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26篇 您的检索式:作者名="Shi Xianjun"
    题名 作者 年代 出处 被引量
1ERK kinase phosphorylates and destabilizes the tumor suppressor FBW7 in pancreatic cancer显示文摘Shunrong Ji Yi Qin Si Shi Xiangyuan Liu Hongli HU Hu Zhou Jing Gao Bo Zhang Wenyan Xu Jiang Liu Dingkong Liang Liang Liu Chen Liu Jiang Long Haijun Zhou Paul J Chiao Jin Xu Quanxing Ni Daming Gao Xianjun Yu 2015Cell Research2015,25,5:19
2Neuroprotective effect of pretreatment with ganoderma lucidum in cerebral ischemia/reperfusion injury in rat hippocampus显示文摘Ganoderma lucidum is a traditional Chinese medicine,which has been shown to have both anti-oxidative and anti-inflammatory effects,and noticeably decreases both the infarct area and neuronal apoptosis of the ischemic cortex.This study aimed to investigate the protective effects and mechanisms of pretreatment with ganoderma lucidum(by intragastric administration)in cerebral ischemia/reperfusion injury in rats.Our results showed that pretreatment with ganoder-ma lucidum for 3 and 7 days reduced neuronal loss in the hippocampus,diminished the content of malondialdehyde in the hippocampus and serum,decreased the levels of tumor necrosis fac-tor-αand interleukin-8 in the hippocampus,and increased the activity of superoxide dismutase in the hippocampus and serum.These results suggest that pretreatment with ganoderma lucidum was protective against cerebral ischemia/reperfusion injury through its anti-oxidative and an-ti-inflammatory actions.Wangxin Zhang Qiuling Zhang Wen Deng Yalu Li Guoqing Xing Xianjun Shi Yifeng Du 2014Neural Regeneration Research2014,9,15:6
3Signaling pathways in cancer-associated fibroblasts:recent advances and future perspectives显示文摘As a critical component of the tumor microenvironment(TME),cancerassociated fibroblasts(CAFs)play important roles in cancer initiation and progression.Well-known signaling pathways,including the transforming growth factor-β(TGF-β),Hedgehog(Hh),Notch,Wnt,Hippo,nuclear factor kappa-B(NF-κB),Janus kinase(JAK)/signal transducer and activator of transcription(STAT),mitogen-activated protein kinase(MAPK),and phosphoinositide 3-kinase(PI3K)/AKT pathways,as well as transcription factors,including hypoxia-inducible factor(HIF),heat shock transcription factor 1(HSF1),P53,Snail,and Twist,constitute complex regulatory networks in theTMEtomodulate the formation,activation,heterogeneity,metabolic characteristics and malignant phenotype of CAFs.Activated CAFs remodel the TME and influence the malignant biological processes of cancer cells by altering the transcriptional and secretory characteristics,and this modulation partially depends on the regulation of signaling cascades.The results of preclinical and clinical trials indicated that therapies targeting signaling pathways in CAFs demonstrated promising efficacy but were also accompanied by some failures(e.g.,NCT01130142 and NCT01064622).Hence,a comprehensive understanding of the signaling cascades in CAFs might help us better understand the roles of CAFs and the TME in cancer progression and may facilitate the development of more efficient and safer stroma-targeted cancer therapies.Here,we review recent advances in studies of signaling pathways in CAFs and briefly discuss some future perspectives on CAF research.Zengli Fang Qingcai Meng Jin Xu Wei Wang Bo Zhang Jiang Liu Chen Liang Jie Hua Yingjun Zhao Xianjun Yu Si Shi 2023Cancer Communications2023,43,1:5
4Energy sources identify metabolic phenotypes n pancreatic cancer显示文摘Chen Liang Yi Qin Bo Zhang Shunrong Ji Si Shi Wenyan Xu Jiang Liu Jinfeng Xiang Dingkong Liang Qiangsheng Hu Liang Liu Chen Liu Guopei Luo Quanxing Ni Jin xu Xianjun Yu 2016Acta Biochimica et Biophysica Sinica2016,48,11:3
