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  • 90
    Alomone Labs sligkv nh2
    Sligkv Nh2, supplied by Alomone Labs, 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/sligkv nh2/product/Alomone Labs
    Average 90 stars, based on 1 article reviews
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    93
    R&D Systems recombinant human sgp130 fc
    IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus <t>sgp130-Fc</t> or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P
    Recombinant Human Sgp130 Fc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human sgp130 fc/product/R&D Systems
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    93
    R&D Systems recombinant human gp130 fc chimera protein cf
    STAT-independent HyperIL6 activity inhibits APAP- or IL11-stimulated cell death through competitive binding to the shared <t>gp130</t> co-receptor. ( A ) Representative fluorescent images and ( B ) quantification of DRAQ7 staining for cell death (scale bars, 200 µm) (n=3 independent experiments, 23 images per experiment) in APAP (20 mM) -treated hepatocytes in the presence of IgG (2 µg/ml), DMSO, anti-IL11RA (X209, 2 µg/ml), HyperIL6 (20 ng/ml), HyperIL6 supplemented with iSTAT3 (S3I-201, 20 µM), or anti-gp130 (2 µg/ml). ( C ) Western blots showing phospho-ERK, ERK, phospho-STAT3, STAT3, phospho-JNK, JNK, NOX4, and GAPDH levels in APAP-treated hepatocytes in the presence of IgG, X209, HyperIL6, or anti-gp130. ( D ) Western blots of phosphorylated ERK, AKT and STAT3 protein and their respective total expression in hepatocytes in response to HyperIL6 stimulation. ( E ) GSH levels (n=4) in APAP-treated hepatocytes. ( F ) Representative fluorescent images of DCFDA (2’, 7’-dichlorofluorescein diacetate) staining for ROS detection (scale bars, 100 µm) (n=4 independent experiments, 10 images per experiment) in APAP-treated hepatocytes. ( G ) Western blots showing ERK, STAT3 and JNK activation status, NOX4 protein expression in APAP-treated hepatocytes in the presence of DMSO, HyperIL6, or HyperIL6 supplemented with iSTAT3. ( H ) Proposed mechanism for competition of IL11 cis-signaling and IL6 trans-signaling by binding to gp130. ( I ) ALT secretion (n=4) and ( J ) Western blots showing ERK, STAT3, and JNK activation status, NOX4 protein expression by rhIL11 (10 ng/ml) -treated hepatocytes following a dose range stimulation of either HyperIL6 or sgp130 in the presence of iSTAT3. ( A-G, I-J ) Primary human hepatocytes; ( A-C, E-G, I-J ) 24 h stimulation. ( E, I ) Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box) and min-max values (whiskers), one-way ANOVA with Dunnett’s correction.
    Recombinant Human Gp130 Fc Chimera Protein Cf, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human gp130 fc chimera protein cf/product/R&D Systems
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human gp130 fc chimera protein cf - by Bioz Stars, 2022-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling converts non-stem cells into stem-like cells. a MCF 10A spheres cultured without or with IL6, IL6 plus sgp130-Fc or with HIL6. b CFSE-labeled MCF 10A cells were cultured as spheres with or without activators (IL6, HIL6) and inhibitors of classical (an anti-IL6 antibody) and trans-signaling (sgp130-Fc). CFSE-dilution in CD44 high CD24 low , CD44 high CD24 high and CD44 low CD24 high/intermediate cells was determined by flow cytometry at day 4. The CFSE-fluorescence intensity of all cells at day one is included as reference. Data are representative for three 3 independently performed experiments. c The absolute number of CD44 high CD24 low , CD44 high CD24 high , CD44 low CD24 high/intermediate cells (upper panel) and LRCs (CFSE high , lower panel) was determined as cell/bead ratio at day 4 by flow cytometry (N=4-5 per group). d Fold-change correlation analysis comparing gene expression changes induced by IL6 plus sgp130 (classical signaling) and HIL6 (trans signaling) in MCF 10 A cells at 12 and 24 hrs with the gene expression signatures of luminal progenitor (LumProg), mature luminal (MatLum) and mammary stem cell enriched cells (MaSC) according to the study of Lim et al. 35 Nc cor: non-centered correlation between fold-changes, Num: number of common differentially expressed genes. e nLRCs from primary, PKH26-labelled control mammosphere-cultures were sorted by flow cytometry as PKH - cells. f Primary HMECs were cultured as spheres for two consecutive rounds in the absence (N=26) or presence of HIL6 and IL6 (HIL6+HIL6, N=18; IL6+HIL6, N=15; HIL6+IL6, N=14; IL6+IL6, N=17). P values in panel c: one-way ANOVA with Dunett’s multiple comparisons test (post-hoc); panel d: P values according to Student’s t-distribution for Nc cor and hypergeometric testing for Num. panel f: one-way ANOVA with Tukey’s multiple comparisons test (post-hoc); comparisons between groups labeled in red are depicted in the bar graph. Asterisks indicate significance between groups (* P

