p53, but not its E3 ligase activity toward p53 plays key role in suppressing Axin-stimulated p53 activation. Our results thus have revealed a novel aspect of the mechanism by which MDM2 regulates p53 activities. | |||
TO cite this article:He Ying,Lian Guili,Ma Huanhuan, et al. E3 Activity of MDM2 is not required for MDM2 to Inhibits Axin-induced p53 Activation[OL].[11 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4688749 |
6. Positive Regulatory Function of miR-92a During Osteoblast Differentiation | |||
LI Zhaoyong | |||
Biology 01 March 2016 | |||
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Abstract:MicroRNAs regulate biological processes by binding to mRNA 3'-untranslated region (UTR) sequences to attenuate protein synthesis. Here we identified that miR-92a are up-regulated through stages of osteoblast differentiation. Twist-1, a negative regulator of osteoblast differentiation, is validated to be a direct target of miR-92a by luciferase activity assay. Overexpression of miR-92a down-regulates Twist-1 protein expression, but not its mRNA level. Inversely, ectopic miR-92a expresson increases Runx2 expression, as well as alkaline phosphatase and osteocalcin mRNA level. Twist-1 protein shows reverse profile as miR-92a and Runx2 during osteoblast differentiation. Thus, we propose that miR-92a functions as a positive regulator during osteoblast differentiation by targeting anti-osteogenic factors and activating osteogenic marker genes. | |||
TO cite this article:LI Zhaoyong. Positive Regulatory Function of miR-92a During Osteoblast Differentiation[OL].[ 1 March 2016] http://en.paper.edu.cn/en_releasepaper/content/4679112 |
7. High EPHA4 outside-inside-out interactive neuro-induced regulation of growth through ALK-C9orf127-ARHGDIG | |||
ZHANG Liming,WANG Lin | |||
Biology 26 September 2015 | |||
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Abstract:13 different Pearson mutual-positive-correlation EPHA4-activation molecular network was constructed from 53 overlapping of 166 GRNInfer and 70 Pearson under EPHA4 CC ≥0.25 in high human hepatocellular carcinoma (HCC) compared with low no-tumor hepatitis/cirrhotic tissues (HBV or HCV infection). Our identified EPHA4 outside-inside-out interactive molecular network showed ALK (anaplastic lymphoma receptor tyrosine kinase), C9orf127 (chromosome 9 open reading frame 127), ARHGDIG (Rho GDP dissociation inhibitor (GDI) gamma) in high HCC. EPHA4 outside-inside-out interactive terms network includes integral to plasma membrane, membrane, transmembrane receptor protein tyrosine kinase signaling pathway, nucleus, cytoplasm, mitochondrion, endoplasmic reticulum, plasma membrane, cell surface, integral to membrane, membrane fraction, cytoplasmic membrane-bound vesicle; neurogenesis, axon guidance; nervous system development, brain development, cell adhesion, cell-matrix adhesion, regulation of progression through mitotic cell cycle, regulation of growth, negative regulation of cell adhesion; nucleotide-binding, transmembrane receptor protein tyrosine kinase activity, receptor signaling protein tyrosine kinase activity, receptor activity, protein-binding, ATP-binding, transferase activity, protein-tyrosine kinase activity, ephrin receptor activity, Rho GDP-dissociation inhibitor activity, GTPase activator activity based on integrative GO, KEGG, GenMAPP, BioCarta and disease databases in high HCC. Therefore, we propose high EPHA4 outside-inside-out interactive neuro-induced regulation of growth through ALK-C9orf127-ARHGDIG in HCC.????? | |||
TO cite this article:ZHANG Liming,WANG Lin. High EPHA4 outside-inside-out interactive neuro-induced regulation of growth through ALK-C9orf127-ARHGDIG[OL].[26 September 2015] http://en.paper.edu.cn/en_releasepaper/content/4655855 |
8. Mechanism of fungal growth suppression by excessive soil phosphorus | |||
CAO Zhiping | |||
Biology 06 November 2014 | |||
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Abstract:Phosphorus is an underappreciated resource that has nearly run out. On the other hand, it has been accumulated in agricultural soil at an accelerated rate during recent decades, which may results in migration of agricultural soil from carbon sink to resource, deterioration of soil quality, reduction in agricultural productivity and speed up of global climate changes. This blooming crisis forces us to reveal the mechanism of fungal suppression by excessive soil phosphorus. Here I propose a hypothesis to explain why excessive phosphorus inhibits fungal growth. High concentrations of phosphate ions change the structural stability of the fungal cell membrane and possibly increase the fluidity of the membrane lipids. Under a relatively high temperature, membrane fluidity may be further exacerbated, thereby undermining the structure of the fungal cell membrane. Technical strategies to test the hypothesis were stated. Meanwhile, the various applications based on the elucidation of this mechanism in biology and medical sciences were also discussed. The finding presented in this study explains the worldwide problem caused by the application of conventional chemical fertilizers, and sheds light on new development in medical science, pharmacy, agriculture and industry. | |||
