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 OAS1, then constructed OAS1 up- and down-stream network by infer and further data-mined the main OAS1 modules including response to stimulus, catalytic activity, organelle, metabolic process, alternative splicing and sequence variant from 16 frontal cortex of HIV encephalitis (HIVE) and 12 no-encephalitis HIV patients in the same GEO Dataset GDS1726. Our infer OAS1 network result showed the different gene rate of HIVE as 78% (21/27) compared with the control considering activation and inhibition relationship. The different active genes in HIVE include HLA_B, ISG15_1, ISG15_2, LCAT, LY96, M33210, PDCD4, STAT1, VEZF1, ADH1B, DGKG, IFI35, LSM7, TSPAN4, ZC3HAV1 and the different inhibitory genes include DGKG, CREB5, GAS1, M33210, TENC1, VEZF1. Our integrative analysis showed the positive results of OAS1 response to stimulus, catalytic activity, organelle, metabolic process, alternative splicing and sequence variant through the net numbers of activation minus inhibition compared with the control and predicted the increases of these modules in HIVE.

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	1. OAS1 network construction and analysis of the frontal cortex with HIV encephalitis (HIVE) compared with no-encephalitis HIV patients by integrative biocomputation
	LI Hao,WANG Lin,HUANG Juxiang
	Basic Medicine 14 November 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 OAS1, then constructed OAS1 up- and down-stream network by infer and further data-mined the main OAS1 modules including response to stimulus, catalytic activity, organelle, metabolic process, alternative splicing and sequence variant from 16 frontal cortex of HIV encephalitis (HIVE) and 12 no-encephalitis HIV patients in the same GEO Dataset GDS1726. Our infer OAS1 network result showed the different gene rate of HIVE as 78% (21/27) compared with the control considering activation and inhibition relationship. The different active genes in HIVE include HLA_B, ISG15_1, ISG15_2, LCAT, LY96, M33210, PDCD4, STAT1, VEZF1, ADH1B, DGKG, IFI35, LSM7, TSPAN4, ZC3HAV1 and the different inhibitory genes include DGKG, CREB5, GAS1, M33210, TENC1, VEZF1. Our integrative analysis showed the positive results of OAS1 response to stimulus, catalytic activity, organelle, metabolic process, alternative splicing and sequence variant through the net numbers of activation minus inhibition compared with the control and predicted the increases of these modules in HIVE.
	TO cite this article:LI Hao,WANG Lin,HUANG Juxiang. OAS1 network construction and analysis of the frontal cortex with HIV encephalitis (HIVE) compared with no-encephalitis HIV patients by integrative biocomputation[OL].[14 November 2018] http://en.paper.edu.cn/en_releasepaper/content/4746438


	2. Dental Pulp Stem Cells in Tooth Regeneration: Characterizations and Applications
	Su Cheng,Zhu Guanyin,Zheng Yi,Gao Bo
	Basic Medicine 04 November 2017
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	Abstract:In order to make up the deficiency of traditional medical treatment method, regenerative medicine as a new research field has received extensive attention in the recent years. Dental pulp stem cells(DPSCs), originating from the neural crest, become a promising source for tooth regeneration applications for their unique advantages, such as easily isolated and minimally invasive. As a kind of mesenchymal stem cells, DPSCs have the ability to differentiate in several cell phenotypes including odontogenic differentiation, vascularization and neural differentiation. To be applied in tissue engineering, DPSCs are usually combined with various scaffolds and growth factors. Based on the characterizations of DPSCs, they are considered to be a great candidate for application used in regenerative endodontic procedures and whole tooth regeneration. In this review, we have carefully described the important aspects of DPSCs and discussed the practical applications in the present studies. this paper.
	TO cite this article:Su Cheng,Zhu Guanyin,Zheng Yi, et al. Dental Pulp Stem Cells in Tooth Regeneration: Characterizations and Applications[OL].[ 4 November 2017] http://en.paper.edu.cn/en_releasepaper/content/4741871

