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p38 β mapk c28c2 rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p38 β mapk c28c2 rabbit mab
    Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the <t>p38</t> genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.
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    Images

    1) Product Images from "Temporal variation in p38-mediated regulation of DUX4 in facioscapulohumeral muscular dystrophy"

    Article Title: Temporal variation in p38-mediated regulation of DUX4 in facioscapulohumeral muscular dystrophy

    Journal: Scientific Reports

    doi: 10.1038/s41598-024-77911-8

    Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.
    Figure Legend Snippet: Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.

    Techniques Used: Inhibition, CRISPR, Western Blot, Generated, Expressing, Immunostaining, Imaging, Control, Knock-Out, Targeted Gene Expression



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    Image Search Results


    Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.

    Journal: Scientific Reports

    Article Title: Temporal variation in p38-mediated regulation of DUX4 in facioscapulohumeral muscular dystrophy

    doi: 10.1038/s41598-024-77911-8

    Figure Lengend Snippet: Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.

    Article Snippet: Proteins were separated through SDS-PAGE and transferred to nitrocellulose or PVDF membranes which were then blotted with antibodies specific for α -tubulin mouse mAb (926-42213; Li-Cor Biosciences); p38 α MAPK polyclonal Rabbit Ab (9218 S; Cell Signaling Technology, Danvers, MA); p38 β MAPK (C28C2) Rabbit mAb (2339; Cell Signaling Technology); IRDye 680 goat anti-mouse secondary (926-68070; Li-Cor Biosciences); and IRDye 800 goat anti-rabbit secondary (926-32211; Li-Cor Biosciences).

    Techniques: Inhibition, CRISPR, Western Blot, Generated, Expressing, Immunostaining, Imaging, Control, Knock-Out, Targeted Gene Expression

    Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.

    Journal: Scientific Reports

    Article Title: Temporal variation in p38-mediated regulation of DUX4 in facioscapulohumeral muscular dystrophy

    doi: 10.1038/s41598-024-77911-8

    Figure Lengend Snippet: Myogenic induction of DUX4 and DUX4 target genes in FSHD cells with genetic depletion or pharmacological inhibition of p38α/β (MAPK14/11). ( A ) Deletion of the p38 genes by CRISPR/Cas9 editing in FSHD cells. Western blot analysis of lysates generated from p38 MAPK CRISPR knockouts. Bands for MAPK14 and MAPK11 are shown in parental (Unmodified), Cas9 expressing (Cas9) or genome-edited cell lines with deletion of p38α (MAPK14-/-), p38β (MAPK11-/-) or p38α/β (MAPK14/11-/-). α-Tubulin expression is detected to ensure equal loading. ( B ) Relative RNA levels for DUX4 and DUX4 targets ZSCAN4 , MBD3L2 , and LEUTX in differentiating FSHD1 (FSHD1_Cas9), FSHD2 (FSHD2_Cas9) and corresponding double KO lines (_MAPK14/11-/-) at the indicated time points (72 and 120 h) after initiating myogenic differentiation. ( C ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). ( D ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 Cas9 and FSHD1 MAPK14/11-/- cells at 120 h time point with an image magnification at 60X. Scale bar: 100 μm. ( E ) Quantification of MHC + cells from figure B. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between unmodified and p38α/β double KO FSHD cells ( p > 0.05). ( F ) Immunostaining images of MyHC (Red) and nuclei (DAPI, blue) on differentiated FSHD1 and FSHD2 cells that were treated losmapimod (_LOS) at 120 h time point. Scale bar: 100 μm. ( G ) Quantification of MHC + cells from figure F. MHC + and MHC − nuclei counts were aggregated from three separate imaging fields for each sample. The mean MI values ± Standard Error of the Mean (SEM) were calculated for three samples. Statistical significance was assessed using one-way ANOVA with Dunnett’s post-testing for multiple comparisons. The “ns” indicates that the observed differences were not statistically significant between untreated and losmapimod-treated FSHD cells ( p > 0.05). ( H ) Relative DUX4 and DUX4 target RNA levels in FSHD1 and FSHD2 myocytes treated with vehicle (_Unmodified_Unmod) or 1 μm losmapimod (_LOS) during a 120-hour differentiation period. Myoblasts in growth media (120 h MB) were compared to differentiated myotubes (120 h MT). In all the qPCR data analysis RNA levels were normalized to housekeeping gene RPL30, followed by respective control groups (considered as 1) and knockout and pharmacological inhibition induced DUX4 and target gene expression fold changes to control were represented.

    Article Snippet: Proteins were separated through SDS-PAGE and transferred to nitrocellulose or PVDF membranes which were then blotted with antibodies specific for α -tubulin mouse mAb (926-42213; Li-Cor Biosciences); p38 α MAPK polyclonal Rabbit Ab (9218 S; Cell Signaling Technology, Danvers, MA); p38 β MAPK (C28C2) Rabbit mAb (2339; Cell Signaling Technology); IRDye 680 goat anti-mouse secondary (926-68070; Li-Cor Biosciences); and IRDye 800 goat anti-rabbit secondary (926-32211; Li-Cor Biosciences).

    Techniques: Inhibition, CRISPR, Western Blot, Generated, Expressing, Immunostaining, Imaging, Control, Knock-Out, Targeted Gene Expression

    Antibodies used in this study

    Journal: Endocrinology

    Article Title: Roles of Growth Hormone–Dependent JAK-STAT5 and Lyn Kinase Signaling in Determining Lifespan and Cancer Incidence

    doi: 10.1210/endocr/bqae136

    Figure Lengend Snippet: Antibodies used in this study

    Article Snippet: P-p38 MAPK (Thr180/Tyr182) , 4511 , AB 2139682 , Cell Signaling Technology.

