mouse il 21  (Sino Biological)


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    Name:
    IL21 cDNA ORF Clone in Cloning Vector Mouse
    Description:
    Full length Clone DNA of Mouse interleukin 21
    Catalog Number:
    mg50137-m
    Product Aliases:
    IL-21 cDNA ORF Clone Mouse
    Price:
    75.0
    Size:
    1Unit
    Category:
    cDNA Clone
    Molecule Name:
    IL21,IL-21,
    Buy from Supplier


    Structured Review

    Sino Biological mouse il 21
    Serum <t>IL-21</t> and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p
    Full length Clone DNA of Mouse interleukin 21
    https://www.bioz.com/result/mouse il 21/product/Sino Biological
    Average 90 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    mouse il 21 - by Bioz Stars, 2021-02
    90/100 stars

    Images

    1) Product Images from "Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance"

    Article Title: Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance

    Journal: Nature Communications

    doi: 10.1038/s41467-017-02304-7

    Serum IL-21 and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p
    Figure Legend Snippet: Serum IL-21 and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p

    Techniques Used: Mouse Assay, Multiplex Assay, Two Tailed Test

    IL-21 or IL-33 treatments induce clearance of established BPS persistence. Plasmids expressing murine IL-21 or IL-33 and empty vector control were injected into BPS HDI mice at 4 and 7 weeks post injection (w.p.i.) (arrows). Sera were collected at indicated time points and levels of IL-21 and IL-33 ( a ), HBsAg ( b ), HBsAb ( c ) and HBeAg ( d ) were analysed using ELISA. Group means and s.e.m. within group are presented with group sizes ( n ) indicated. Group positivity percentage data are also presented for HBsAg ( b , right panel), HBsAb ( c , right panel) and HBeAg ( d , right panel). HBV DNA for each group were analysed using pooled serum in commercial quantitative assay ( e ). Dotted lines represent cut-off thresholds ( a , b – d , right panels) and lower limit of quantification ( e ) respectively. geq genome equivalents
    Figure Legend Snippet: IL-21 or IL-33 treatments induce clearance of established BPS persistence. Plasmids expressing murine IL-21 or IL-33 and empty vector control were injected into BPS HDI mice at 4 and 7 weeks post injection (w.p.i.) (arrows). Sera were collected at indicated time points and levels of IL-21 and IL-33 ( a ), HBsAg ( b ), HBsAb ( c ) and HBeAg ( d ) were analysed using ELISA. Group means and s.e.m. within group are presented with group sizes ( n ) indicated. Group positivity percentage data are also presented for HBsAg ( b , right panel), HBsAb ( c , right panel) and HBeAg ( d , right panel). HBV DNA for each group were analysed using pooled serum in commercial quantitative assay ( e ). Dotted lines represent cut-off thresholds ( a , b – d , right panels) and lower limit of quantification ( e ) respectively. geq genome equivalents

    Techniques Used: Expressing, Plasmid Preparation, Injection, Mouse Assay, Enzyme-linked Immunosorbent Assay

    IL-21-induced or IL-33-induced clearance of BPS persistence engenders protection from re-challenge. HDI mice harbouring BPS persistence were treated with injections of plasmids expressing IL-21 ( a ) or IL-33 ( b ) at 4 and 7 w.p.i. and those displaying at least 4 weeks of sustained HBsAg negativity (see Fig. 6 ) were re-challenged in the same way as initial BPS HDI. BPS HDI mice treated with vector control were used as control and re-challenged similarly ( c ). Sera were collected at indicated time points and levels of HBsAg (left), HBsAb (middle) and HBeAg (right) were analysed using ELISA. Dotted lines represent cut-off thresholds. w.p.i. weeks post injection of BPS re-challenge
    Figure Legend Snippet: IL-21-induced or IL-33-induced clearance of BPS persistence engenders protection from re-challenge. HDI mice harbouring BPS persistence were treated with injections of plasmids expressing IL-21 ( a ) or IL-33 ( b ) at 4 and 7 w.p.i. and those displaying at least 4 weeks of sustained HBsAg negativity (see Fig. 6 ) were re-challenged in the same way as initial BPS HDI. BPS HDI mice treated with vector control were used as control and re-challenged similarly ( c ). Sera were collected at indicated time points and levels of HBsAg (left), HBsAb (middle) and HBeAg (right) were analysed using ELISA. Dotted lines represent cut-off thresholds. w.p.i. weeks post injection of BPS re-challenge