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	3. The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury
	ZHOU Beiqun,ZHU Jiangtao
	Basic Medicine 17 May 2016
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	Abstract:Mixed lineage kinase domain-like protein (MLKL) was recently identified to play a critical role in necrotic cell death. To examine its role in ischemia injury, we examined its expression and the degradation of MLKL on neuroprotective effects in a middle cerebral artery occlusion (MCAO) model. We found that MLKL expression was significantly increased at 6 h after reperfusion and reached peak at 48 h after I/R injury. Our findings further demonstrated that a small chemical Necrosulfonamide (NSA) decreased MLKL level after I/R injury by increasing the degradation of MLKL through the ubiquitination proteasome pathway. The degradation of MLKL by NSA also increased cleaved PARP-1 level, a marker of apoptosis. The reduction of MLKL by NSA markedly improved neurological deficits compared with vehicle-treated mice after MCAO. NSA pre-treatment and post-treatment reduced infarct volume even when NSA was administrated at 4 h after I/R injury, indicating a long therapeutic window of NSA treatment. These findings suggest that MLKL plays a critical role in ischemic injury and is a new therapeutic target for stroke. Therefore, Promoting the degradation of MLKL may represent a novel avenue for reducing necrotic cell death after ischemic brain injury.
	TO cite this article:ZHOU Beiqun,ZHU Jiangtao. The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury[OL].[17 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4690231


	4. 3D rotary culture system augment megakaryopoiesis and thrombopoiesis
	YANG Yiqing,Liu Cuicui,Lei Xiaohua,Zhou Jiaxi
	Basic Medicine 25 November 2015
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	Abstract:Platelets transfusion has been widely used by patients undergoing chemotherapy or radiotherapy, but the shortage of platelet supply limits the care of patients. While derivation of clinical-scale platelets in vitro would provide new source for transfusion, devices and procedures for deriving scalable platelets for clinical applications have not been established. In this study, we found that a rotary cell culture system (RCCS) can potentiate megakaryopoiesis and significantly improve the efficiency of platelet generation. Shear force, simulated microgravity and better diffusion of nutrients and oxygen from RSCCS altogether may account for the improved efficient platelet generation. The cost-effective and highly controllable strategy and methodology represent an important step toward large-scale platelet production for future biomedical and clinical applications.?
	TO cite this article:YANG Yiqing,Liu Cuicui,Lei Xiaohua, et al. 3D rotary culture system augment megakaryopoiesis and thrombopoiesis[OL].[25 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4664369


	5. SHIP2 interacts with MLK3 and regulates its tyrosine phosphorylation
	WU Zhe,XIE Jingwei
	Basic Medicine 09 November 2015
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	Abstract:MLK3, a serine/threonine MAP3K, implicates in various physiological functions as neurodegenerative disease, cell cycle regulation, apoptosis and T-cell activation etc. Phosphorylation of MLK3 is essential for its activation. Ocassionally, in our previous study, MLK3 was found to be phosphorylated at tyrosine site which had not reported yet. Data in the present study show that SHIP2 positively regulated MLK3 tyrosine phosphorylation through SHIP2-MLK3 interaction, and JIP1 showed negative effect on this tyrosine phosphorylation. In addition, SHIP2-MLK3 association was not modulated in response to EGF or TNF-α. Domain tests demonstrate that the catalytic domain of SHIP2 was responsible for the interaction with MLK3. All together, our data may provide a new potential regulating mechaniam of cross-talk between SHIP2 and MLK3-mediated MAPK pathway.
	TO cite this article:WU Zhe,XIE Jingwei. SHIP2 interacts with MLK3 and regulates its tyrosine phosphorylation[OL].[ 9 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4660744


	6. JIP1 negatively regulates SHIP2 catalytic activity through protein-protein interaction
	WU Zhe,XIE Jingwei
	Basic Medicine 09 November 2015
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	Abstract:SHIP2, a SH2-containing inositol polyphosphate 5-phosphatase 2, plays a role in insulin and growth factor signaling, cytoskeletal organization, neurodegenerative diseases etc. In our previous study, JIP1 (JNK-interacting protein 1) was identified as a new protein partner of SHIP2 and SHIP2 showed negative effect on JIP1-mediated JNK activity. Herein, the region of SHIP2 involved in the interaction with JIP1 and the effect of JIP1 on SHIP2 were inverstigated. Data showd that there existed other region than PR domain of SHIP2 implicating in the association with JIP1, and JIP1 negatively regulated SHIP2 catalytic activity. In addition, SHIP2 might be phosphorylated by JIP1-mediated JNK on serine/threonine sites. Taken together, through JIP1-SHIP2 interaction, JIP1 might be implicated in the signalling functional consequences such as neurodegenerative diseases, cells proliferation and insulin resistance etc.
	TO cite this article:WU Zhe,XIE Jingwei. JIP1 negatively regulates SHIP2 catalytic activity through protein-protein interaction[OL].[ 9 November 2015] http://en.paper.edu.cn/en_releasepaper/content/4660362