    Article Snippet: mRNA microarray experiments MCF 10A cells were cultured as mammospheres in the presence or absence of 10 ng/ml IL6 (Sigma-Aldrich, Germany), 10 ng/ml IL6 + 0.1 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany) or 20 ng/ml Hyper-IL6 (kind gift of S. Rose-John, Christian-Albrechts-University, Germany) for 12 and 24 hours.

    Techniques: Cell Culture, Labeling, Flow Cytometry, Fluorescence, Expressing

    IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Journal: bioRxiv

    Article Title: Interleukin-6 trans-signaling is a candidate mechanism to drive progression of human DCCs during periods of clinical latency

    doi: 10.1101/2020.05.28.121145

    Figure Lengend Snippet: IL6 trans-signaling regulates the frequency of MCF 10A, hTERT-HME1 and primary HMECs with sphere-forming ability. a MCF 10A cells were cultured as spheres in the absence (N=18) or presence of IL6 (N=18), an IL6-blocking antibody (N=6) or Hyper-IL6 (N=6). b hTERT-HME1 were cultured as spheres in the absence (N=3) or presence (N=3) of Hyper-IL6. c HMECs were cultured without or with IL6, with an IL6 blocking antibody or Hyper-IL6. N=3 patients, each patient analyzed in triplicate. d hTERT-HME1-EGFR Δ746–750 cells were cultured as spheres in the absence or presence of HIL6 (each N=12). e MCF 10A cells were cultured as spheres without (N=6) or with IL6 (N=6) and IL6 plus sgp130-Fc at indicated concentrations (each N=6). f Sphere formation of hTERT-HME1-EGFR Δ746-750 in the absence (N=10) or presence of an anti-IL6 antibody (N=9) or with sgp130-Fc at indicated concentrations (each N=12). Cumulative data of three experiments. P values in panel a, c, f: one-way ANOVA with Dunnett’s multiple comparisons test (post hoc); panel b, d: two-sided Student’s t-test; panel e: one-way ANOVA with Tukey’s multiple comparisons test (post hoc); asterisks indicate significance between groups (*P

    Article Snippet: mRNA microarray experiments MCF 10A cells were cultured as mammospheres in the presence or absence of 10 ng/ml IL6 (Sigma-Aldrich, Germany), 10 ng/ml IL6 + 0.1 ng/ml recombinant human sgp130-Fc (R & D Systems, Germany) or 20 ng/ml Hyper-IL6 (kind gift of S. Rose-John, Christian-Albrechts-University, Germany) for 12 and 24 hours.