5SETD8 induces stemness and epithelial–mesenchymal transition of pancreatic cancer cells by regulating ROR1 expression显示文摘Pancreatic cancer(PC)is one of the most deadly diseases,and its incidence is increasing year by year.The methyltransferase SETD8 has been demonstrated to play an important role in tumor cell proliferation and metastasis.However,little is known about whether SETD8 could affect the invasion and metastasis of PC and the mechanism underlying the regulation.Based on our previous report,here,we further found that SETD8 could promote the invasion and migration of PC cells by inducing the expression of receptor tyrosine kinase-like orphan receptor 1(ROR1).ROR1 was predominantly upregulated in PC tissues and was correlated with lymph node metastasis and worse prognosis.Mechanistically,SETD8 mediated ROR1 activity and regulated PC cells invasion and migration,although promoting the expression of stemness and epithelial–mesenchymal transition-related molecules.This promotion effect disappeared when the catalytically inactive mutant SETD8 was overexpressed,which could be counteracted by the SETD8-specific methyltransferase inhibitor UNC0379.Collectively,our results demonstrate that SETD8 may be a novel prognostic factor and a therapeutic target of PC.Mengqi Liu Yihua Shi Qiangsheng Hu Yi Qin Shunrong Ji Wensheng Liu Qifeng Zhuo Guixiong Fan Zeng Ye Changfeng Song Xianjun Yu Xiaowu Xu Wenyan Xu 2021Acta Biochimica et Biophysica Sinica2021,53,12:2
6The association of interleukin-16 gene polymorphisms with IL-16 serum levels and risk of nasopharyngeal carcinoma in a Chinese population显示文摘Xue Qin Qiliu Peng Xiaoxia Lao Zhiping Chen Yu Lu Xianjun Lao Cuiju Mo Jingzhe Sui Junrong Wu Limin Zhai Shi Yang Shan Li Jinmin Zhao 2014Tumor Biology2014,,3:2
7LSD1 sustains pancreatic cancer growth via maintaining HIF1α-dependent glycolytic process显示文摘Yi Qin Wenwei Zhu Wenyan Xu Bo Zhang Si Shi Shunrong Ji Jiang Liu Jiang Long Chen Liu Liang Liu Jin Xu Xianjun Yu 2014Cancer Letters2014,,:1
8Analysis of water transport properties for plant structured textile fabric 显示文摘SHI Xianjun WU Jihong 2009Advanced Materials Research2009,79,82:1
9A QTL for rice grain width and weight encodes a previously unknown RING-type E3 ubiquitin ligase显示文摘Song Xianjun Huang Wei Shi Min etal 2007Nature Genetics2007,39,5:1
10Metabolic tumor burden is associated with major oncogenomic alterations and serum tumor markers in patients with resected pancreatic cancer显示文摘Si Shi Shunrong Ji Yi Qin Jin Xu Bo Zhang Wenyan Xu Jiang Liu Jiang Long Chen Liu Liang Liu Quanxing Ni Xianjun Yu 2015Cancer Letters2015,,2:1
11Terminalsliding mode control for STT missile based on RBFneural network 显示文摘Shi Xianjun Zhao Hongchao Chen Jie 2012Advances in Intelligent and SoftComputing2012,169,:1
12A QTL for rice grain width and weight encodes a previously unknown RING-type E3 ubiquitin ligase 显示文摘XianJun Song Wei Huang Min Shi 2007Nature Genetics2007,39,:1
13A QTL for rice grain width and weight encodes a reviously unknown RING-type E3 ubiquitin ligase显示文摘SONG Xianjun HUANG Wei SHI Min 2007Nat Genet2007,39,5:1
14Approaches for automated detection and classification of masses in mammograms显示文摘Cheng Hengda Shi Xianjun Min Rui 2006Pattern Recognition2006,39,4:1
15Epigenetic regulation in the tumor microenvironment:molecular mechanisms and therapeutic targets显示文摘Over decades,researchers have focused on the epigenetic control of DNA-templated processes.Histone modification,DNA methylation,chromatin remodeling,RNA modification,and noncoding RNAs modulate many biological processes that are crucial to the development of cancers.Dysregulation of the epigenome drives aberrant transcriptional programs.A growing body of evidence suggests that the mechanisms of epigenetic modification are dysregulated in human cancers and might be excellent targets for tumor treatment.Epigenetics has also been shown to influence tumor immunogenicity and immune cells involved in antitumor responses.Thus,the development and application of epigenetic therapy and cancer immunotherapy and their combinations may have important implications for cancer treatment.Here,we present an up-to-date and thorough description of how epigenetic modifications in tumor cells influence immune cell responses in the tumor microenvironment(TME)and how epigenetics influence immune cells internally to modify the TME.Additionally,we highlight the therapeutic potential of targeting epigenetic regulators for cancer immunotherapy.Harnessing the complex interplay between epigenetics and cancer immunology to develop therapeutics that combine thereof is challenging but could yield significant benefits.The purpose of this review is to assist researchers in understanding how epigenetics impact immune responses in the TME,so that better cancer immunotherapies can be developed.Jing Yang Jin Xu Wei Wang Bo Zhang Xianjun Yu Si Shi 2023Signal Transduction and Targeted Therapy2023,8,6:1