	7. Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases
	ZHANG Qiuyu,WU Linqing,HAN Yangfei,XU weiqun,ZHANG Tao
	Basic Medicine 25 December 2014
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	Abstract:OBJECT: To investigate the effect of extracellular high-mobility group box 1（HMGB1）on cell proliferation and signaling pathway in human gastric cancer cell. Methods: Immunohistochemistry and immunocytochemistry localized HMGB1 in gastric cancer tissues and gastric carcinoma cell lines. The protein level of microtubule light chain 3（LC3-I, LC3-II）and the formation of autophagic vesicles in gefitinib -induced BGC-823 cells were assessed by western blotting and confocal microscopy respectively. Western blot and ELISA were used to assess the effects of gefitinib, an epidermal growth factor receptor inhibitor, on autophagy and HMGB1 release in BGC-823 cells. MTT and Western blot assessed the effects of extracellular HMGB1 on cell proliferation and signaling transduction. Results: Released HMGB1 promoted proliferation through activation of ERK1/2 MAPK. HMGB1 expression in gastric cancer tissue and serum was significantly increased compared to control and healthy serum. Gastric carcinoma cells showed elevated HMGB1 in nuclei and cytoplasm, whereas GES-1 cells exhibited lower HMGB1 with nuclear localization. Gefitinib increased autophagy and cytoplasmic HMGB1 release from BGC-823 cells. Extracellular HMGB1 in autophagic cell supernatant promoted proliferation that was abolished by glycyrrhizic acid, an HMGB1 inhibitor. BGC-823 cells incubated with HMGB1 increased ERK1/2 phosphorylation, but did not affect JNK, p38 or AKT. Blocking RAGE-HMGB1 interaction with antibody or siRNA suppressed ERK1/2 activation and gastric cancer cell growth, indicating RAGE-mediated ERK1/2 signaling was necessary for tumor progression. Conclusions: Extracellular HMGB1 promoted growth through RAGE-dependent activation of ERK1/2 in gastric cancer.
	TO cite this article:ZHANG Qiuyu,WU Linqing,HAN Yangfei, et al. Autophagy-mediated HMGB1 release promotes survival of gastric cancer cells via the activation of ERK1/2 MAPK kinases[OL].[25 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4624561


	8. Inhibition of the mevalonate pathway ameliorates anoxia-induced down-regulation of FKBP12.6 and intracellular calcium handling dysfunction in H9c2 cells
	YANG Ying,LV Xue,Rong Xiqing,LAI Dongwu,FU Guosheng
	Basic Medicine 16 November 2014
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	Abstract:Statins have beneficial pleiotropic effects beyond lipid lowering on the cardiovascular system. These cardio-protective effects are mediated through inhibition of the intracellular mevalonate pathway, by decreasing isoprenoid intermediates synthesis and the subsequent post-translational modification of small GTPases, such as Ras, Rho, and Rac. Impaired intracellular calcium handling is considered an important physiopathologic mechanism responsible for cardiac dysfunction. Our study aimed at investigating the influence of mevalonate pathway, including its downstream small GTPases (Ras, RhoA, and Rac1) on anoxia-mediated alterations of calcium handling in H9c2 cardiomyocytes. Cultured H9c2 cardiomyocytes were exposed to acute anoxia after pretreatment with different drugs that specifically antagonize five key components in the mevalonate pathway, including 3-hydroxy-3-methylgutaryl-CoA reductase, farnesyl pyrophosphate synthase, Rho-kinase, Rac1 and Ras farnesyltransferase. Thereafter, we evaluated the effects of t?he mevalonate pathway on anoxia-induced cell death, expression of the sarcoplasmic reticulum calcium release channel (ryanodine receptor 2) and its regulator FK506-binding protein 12.6. Our experiments confirmed the role of prenylated proteins in regulating cardiomyocyte dysfunction, especially via RhoA- and Ras-related signaling pathways. Furthermore, our data demonstrated that inhibition of the mevalonate pathway could ameliorate anoxia-mediated calcium handling dysfunction with the up-regulated expression of FK506-binding protein 12.6 and consequently provided evidence for FK506-binding protein 12.6 as a "stabilizer" of ryanodine receptor 2.
	TO cite this article:YANG Ying,LV Xue,Rong Xiqing, et al. Inhibition of the mevalonate pathway ameliorates anoxia-induced down-regulation of FKBP12.6 and intracellular calcium handling dysfunction in H9c2 cells[OL].[16 November 2014] http://en.paper.edu.cn/en_releasepaper/content/4618949