    Techniques Used: Mouse Assay, Expressing, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Injection

    2) Product Images from "Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis"

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    Journal: Molecular Cancer

    doi: 10.1186/s12943-020-01253-y

    CDR1as functions in a p53-dependent manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p
    Figure Legend Snippet: CDR1as functions in a p53-dependent manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p

    Techniques Used: Expressing, Transfection, Plasmid Preparation

    CDR1as serves as a protective machinery to preserve p53 function against DNA damage in U87MG cells. a Western blot analysis of p53 and p21 expression (left); and RT-qPCR analysis of CDR1as expression (right) in U87MG cells after 48 h treatment with DOXO, VP16 or DMSO (as control). b Western blot analysis of p53 and p21 expression (left); and densitometric analysis of p53 expression normalized to GAPDH (right) in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. c Flow cytometric analysis of cell cycle in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO. d Flow cytometric analysis of apoptosis in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. e IF analysis of γH2A.X (DNA damage marker) in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO (left); quantification of number of γH2A.X positive cells with equal or more than 10 γH2A.X foci/nucleus (right). * p
    Figure Legend Snippet: CDR1as serves as a protective machinery to preserve p53 function against DNA damage in U87MG cells. a Western blot analysis of p53 and p21 expression (left); and RT-qPCR analysis of CDR1as expression (right) in U87MG cells after 48 h treatment with DOXO, VP16 or DMSO (as control). b Western blot analysis of p53 and p21 expression (left); and densitometric analysis of p53 expression normalized to GAPDH (right) in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. c Flow cytometric analysis of cell cycle in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO. d Flow cytometric analysis of apoptosis in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. e IF analysis of γH2A.X (DNA damage marker) in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO (left); quantification of number of γH2A.X positive cells with equal or more than 10 γH2A.X foci/nucleus (right). * p

    Techniques Used: Western Blot, Expressing, Quantitative RT-PCR, Transfection, Marker

    p53 physically interacts with CDR1as indicating glioma prognosis. a Heatmap of 30 most enriched lncRNAs binding to p53 protein determined by RIP-seq. b Validation of 30 candidate lncRNAs binding to p53 protein by RIP-qPCR. c Plots of the correlation between the scores of p53 pathway gene sets and expression of candidate lncRNAs in glioma samples in the CGGA cohort. d CDR1as expression in glioma with different WHO grades in the CGGA cohort. e , f Kaplan-Meier curves of the overall survival ( e ) and ROC curves ( f ) of glioma patients in the CGGA cohort. g RT-qPCR assays of CDR1as expression in glioma samples collected by ourselves. h Mapping of RIP-seq reads back to genomic locus of CDR1as . i Validation of the p53- CDR1as interaction by CHIRP. j Co-localization analysis of p53 and CDR1as in U87MG cells using protein IF and RNA FISH assays respectively. ns, no significance; * p
    Figure Legend Snippet: p53 physically interacts with CDR1as indicating glioma prognosis. a Heatmap of 30 most enriched lncRNAs binding to p53 protein determined by RIP-seq. b Validation of 30 candidate lncRNAs binding to p53 protein by RIP-qPCR. c Plots of the correlation between the scores of p53 pathway gene sets and expression of candidate lncRNAs in glioma samples in the CGGA cohort. d CDR1as expression in glioma with different WHO grades in the CGGA cohort. e , f Kaplan-Meier curves of the overall survival ( e ) and ROC curves ( f ) of glioma patients in the CGGA cohort. g RT-qPCR assays of CDR1as expression in glioma samples collected by ourselves. h Mapping of RIP-seq reads back to genomic locus of CDR1as . i Validation of the p53- CDR1as interaction by CHIRP. j Co-localization analysis of p53 and CDR1as in U87MG cells using protein IF and RNA FISH assays respectively. ns, no significance; * p

    Techniques Used: Binding Assay, Real-time Polymerase Chain Reaction, Expressing, Quantitative RT-PCR, Fluorescence In Situ Hybridization