16Defective EMC1 drives abnormal retinal angiogenesis via Wnt/β-catenin signaling and may be associated with the pathogenesis of familial exudative vitreoretinopathy显示文摘Endoplasmic reticulum(ER)membrane protein complex(EMC)is required for the co-translational insertion of newly synthesized multi-transmembrane proteins.Compromised EMC function in different cell types has been implicated in multiple diseases.Using inducible genetic mouse models,we revealed defects in retinal vascularization upon endothelial cell(EC)specific deletion of Emc1,the largest subunit of EMC.Loss of Emc1 in ECs led to reduced vascular progression and vascular density,diminished tip cell sprouts,and vascular leakage.We then performed an unbiased transcriptomic analysis on human retinal microvascular endothelial cells(HRECs)and revealed a pivotal role of EMC1 in theβ-catenin signaling pathway.Further in-vitro and in-vivo experiments proved that loss of EMC1 led to compromisedβ-catenin signaling activity through reduced expression of Wnt receptor FZD4,which could be restored by lithium chloride(LiCl)treatment.Driven by these findings,we screened genomic DNA samples from familial exudative vitreoretinopathy(FEVR)patients and identified one heterozygous variant in EMC1 that co-segregated with FEVR phenotype in the family.In-vitro expression experiments revealed that this variant allele failed to facilitate the expression of FZD4 on the plasma membrane and activate theβ-catenin signaling pathway,which might be a main cause of FEVR.In conclusion,our findings reveal that variants in EMC1 gene cause compromisedβ-catenin signaling activity,which may be associated with the pathogenesis of FEVR.Shujin Li Mu Yang Rulian Zhao Li Peng Wenjing Liu Xiaoyan Jiang Yunqi He Erkuan Dai Lin Zhang Yeming Yang Yi Shi Peiquan Zhao Zhenglin Yang Xianjun Zhu 2023Genes & Diseases2023,10,6:1
17Calculating on Permanent Magnet with Distributing Leakage Flux 显示文摘Liu Lingshun Shi Xianjun and WangDong 2011EI Lecture Notes in Electrical Engineering2011,1,3:1
18Variants in the Wnt co-receptor LRP6 are associated with familial exudative vitreoretinopathy显示文摘Familial exudative vitreoretinopathy(FEVR),an inherited eye disease,is characterized by abnormal retinal vascular development,such as neovascularization,vitreous hemorrhage,exudation,and retinal detachment(Criswick and Schepens,1969;Robitaille et al.,2002).FEVR is inherited as autosomal dominant,autosomal recessive,and X-linked patterns(de Crecchio et al.,1998).Shujin Li Mu Yang Yunqi He Xiaoyan Jiang Rulian Zhao Wenjing Liu Lulin Huang Yi Shi Xiao Li Kuanxiang Sun Yeming Yang Periasamy Sundaresan Peiquan Zhao Zhenglin Yang Xianjun Zhu 2022Journal of Genetics and Genomics2022,49,6:1
19Highly lymphatic metastatic pancreatic cancer cells possess stem cell-likeproperties显示文摘Guopei Luo Jiang Long Xiaobo Cui Zhiwen Xiao Zuqiang Liu Si Shi Liang Liu Chen Liu Jin Xu Min Li Xianjun Yu 2013International Journal of Oncology2013,,:1
20Loss of Wtap results in cerebellar ataxia and degeneration of Purkinje cells显示文摘N^(6)-methyladenosine(m^(6)A)modification,which is achieved by the METTL3/METTL14/WTAP methyltransferase complex,is the most abundant internal mRNA modification.Although recent evidence indicates that m^(6)A can regulate neurodevelopment as well as synaptic function,the roles of m^(6)A modification in the cerebellum and related synaptic connections are not well established.Here,we report that Purkinje cell(PC)-specific WTAP knockout mice display early-onset ataxia concomitant with cerebellar atrophy due to extensive PC degeneration and apoptotic cell death.Loss of Wtap also causes the aberrant degradation of multiple PC synapses.WTAP depletion leads to decreased expression levels of METTL3/14 and reduced m^(6)A methylation in PCs.Moreover,the expression of GFAP and NF-L in the degenerating cerebellum is increased,suggesting severe neuronal injuries.In conclusion,this study demonstrates the critical role of WTAP-mediated m^(6)A modification in cerebellar PCs,thus providing unique insights related to neurodegenerative disorders.Yeming Yang Guo Huang Xiaoyan Jiang Xiao Li Kuanxiang Sun Yi Shi Zhenglin Yang Xianjun Zhu 2022Journal of Genetics and Genomics2022,49,9:1
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