    Techniques:

    Altered hepatic transcripts involved in inflammatory stimuli in 12-week-old Ghr -mutant mice fed ad libitum. (A) Elevated transcripts of IL-10rα and IL-10rβ in male Ghr mutant and interleukin 1 receptor antagonist ( IL-1Ra ), cyclin-dependent kinase inhibitor 1A ( Cdkn1a ), in Ghr −/− males and females. No change was evident in IL-1β levels. (B) Decreased protein levels of inflammation modulators in livers of 12-week-old male Ghr mutants fed ad libitum. Decrease expression of acetylated tubulin (K40), phosphorylated p38 stress kinase, as well as inflammatory and immune response modulator nuclear factor (NF)κB p65 subunit and oxidative stress generator NADPH oxidase 4 (Nox4) in Ghr −/− and GhrBox1 −/− mice. Blots representative of n = 3 mice/genotype. Data represented as mean ± SEM (n = 4 mice/genotype). * P less than .05; ** P less than .01; *** P less than .001; **** P less than .0001 compared to wild-type (WT) of the same sex by analysis of variance.

    Journal: Endocrinology

    Article Title: Roles of Growth Hormone–Dependent JAK-STAT5 and Lyn Kinase Signaling in Determining Lifespan and Cancer Incidence

    doi: 10.1210/endocr/bqae136

    Figure Lengend Snippet: Altered hepatic transcripts involved in inflammatory stimuli in 12-week-old Ghr -mutant mice fed ad libitum. (A) Elevated transcripts of IL-10rα and IL-10rβ in male Ghr mutant and interleukin 1 receptor antagonist ( IL-1Ra ), cyclin-dependent kinase inhibitor 1A ( Cdkn1a ), in Ghr −/− males and females. No change was evident in IL-1β levels. (B) Decreased protein levels of inflammation modulators in livers of 12-week-old male Ghr mutants fed ad libitum. Decrease expression of acetylated tubulin (K40), phosphorylated p38 stress kinase, as well as inflammatory and immune response modulator nuclear factor (NF)κB p65 subunit and oxidative stress generator NADPH oxidase 4 (Nox4) in Ghr −/− and GhrBox1 −/− mice. Blots representative of n = 3 mice/genotype. Data represented as mean ± SEM (n = 4 mice/genotype). * P less than .05; ** P less than .01; *** P less than .001; **** P less than .0001 compared to wild-type (WT) of the same sex by analysis of variance.

    Article Snippet: P-p38 MAPK (Thr180/Tyr182) , 4511 , AB 2139682 , Cell Signaling Technology.

    Techniques: Mutagenesis, Expressing

    Antibodies used in this study

    Journal: Endocrinology

    Article Title: Roles of Growth Hormone–Dependent JAK-STAT5 and Lyn Kinase Signaling in Determining Lifespan and Cancer Incidence

    doi: 10.1210/endocr/bqae136

    Figure Lengend Snippet: Antibodies used in this study

    Article Snippet: p38 MAPK , 9212 , AB 330713 , Cell Signaling Technology.

    Techniques:

    Altered hepatic transcripts involved in inflammatory stimuli in 12-week-old Ghr -mutant mice fed ad libitum. (A) Elevated transcripts of IL-10rα and IL-10rβ in male Ghr mutant and interleukin 1 receptor antagonist ( IL-1Ra ), cyclin-dependent kinase inhibitor 1A ( Cdkn1a ), in Ghr −/− males and females. No change was evident in IL-1β levels. (B) Decreased protein levels of inflammation modulators in livers of 12-week-old male Ghr mutants fed ad libitum. Decrease expression of acetylated tubulin (K40), phosphorylated p38 stress kinase, as well as inflammatory and immune response modulator nuclear factor (NF)κB p65 subunit and oxidative stress generator NADPH oxidase 4 (Nox4) in Ghr −/− and GhrBox1 −/− mice. Blots representative of n = 3 mice/genotype. Data represented as mean ± SEM (n = 4 mice/genotype). * P less than .05; ** P less than .01; *** P less than .001; **** P less than .0001 compared to wild-type (WT) of the same sex by analysis of variance.

    Journal: Endocrinology

    Article Title: Roles of Growth Hormone–Dependent JAK-STAT5 and Lyn Kinase Signaling in Determining Lifespan and Cancer Incidence

    doi: 10.1210/endocr/bqae136

    Figure Lengend Snippet: Altered hepatic transcripts involved in inflammatory stimuli in 12-week-old Ghr -mutant mice fed ad libitum. (A) Elevated transcripts of IL-10rα and IL-10rβ in male Ghr mutant and interleukin 1 receptor antagonist ( IL-1Ra ), cyclin-dependent kinase inhibitor 1A ( Cdkn1a ), in Ghr −/− males and females. No change was evident in IL-1β levels. (B) Decreased protein levels of inflammation modulators in livers of 12-week-old male Ghr mutants fed ad libitum. Decrease expression of acetylated tubulin (K40), phosphorylated p38 stress kinase, as well as inflammatory and immune response modulator nuclear factor (NF)κB p65 subunit and oxidative stress generator NADPH oxidase 4 (Nox4) in Ghr −/− and GhrBox1 −/− mice. Blots representative of n = 3 mice/genotype. Data represented as mean ± SEM (n = 4 mice/genotype). * P less than .05; ** P less than .01; *** P less than .001; **** P less than .0001 compared to wild-type (WT) of the same sex by analysis of variance.

    Article Snippet: p38 MAPK , 9212 , AB 330713 , Cell Signaling Technology.

    Techniques: Mutagenesis, Expressing