Epithelial-mesenchymal transition（EMT） induced by transforming growth factor beta（TGF-P） is implicated in hepatocarcinogenesis and hepatocellular carcinoma（HCC） ***18G/CD147, which belongs to the CD147 family,is...
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Epithelial-mesenchymal transition（EMT） induced by transforming growth factor beta（TGF-P） is implicated in hepatocarcinogenesis and hepatocellular carcinoma（HCC） ***18G/CD147, which belongs to the CD147 family,is an HCC-associated antigen that plays a crucial role in tumor invasion and *** goal of this study was to investigate the role of HAb18G/CD147 during EMT in *** normal hepatic cell lines QZG and L02,primary mouse hepatocytes,and nude mouse models were used to determine the role of HAb18G/CD147 in EMT and the involvement of the TGF-P-driven pathway.A dual-luciferase reporter assay and chromatin immunoprecipitation were used to investigate the transcriptional regulation of the CD147 *** from patients with liver disease were assessed to determine the relationship between HAb18G/CD147 and typical markers for *** results show that upregulation of HAb18G/CD147 is induced by TGF-p coupled with the downregulation of E-cadherin and the upregulation of N-cadherin and *** expression of HAb18G/CD147 is controlled by the cell survival PI3K/Akt/GSK3p signaling pathway and is directly regulated by the transcription factor *** of CD147 also induces an elevated expression of TGF-β. CD147-transfected hepatocytes have mesenchymal phenotypes that accelerate tumor formation and tumor metastasis in *** analysis displays a negative correlation between HAb18G/CD147 and E-cadherin expression（r=-0.3622,P=0.0105） and a positive correlation between HAb18G/CD147 and Slug expression（r=0.3064,P=0.0323） in human HCC *** study reveals a novel role of HAb18G/CD147 in mediating EMT in the process of HCC progression and demonstrated that CD147 is a Slug target gene in the signaling cascade TGF-β→PI3K/Akt→GSK3β→Snail→Slug→CD147. Our results suggest that CD147 may be a potential target for the treatment and prevention of HCC.
Background:Abnormal alternative splicing of tau exon 10 results in imbalance of 3R-tau and 4R-tau expression,which is sufficient to cause neurofibrillary *** factor SC35,a member of the superfamily of the serine/argin...
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Background:Abnormal alternative splicing of tau exon 10 results in imbalance of 3R-tau and 4R-tau expression,which is sufficient to cause neurofibrillary *** factor SC35,a member of the superfamily of the serine/arginine-rich(SR) proteins,promotes tau exon 10 *** function of SC35 is tightly regulated by *** of DyrklA(dual-specificity tyrosine-phosphorylated and regulated kinase 1A) due to trisome in Down syndrome brain may contribute to the dysregulation of tau exon 10 ***1(protein phosphatase 1) dysregulated in Alzheimer's desease brain is an abundant neuronal serine/threoning ***:By mutation of mini-tau gene,pCI/SI9-SI10 which consists of exons 9,10,11,a part of intron 9 and intron 10 and RNA co-immunoprecipitation(RNA-IP),we elucidated the molecular mechanism by which SC35 works on tau exon 10 splicing and whether and how Dyrk1A or PP1 regulates SC35-promoted tau exon 10 inclusion in vitro and in cultured ***:We observed that tau pre-mRNA could be precipitated by anti-SC35 *** of the SC35-like exonic splicing enhancer located at exon 10 of tau affected both the binding of SC35 to tau pre-mRNA and promotion of tau exon 10 inclusion,suggesting that SC35 acts on the SC35-like exonic splicing enhancer to promote tau exon 10 ***1A interacted with and phosphorylated *** affected the interaction between SC35 and tau pre-mRNA and suppressed SC35-promoted tau exon 10 ***1 also interacted with SC35 and downregulated the tau exon 10 ***:The phosphorylation of SC35 is regulated by DyrklA or PP1,which may cause dysregulation of tau exon 10 splicing,leading to the imbalance in 3R-tau and 4R-tau expression,which may initiate or accelerate tau pathology.
Objective:To study the CDR3 Spectratyping of CD4 T and CD8T cell before and after immunized with HBV *** to analyze the association between CD8T cell CDR3 bias and HLA-A,so as CD4 T cell CDR3 bias and ***:（1） 20 vol...
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Objective:To study the CDR3 Spectratyping of CD4 T and CD8T cell before and after immunized with HBV *** to analyze the association between CD8T cell CDR3 bias and HLA-A,so as CD4 T cell CDR3 bias and ***:（1） 20 volunteers（Buyi,Dong,Miao and Han,who come from the national class of 2008 of zunyi medical college） with HBV vaccine immunized（all volunteers with negative hepatitis B surface five markers by electricity chemiluminescence screen）;（2）According to HBV Vaccination procedures and requirements to complete the three times HBV vaccine inoculation;（3） Peripheral blood samples were collected（15ml/times） before and after the vaccination（three times）;（4）Immunomagnetic beads（Magnetic Activated Cell ***） separate CD4T cells and CD8T cells from the PBL samples;（5） Extracted the total RNA of CD4T cells and CD8T cells,then reverse transcribed RNA to cDNA,Using fluorescence quantitative PCR amplification of 26 TRBV family CDR3（cDNA）;Analysis of CD4T and CD8T cells CDR3 Spectratyping（before immunized / 2 months / 6 months） by FQ-PCR melting curve;（6） Sequencing HLA-A/ HLA -DR allele sequence by using PCR-SBT（Sequencing based ***） in the genomic DNA of 20 volunteers;（7） Cloned and sequence the purified PCR product of part of HBV vaccine volunteers after vaccination CD8 T cells and CD4 T cells TRBV family CDR3 with showed a single peak of ***:（1） HBV surface antibodies titer were greater than 10IU / L after third HBV vaccine vaccinated in all of 20 volunteers;（2） Each volunteer have one family or a few TRBV CDR3 melting curve shows bias after the second/third HBV vaccine immunized;（3） Different vaccinated volunteers with same HLA have more common TCR CDR3 bias;（4） Significant bias of CDR3 in the same national volunteers were not *** of the multi-peak into a single peak from the family of volunteers（with same HLA） was sequenced and was not found the public CDR3 ***:（1） The HBS-Ab titer（greater than 10IU
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