    CDR1as up-regulates expression of p53 protein by inhibiting its ubiquitination in U87MG cells. a Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . b Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with different siCDR1as or siNC. c Western blot analysis of p53 and its targets in CDR1as knocked-down U87MG cells treated with Nutlin3 or DMSO. d Luciferase reporter assays for p53 transcription activity in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as (left); and in U87MG cells transfected with different siCDR1as or siNC (right). e , f Immunoblot of p53 and MDM2 protein and quantification of p53 relative level at the indicated time in U87MG cells transfected with plasmid encoding CDR1as or control plasmid ( e ); and in U87MG cells transfected with siCDR1as-1 or siNC ( f ) after CHX treatment to block protein synthesis. g Immunoblot of p53 ubiquitination in U87MG cells co-transfected with the plasmids encoding HA-ubiquitin ( HA-Ub ), Myc-MDM2 and CDR1as after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). h Immunoblot of p53 ubiquitination in CDR1as knocked-down (or siNC treated) U87MG cells transfected with the plasmids encoding HA-Ub and Myc-MDM2 after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). * p
    Figure Legend Snippet: CDR1as up-regulates expression of p53 protein by inhibiting its ubiquitination in U87MG cells. a Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . b Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with different siCDR1as or siNC. c Western blot analysis of p53 and its targets in CDR1as knocked-down U87MG cells treated with Nutlin3 or DMSO. d Luciferase reporter assays for p53 transcription activity in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as (left); and in U87MG cells transfected with different siCDR1as or siNC (right). e , f Immunoblot of p53 and MDM2 protein and quantification of p53 relative level at the indicated time in U87MG cells transfected with plasmid encoding CDR1as or control plasmid ( e ); and in U87MG cells transfected with siCDR1as-1 or siNC ( f ) after CHX treatment to block protein synthesis. g Immunoblot of p53 ubiquitination in U87MG cells co-transfected with the plasmids encoding HA-ubiquitin ( HA-Ub ), Myc-MDM2 and CDR1as after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). h Immunoblot of p53 ubiquitination in CDR1as knocked-down (or siNC treated) U87MG cells transfected with the plasmids encoding HA-Ub and Myc-MDM2 after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). * p

    Techniques Used: Expressing, Western Blot, Quantitative RT-PCR, Transfection, Plasmid Preparation, Luciferase, Activity Assay, Blocking Assay

    CDR1as suppresses gliomagenesis of U87MG cells in vitro and in vivo . a-d Colony formation assays ( a ), cell proliferation assays ( b ), flow cytometric cell cycle assays ( c ) and flow cytometric apoptosis assays ( d ) for U87MG cells treated with different siCDR1as or siNC. e Excised tumors from nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. f Volume of xenografted tumors derived from U87MG cells treated with siCDR1as-1 or siNC. g Kaplan-Meier curves of the overall survival of nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. h IHC assays for xenografted tumors derived from U87MG cells stained with H E, PCNA antibody and p53 antibody respectively. * p
    Figure Legend Snippet: CDR1as suppresses gliomagenesis of U87MG cells in vitro and in vivo . a-d Colony formation assays ( a ), cell proliferation assays ( b ), flow cytometric cell cycle assays ( c ) and flow cytometric apoptosis assays ( d ) for U87MG cells treated with different siCDR1as or siNC. e Excised tumors from nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. f Volume of xenografted tumors derived from U87MG cells treated with siCDR1as-1 or siNC. g Kaplan-Meier curves of the overall survival of nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. h IHC assays for xenografted tumors derived from U87MG cells stained with H E, PCNA antibody and p53 antibody respectively. * p

    Techniques Used: In Vitro, In Vivo, Mouse Assay, Derivative Assay, Immunohistochemistry, Staining

    CDR1as directly binds with the DBD region of p53 and disrupts the p53/MDM2 complex. a A schema showing four constructs containing full-length or different domains of p53. b RIP-qPCR analysis of CDR1as binding with the indicated p53 constructs. c IP analysis of interaction between MDM2 and p53 in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . d IP analysis of interaction between MDM2 and p53 in U87MG cells co-transfected with plasmids encoding CDR1as , Myc-p53 or Myc-MDM2 . e-h IP analysis of interaction between MDM2 and the indicated p53 constructs in MEF DKO ( p53 −/− ; MDM2 −/− ) cells co-transfected with plasmids encoding CDR1as , HA-MDM2 , and the indicated p53 constructs. * p
    Figure Legend Snippet: CDR1as directly binds with the DBD region of p53 and disrupts the p53/MDM2 complex. a A schema showing four constructs containing full-length or different domains of p53. b RIP-qPCR analysis of CDR1as binding with the indicated p53 constructs. c IP analysis of interaction between MDM2 and p53 in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . d IP analysis of interaction between MDM2 and p53 in U87MG cells co-transfected with plasmids encoding CDR1as , Myc-p53 or Myc-MDM2 . e-h IP analysis of interaction between MDM2 and the indicated p53 constructs in MEF DKO ( p53 −/− ; MDM2 −/− ) cells co-transfected with plasmids encoding CDR1as , HA-MDM2 , and the indicated p53 constructs. * p