    Techniques: Cell Culture, Blocking Assay

    STAT-independent HyperIL6 activity inhibits APAP- or IL11-stimulated cell death through competitive binding to the shared gp130 co-receptor. ( A ) Representative fluorescent images and ( B ) quantification of DRAQ7 staining for cell death (scale bars, 200 µm) (n=3 independent experiments, 23 images per experiment) in APAP (20 mM) -treated hepatocytes in the presence of IgG (2 µg/ml), DMSO, anti-IL11RA (X209, 2 µg/ml), HyperIL6 (20 ng/ml), HyperIL6 supplemented with iSTAT3 (S3I-201, 20 µM), or anti-gp130 (2 µg/ml). ( C ) Western blots showing phospho-ERK, ERK, phospho-STAT3, STAT3, phospho-JNK, JNK, NOX4, and GAPDH levels in APAP-treated hepatocytes in the presence of IgG, X209, HyperIL6, or anti-gp130. ( D ) Western blots of phosphorylated ERK, AKT and STAT3 protein and their respective total expression in hepatocytes in response to HyperIL6 stimulation. ( E ) GSH levels (n=4) in APAP-treated hepatocytes. ( F ) Representative fluorescent images of DCFDA (2’, 7’-dichlorofluorescein diacetate) staining for ROS detection (scale bars, 100 µm) (n=4 independent experiments, 10 images per experiment) in APAP-treated hepatocytes. ( G ) Western blots showing ERK, STAT3 and JNK activation status, NOX4 protein expression in APAP-treated hepatocytes in the presence of DMSO, HyperIL6, or HyperIL6 supplemented with iSTAT3. ( H ) Proposed mechanism for competition of IL11 cis-signaling and IL6 trans-signaling by binding to gp130. ( I ) ALT secretion (n=4) and ( J ) Western blots showing ERK, STAT3, and JNK activation status, NOX4 protein expression by rhIL11 (10 ng/ml) -treated hepatocytes following a dose range stimulation of either HyperIL6 or sgp130 in the presence of iSTAT3. ( A-G, I-J ) Primary human hepatocytes; ( A-C, E-G, I-J ) 24 h stimulation. ( E, I ) Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box) and min-max values (whiskers), one-way ANOVA with Dunnett’s correction.

    Journal: bioRxiv

    Article Title: Overturning the paradigm that IL6 signaling drives liver regrowth while shining light on a new therapeutic target for regenerative medicine

    doi: 10.1101/2021.04.05.438446

    Figure Lengend Snippet: STAT-independent HyperIL6 activity inhibits APAP- or IL11-stimulated cell death through competitive binding to the shared gp130 co-receptor. ( A ) Representative fluorescent images and ( B ) quantification of DRAQ7 staining for cell death (scale bars, 200 µm) (n=3 independent experiments, 23 images per experiment) in APAP (20 mM) -treated hepatocytes in the presence of IgG (2 µg/ml), DMSO, anti-IL11RA (X209, 2 µg/ml), HyperIL6 (20 ng/ml), HyperIL6 supplemented with iSTAT3 (S3I-201, 20 µM), or anti-gp130 (2 µg/ml). ( C ) Western blots showing phospho-ERK, ERK, phospho-STAT3, STAT3, phospho-JNK, JNK, NOX4, and GAPDH levels in APAP-treated hepatocytes in the presence of IgG, X209, HyperIL6, or anti-gp130. ( D ) Western blots of phosphorylated ERK, AKT and STAT3 protein and their respective total expression in hepatocytes in response to HyperIL6 stimulation. ( E ) GSH levels (n=4) in APAP-treated hepatocytes. ( F ) Representative fluorescent images of DCFDA (2’, 7’-dichlorofluorescein diacetate) staining for ROS detection (scale bars, 100 µm) (n=4 independent experiments, 10 images per experiment) in APAP-treated hepatocytes. ( G ) Western blots showing ERK, STAT3 and JNK activation status, NOX4 protein expression in APAP-treated hepatocytes in the presence of DMSO, HyperIL6, or HyperIL6 supplemented with iSTAT3. ( H ) Proposed mechanism for competition of IL11 cis-signaling and IL6 trans-signaling by binding to gp130. ( I ) ALT secretion (n=4) and ( J ) Western blots showing ERK, STAT3, and JNK activation status, NOX4 protein expression by rhIL11 (10 ng/ml) -treated hepatocytes following a dose range stimulation of either HyperIL6 or sgp130 in the presence of iSTAT3. ( A-G, I-J ) Primary human hepatocytes; ( A-C, E-G, I-J ) 24 h stimulation. ( E, I ) Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box) and min-max values (whiskers), one-way ANOVA with Dunnett’s correction.

    Article Snippet: Recombinant proteinsCommercial recombinant proteins: rhIL11 (UniProtKB: P20809, Genscript), rmIL11 (UniProtKB: P47873, Genscript), rh-HyperIL6 (IL6R:IL6 fusion protein, 8954-SR, R & D systems), rm-HyperIL6 (IL6R:IL6 fusion protein, 9038-SR, R & D systems), human soluble gp130 Fc (671-GP-100, R & D systems).

    Techniques: Activity Assay, Binding Assay, Staining, Western Blot, Expressing, Activation Assay, Whisker Assay