TO cite this article:CAO Zhiping. Mechanism of fungal growth suppression by excessive soil phosphorus[OL].[ 6 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4616954 |
9. Parkin RING1 domain mutant impair its mitochondrial translocation and interaction with PINK1 | |||
YANG Hui,YANG Ling,GAO Peiye,ZUO Ji,YE Xiaofei,LIU Wen | |||
Biology 30 November 2013 | |||
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Abstract:In Mutations in Parkin and PTEN-induced putative kinase 1 (PINK1) could cause autosomal recessive forms of Parkinson's disease (PD), but how these mutations trigger mitochondrial dysfunction and the precise relationship between Parkin and PINK1 are still poorly understood. Recent studies indicate that with the help of PINK1, Parkin can promote the clearance of impaired mitochondria by mitophagy. Especially, it remains to be clarified the role of RING1 domain of Parkin in the interaction with PINK1 and its mitochondrial recruitment. In the present study, we reported that in a non-neuronal human HeLa cell line, the RING1 finger related mutation of Parkin (T240R) affected its ability to interact with full-length PINK1 under normal condition. Furthermore our immunofluorescence results shows that RING1 finger related mutations of Parkin did not affect its subcellular localization, but minimal co-localization of mutant Parkin (T240R and RING1 Del) with mitochondria were observed when cotransfection with PINK1. Our results provide the links between PINK1 and Parkin are important to sustain the mitochondrial integrity and may shed a light on the pathogenesis of PD, especially in the aspect of the PINK1-Parkin pathway. | |||
TO cite this article:YANG Hui,YANG Ling,GAO Peiye, et al. Parkin RING1 domain mutant impair its mitochondrial translocation and interaction with PINK1[OL].[30 November 2013] http://en.paper.edu.cn/en_releasepaper/content/4571865 |
10. Fibulin-2 regulates Angiotensin II-induced fibrotic response in cultured cardiac fibroblasts via modulating TGF-beta1 signaling | |||
Zhao Yongxi,Wu Jing | |||
Biology 16 November 2013 | |||
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Abstract:Fibulin-2, a typical product of fibroblasts, has been recently implicated in physiological or pathological ECM remodeling and tissue fibrosis, but the roles and underlying mechanisms remain obscure. Angiotensin II (Ang-II) and TGF-beta play a pivotal role in cardiac remodeling, which do not act independently from one another but rather act as part of a signalling network to promote cardiac remodeling. The cardiac fibroblasts (CFs), the most abundant cell type present in the heart, are responsible for the deposition of extracellular matrix. The present study was designed to investigate the role and molecular mechanisms of fibulin-2 in Ang-II-induced ECM changes and TGF-beta signaling pathway in cultured CFs. Methods: CFs were isolated from wild type (WT) and fibulin-2 deficient (Fbln2-/-) adult mice in C57BL/6 background, and treated with Ang-II, Ang-II plus neutralizing antibody to TGF-beta, or recombinant TGF-beta1 for 24h. Real-time RT-PCR was performed to assess mRNA expression of collagen type I (Col I), type III (Col III), fibulin-2 (FBLN2), TGF-beta1 and MMP-2. ELISA assay and gelatin zymographic analysis were performed to examine TGF-beta1 concentration and MMP-2 activity in the conditioned culture medium. Western blot analysis was performed to detect Smad-2 and p-Smad2 protein expression. Results: FBLN2 mRNA was markedly up-regulated in WT CFs by Ang-II, and partially decreased when plus neutralizing antibody to TGF-beta. In FBLN2-/- CFs, there was no FBLN2 mRNA detected. There was no discernible difference in mRNA expression of Col I, Col III, TGF-beta1 and MMP-2 between control WT and Fblin2-/- CFs. Ang-II treated WT CFs showed significant increase in Col I, Col III, TGF-beta1 and MMP-2 mRNA expression from control. Compared to WT CFs, Fbln2-/- CFs induced by Ang-II showed a significantly less extent increase in these markers. MMP-2 activity showed essentially identical patterns to relative MMP-2 mRNA levels. TGF-beta1 concentration in WT supernatants was significantly elevated by Ang-II but not in Fbln2-/- supernatants. Smad2 expression was not changed by Ang-II, however p-Smad2, was significantly increased by Ang-II in WT CFs but not in Fbln2-/- CFs. Plus neutralizing antibody to TGF-beta, up-regulation of Col I, Col III, TGF-beta1 and MMP-2 expression, MMP-2 activity, and Smad2 phosphorylation induced by Ang-II in WT CFs was partially reduced, but no significant effects on FBLN2-/- CFs. Conclusion: Fibulin-2 enhanced Ang-II-induced ECM remodeling (increased collagen synthesis and MMP activation), which was partially mediated by TGF-beta activation. TGF-beta mediated positive feedback loop plays a central role in Ang-II-induced ECM remodeling. Fibulin-2 is required for Ang-II-induced TGF-beta activation in promoting ECM remodeling. | |||
TO cite this article:Zhao Yongxi,Wu Jing. Fibulin-2 regulates Angiotensin II-induced fibrotic response in cultured cardiac fibroblasts via modulating TGF-beta1 signaling[OL].[16 November 2013] http://en.paper.edu.cn/en_releasepaper/content/4564806 |
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