    Techniques Used: Construct, Real-time Polymerase Chain Reaction, Binding Assay, Transfection, Plasmid Preparation

    Related Articles

    Expressing:

    Article Title: Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance
    Article Snippet: .. Mouse IL-21 (MG50137-M-N) and IL-33 (MG50118-M-N) expression plasmids (Sino Biological, China) and rat monoclonal antibodies (anti-mIL-21: 16-9333; anti-mIL-33, 16-7211) (eBioscience, China) were purchased. .. Transfection and analysis of HBV markers and virions Culture and transfection of Huh-7 (TCHu182, Cell Bank of Chinese Academy of Sciences, China) and HepG2 (American Tissue Culture Collection, ATCC® Number: HB-8065™, Manassas, VA) cells were performed as previously described , .

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    Sino Biological mouse il 21
    Serum <t>IL-21</t> and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p
    Mouse Il 21, supplied by Sino Biological, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse il 21/product/Sino Biological
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse il 21 - by Bioz Stars, 2021-02
    90/100 stars
      Buy from Supplier

    93
    Sino Biological myc p53
    CDR1as functions in a <t>p53-dependent</t> manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p
    Myc P53, supplied by Sino Biological, used in various techniques. Bioz Stars score: 93/100, based on 0 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/myc p53/product/Sino Biological
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    myc p53 - by Bioz Stars, 2021-02
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    92
    Sino Biological mouse trkb cdna
    CDR1as functions in a <t>p53-dependent</t> manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p
    Mouse Trkb Cdna, supplied by Sino Biological, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse trkb cdna/product/Sino Biological
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse trkb cdna - by Bioz Stars, 2021-02
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    Image Search Results


    Serum IL-21 and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p

    Journal: Nature Communications

    Article Title: Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance

    doi: 10.1038/s41467-017-02304-7

    Figure Lengend Snippet: Serum IL-21 and IL-33 are stimulated in B6 HDI mice but not BPS HDI mice. Sera from BPS, B6 and pUC18 HDI BALB/c mice were collected at indicated time points and levels of selected cytokines quantitated using multiplex-based assay. Group means and s.e.m. within group of serum IL-21 ( a ) and IL-33 ( b ) measurements are presented with group sizes ( n ) indicated. BPS and B6 mice data are compared against pUC18 mice and statistical significance calculated using unpaired two-tailed t -test. * p

    Article Snippet: Mouse IL-21 (MG50137-M-N) and IL-33 (MG50118-M-N) expression plasmids (Sino Biological, China) and rat monoclonal antibodies (anti-mIL-21: 16-9333; anti-mIL-33, 16-7211) (eBioscience, China) were purchased.

    Techniques: Mouse Assay, Multiplex Assay, Two Tailed Test

    IL-21 or IL-33 treatments induce clearance of established BPS persistence. Plasmids expressing murine IL-21 or IL-33 and empty vector control were injected into BPS HDI mice at 4 and 7 weeks post injection (w.p.i.) (arrows). Sera were collected at indicated time points and levels of IL-21 and IL-33 ( a ), HBsAg ( b ), HBsAb ( c ) and HBeAg ( d ) were analysed using ELISA. Group means and s.e.m. within group are presented with group sizes ( n ) indicated. Group positivity percentage data are also presented for HBsAg ( b , right panel), HBsAb ( c , right panel) and HBeAg ( d , right panel). HBV DNA for each group were analysed using pooled serum in commercial quantitative assay ( e ). Dotted lines represent cut-off thresholds ( a , b – d , right panels) and lower limit of quantification ( e ) respectively. geq genome equivalents