	9. Signal pathways involved in inhibition of berberine on human umbilical vein endothelial cell proliferation induced by oxidized low-density lipoprotein
	Xu Ruixia,Li Xiaolin,Guo Yuanlin,Zhu Chenggang,Li Sha,Sun Jing,Ye Jue,Jiang Lixin,Li Jianjun
	Basic Medicine 18 December 2013
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	Abstract:Objectives: Oxidized low-density lipoprotein (oxLDL) is a proatherogenic lipoprotein, accumulating in the vascular wall and playing an important role in the development of atherosclerosis. This study aims to investigate the effect of berberine on HUVECs proliferation induced by oxLDL and its potential signaling pathways. Methods and results: HUVECs were stimulated with oxLDL and co-cultured with berberine at a variety of concentrations at different time points. The data showed that oxLDL (10-100 μg/ml) remarkably promoted HUVECs proliferation assessed by Cell Counting Kit-8 (CCK-8) and EdU assay. The effects were found to be involved in up-regulation of PCNA, NF-кB and LOX-1 and activation of PI3K/Akt, ERK1/2 and p38MAPK signaling pathways evaluated by either real time PCR or western blot analysis. Interestingly, HUVECs proliferation was significantly inhibited by berberine (5-25 μg/ml), which was associated with down-regulating of PCNA, NF-кB and LOX-1 and decreasing the phosphorylation of Akt, ERK1/2 and p38MAPK. Furthermore, the anti-proliferative effect of berberine on HUVECs was effectively abrogated by a PI3K inhibitor LY294002, an ERK1/2 inhibitor PD98059 and a p38 inhibitor SB202190 partly through the restoration of phosphorylation of Akt, ERK1/2 and p38MAPK. Conclusions: The data firstly demonstrated that berberine inhibited ox-LDL-induced HUVECs proliferation by decreasing the expression of PCNA, NF-кB and LOX-1 and suppressing the activation of PI3K/Akt, ERK1/2 and p38MAPK pathways, suggesting that berberine may be a potential candidate of medications to prevent the oxLDL-induced endothelial cells proliferation involved in endothelial dysfunction and atherosclerosis.
	TO cite this article:Xu Ruixia,Li Xiaolin,Guo Yuanlin, et al. Signal pathways involved in inhibition of berberine on human umbilical vein endothelial cell proliferation induced by oxidized low-density lipoprotein[OL].[18 December 2013] http://en.paper.edu.cn/en_releasepaper/content/4575371


	10. BH3-only proteins in myocardial ischemia: poison or meal?
	Xin Hong,Bao Guangzhi,Wang Minjun,Zhu Yizhun
	Basic Medicine 10 January 2013
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	Abstract:Loss of myocardial cells via apoptosis has been characterized in ischemic heart disease. BH3-only proteins of Bcl-2 family are essential initiators of apoptosis during heart ischemia and hypoxia. Multiple BH3-only proteins, such as Bnip3, Nix, Puma, Bid and Bad, have been upregulated and shown to contribute to the cell death via apoptosis pathway during myocardial ischemia. Autophagic flux is activated in ischemic heart disease due to the short supply of nutrients. BH3-only proteins also control the initiation of autophagy which is another important pathway regulating cell survival and death. A novel BH3-only protein, beclin-1, plays a critical role in autophagy. Autophagy functions as cardioprotective pathway to overcome the stress through against apoptosis, but prolonged activation can result in cell death. Here we review the roles of BH-3 only proteins in myocardial ischemia.
	TO cite this article:Xin Hong,Bao Guangzhi,Wang Minjun, et al. BH3-only proteins in myocardial ischemia: poison or meal?[OL].[10 January 2013] http://en.paper.edu.cn/en_releasepaper/content/4513724

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