    Journal: Nature Communications

    Article Title: Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance

    doi: 10.1038/s41467-017-02304-7

    Figure Lengend Snippet: IL-21 or IL-33 treatments induce clearance of established BPS persistence. Plasmids expressing murine IL-21 or IL-33 and empty vector control were injected into BPS HDI mice at 4 and 7 weeks post injection (w.p.i.) (arrows). Sera were collected at indicated time points and levels of IL-21 and IL-33 ( a ), HBsAg ( b ), HBsAb ( c ) and HBeAg ( d ) were analysed using ELISA. Group means and s.e.m. within group are presented with group sizes ( n ) indicated. Group positivity percentage data are also presented for HBsAg ( b , right panel), HBsAb ( c , right panel) and HBeAg ( d , right panel). HBV DNA for each group were analysed using pooled serum in commercial quantitative assay ( e ). Dotted lines represent cut-off thresholds ( a , b – d , right panels) and lower limit of quantification ( e ) respectively. geq genome equivalents

    Article Snippet: Mouse IL-21 (MG50137-M-N) and IL-33 (MG50118-M-N) expression plasmids (Sino Biological, China) and rat monoclonal antibodies (anti-mIL-21: 16-9333; anti-mIL-33, 16-7211) (eBioscience, China) were purchased.

    Techniques: Expressing, Plasmid Preparation, Injection, Mouse Assay, Enzyme-linked Immunosorbent Assay

    IL-21-induced or IL-33-induced clearance of BPS persistence engenders protection from re-challenge. HDI mice harbouring BPS persistence were treated with injections of plasmids expressing IL-21 ( a ) or IL-33 ( b ) at 4 and 7 w.p.i. and those displaying at least 4 weeks of sustained HBsAg negativity (see Fig. 6 ) were re-challenged in the same way as initial BPS HDI. BPS HDI mice treated with vector control were used as control and re-challenged similarly ( c ). Sera were collected at indicated time points and levels of HBsAg (left), HBsAb (middle) and HBeAg (right) were analysed using ELISA. Dotted lines represent cut-off thresholds. w.p.i. weeks post injection of BPS re-challenge

    Journal: Nature Communications

    Article Title: Hepatitis B virus persistence in mice reveals IL-21 and IL-33 as regulators of viral clearance

    doi: 10.1038/s41467-017-02304-7

    Figure Lengend Snippet: IL-21-induced or IL-33-induced clearance of BPS persistence engenders protection from re-challenge. HDI mice harbouring BPS persistence were treated with injections of plasmids expressing IL-21 ( a ) or IL-33 ( b ) at 4 and 7 w.p.i. and those displaying at least 4 weeks of sustained HBsAg negativity (see Fig. 6 ) were re-challenged in the same way as initial BPS HDI. BPS HDI mice treated with vector control were used as control and re-challenged similarly ( c ). Sera were collected at indicated time points and levels of HBsAg (left), HBsAb (middle) and HBeAg (right) were analysed using ELISA. Dotted lines represent cut-off thresholds. w.p.i. weeks post injection of BPS re-challenge

    Article Snippet: Mouse IL-21 (MG50137-M-N) and IL-33 (MG50118-M-N) expression plasmids (Sino Biological, China) and rat monoclonal antibodies (anti-mIL-21: 16-9333; anti-mIL-33, 16-7211) (eBioscience, China) were purchased.

    Techniques: Mouse Assay, Expressing, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Injection

    CDR1as functions in a p53-dependent manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: CDR1as functions in a p53-dependent manner. a , b Ectopic expression ( a ), and knock-down ( b ) of CDR1as in HCT116 cells in which p53 is intact (HCT116 p53+/+ ) or absent (HCT116 p53−/− ). c , d Colony formation assays for HCT116 p53+/+ cells and HCT116 p53−/− cells in which CDR1as is ectopically expressed ( c ) or knocked down ( d ). e Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with CDR1as expressing plasmid (or control plasmid). f Flow cytometric cell cycle assays (left) and apoptosis assays (right) for the indicated cells transfected with siCDR1as-1 (or siNC). * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: Expressing, Transfection, Plasmid Preparation

    CDR1as serves as a protective machinery to preserve p53 function against DNA damage in U87MG cells. a Western blot analysis of p53 and p21 expression (left); and RT-qPCR analysis of CDR1as expression (right) in U87MG cells after 48 h treatment with DOXO, VP16 or DMSO (as control). b Western blot analysis of p53 and p21 expression (left); and densitometric analysis of p53 expression normalized to GAPDH (right) in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. c Flow cytometric analysis of cell cycle in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO. d Flow cytometric analysis of apoptosis in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. e IF analysis of γH2A.X (DNA damage marker) in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO (left); quantification of number of γH2A.X positive cells with equal or more than 10 γH2A.X foci/nucleus (right). * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: CDR1as serves as a protective machinery to preserve p53 function against DNA damage in U87MG cells. a Western blot analysis of p53 and p21 expression (left); and RT-qPCR analysis of CDR1as expression (right) in U87MG cells after 48 h treatment with DOXO, VP16 or DMSO (as control). b Western blot analysis of p53 and p21 expression (left); and densitometric analysis of p53 expression normalized to GAPDH (right) in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. c Flow cytometric analysis of cell cycle in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO. d Flow cytometric analysis of apoptosis in U87MG cells transfected with siCDR1as-1 or siNC after 48 h treatment of DOXO or DMSO. e IF analysis of γH2A.X (DNA damage marker) in U87MG cells transfected with different siCDR1as or siNC after 48 h treatment of DOXO or DMSO (left); quantification of number of γH2A.X positive cells with equal or more than 10 γH2A.X foci/nucleus (right). * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: Western Blot, Expressing, Quantitative RT-PCR, Transfection, Marker

    p53 physically interacts with CDR1as indicating glioma prognosis. a Heatmap of 30 most enriched lncRNAs binding to p53 protein determined by RIP-seq. b Validation of 30 candidate lncRNAs binding to p53 protein by RIP-qPCR. c Plots of the correlation between the scores of p53 pathway gene sets and expression of candidate lncRNAs in glioma samples in the CGGA cohort. d CDR1as expression in glioma with different WHO grades in the CGGA cohort. e , f Kaplan-Meier curves of the overall survival ( e ) and ROC curves ( f ) of glioma patients in the CGGA cohort. g RT-qPCR assays of CDR1as expression in glioma samples collected by ourselves. h Mapping of RIP-seq reads back to genomic locus of CDR1as . i Validation of the p53- CDR1as interaction by CHIRP. j Co-localization analysis of p53 and CDR1as in U87MG cells using protein IF and RNA FISH assays respectively. ns, no significance; * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: p53 physically interacts with CDR1as indicating glioma prognosis. a Heatmap of 30 most enriched lncRNAs binding to p53 protein determined by RIP-seq. b Validation of 30 candidate lncRNAs binding to p53 protein by RIP-qPCR. c Plots of the correlation between the scores of p53 pathway gene sets and expression of candidate lncRNAs in glioma samples in the CGGA cohort. d CDR1as expression in glioma with different WHO grades in the CGGA cohort. e , f Kaplan-Meier curves of the overall survival ( e ) and ROC curves ( f ) of glioma patients in the CGGA cohort. g RT-qPCR assays of CDR1as expression in glioma samples collected by ourselves. h Mapping of RIP-seq reads back to genomic locus of CDR1as . i Validation of the p53- CDR1as interaction by CHIRP. j Co-localization analysis of p53 and CDR1as in U87MG cells using protein IF and RNA FISH assays respectively. ns, no significance; * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: Binding Assay, Real-time Polymerase Chain Reaction, Expressing, Quantitative RT-PCR, Fluorescence In Situ Hybridization

    CDR1as up-regulates expression of p53 protein by inhibiting its ubiquitination in U87MG cells. a Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . b Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with different siCDR1as or siNC. c Western blot analysis of p53 and its targets in CDR1as knocked-down U87MG cells treated with Nutlin3 or DMSO. d Luciferase reporter assays for p53 transcription activity in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as (left); and in U87MG cells transfected with different siCDR1as or siNC (right). e , f Immunoblot of p53 and MDM2 protein and quantification of p53 relative level at the indicated time in U87MG cells transfected with plasmid encoding CDR1as or control plasmid ( e ); and in U87MG cells transfected with siCDR1as-1 or siNC ( f ) after CHX treatment to block protein synthesis. g Immunoblot of p53 ubiquitination in U87MG cells co-transfected with the plasmids encoding HA-ubiquitin ( HA-Ub ), Myc-MDM2 and CDR1as after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). h Immunoblot of p53 ubiquitination in CDR1as knocked-down (or siNC treated) U87MG cells transfected with the plasmids encoding HA-Ub and Myc-MDM2 after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: CDR1as up-regulates expression of p53 protein by inhibiting its ubiquitination in U87MG cells. a Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . b Western blot analysis of p53 and its targets (left); and validation of RNA levels of CDR1as , TP53 , MDM2 , CDKN1A and PUMA by RT-qPCR (right) in U87MG cells transfected with different siCDR1as or siNC. c Western blot analysis of p53 and its targets in CDR1as knocked-down U87MG cells treated with Nutlin3 or DMSO. d Luciferase reporter assays for p53 transcription activity in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as (left); and in U87MG cells transfected with different siCDR1as or siNC (right). e , f Immunoblot of p53 and MDM2 protein and quantification of p53 relative level at the indicated time in U87MG cells transfected with plasmid encoding CDR1as or control plasmid ( e ); and in U87MG cells transfected with siCDR1as-1 or siNC ( f ) after CHX treatment to block protein synthesis. g Immunoblot of p53 ubiquitination in U87MG cells co-transfected with the plasmids encoding HA-ubiquitin ( HA-Ub ), Myc-MDM2 and CDR1as after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). h Immunoblot of p53 ubiquitination in CDR1as knocked-down (or siNC treated) U87MG cells transfected with the plasmids encoding HA-Ub and Myc-MDM2 after MG132 treatment (left); and validation of CDR1as expression by RT-qPCR (right). * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: Expressing, Western Blot, Quantitative RT-PCR, Transfection, Plasmid Preparation, Luciferase, Activity Assay, Blocking Assay

    CDR1as suppresses gliomagenesis of U87MG cells in vitro and in vivo . a-d Colony formation assays ( a ), cell proliferation assays ( b ), flow cytometric cell cycle assays ( c ) and flow cytometric apoptosis assays ( d ) for U87MG cells treated with different siCDR1as or siNC. e Excised tumors from nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. f Volume of xenografted tumors derived from U87MG cells treated with siCDR1as-1 or siNC. g Kaplan-Meier curves of the overall survival of nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. h IHC assays for xenografted tumors derived from U87MG cells stained with H E, PCNA antibody and p53 antibody respectively. * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: CDR1as suppresses gliomagenesis of U87MG cells in vitro and in vivo . a-d Colony formation assays ( a ), cell proliferation assays ( b ), flow cytometric cell cycle assays ( c ) and flow cytometric apoptosis assays ( d ) for U87MG cells treated with different siCDR1as or siNC. e Excised tumors from nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. f Volume of xenografted tumors derived from U87MG cells treated with siCDR1as-1 or siNC. g Kaplan-Meier curves of the overall survival of nude mice xenografted with U87MG cells treated with siCDR1as-1 or siNC. h IHC assays for xenografted tumors derived from U87MG cells stained with H E, PCNA antibody and p53 antibody respectively. * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: In Vitro, In Vivo, Mouse Assay, Derivative Assay, Immunohistochemistry, Staining

    CDR1as directly binds with the DBD region of p53 and disrupts the p53/MDM2 complex. a A schema showing four constructs containing full-length or different domains of p53. b RIP-qPCR analysis of CDR1as binding with the indicated p53 constructs. c IP analysis of interaction between MDM2 and p53 in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . d IP analysis of interaction between MDM2 and p53 in U87MG cells co-transfected with plasmids encoding CDR1as , Myc-p53 or Myc-MDM2 . e-h IP analysis of interaction between MDM2 and the indicated p53 constructs in MEF DKO ( p53 −/− ; MDM2 −/− ) cells co-transfected with plasmids encoding CDR1as , HA-MDM2 , and the indicated p53 constructs. * p

    Journal: Molecular Cancer

    Article Title: Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis

    doi: 10.1186/s12943-020-01253-y

    Figure Lengend Snippet: CDR1as directly binds with the DBD region of p53 and disrupts the p53/MDM2 complex. a A schema showing four constructs containing full-length or different domains of p53. b RIP-qPCR analysis of CDR1as binding with the indicated p53 constructs. c IP analysis of interaction between MDM2 and p53 in U87MG cells transfected with increasing concentrations of plasmid encoding CDR1as . d IP analysis of interaction between MDM2 and p53 in U87MG cells co-transfected with plasmids encoding CDR1as , Myc-p53 or Myc-MDM2 . e-h IP analysis of interaction between MDM2 and the indicated p53 constructs in MEF DKO ( p53 −/− ; MDM2 −/− ) cells co-transfected with plasmids encoding CDR1as , HA-MDM2 , and the indicated p53 constructs. * p

    Article Snippet: Plasmids of Myc-p53 , Myc-MDM2 , PCDH-p53 and HA-Ub were a gift of Dr. Zhang Lingqiang.

    Techniques: Construct, Real-time Polymerase Chain Reaction, Binding Assay, Transfection, Plasmid Preparation