nfatc1 signalling Search Results


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  • 92
    Cell Signaling Technology Inc nfatc1
    TRAIL inhibits RANKL-induced osteoclast differentiation and activation of <t>NFATc1.</t> a Bone marrow-derived macrophages (BMMs) from wild type (WT) and TRAIL-R knockout ( Trail-r −/− ) mice were plated in 96-well plates and stimulated with the RANKL (50 ng/ml) + M-CSF (20 ng/ml), TRAIL (500 ng/ml), or RANKL + M-CSF + TRAIL as indicated in the figure. After 10 days, cells were analyzed for osteoclast differentiation. After incubation, cells were subjected to a tartrate-resistant acid phosphatase (TRAP) assay. Cell morphology was examined by light microscopy (Scale bars, 100 µm), and the number of TRAP-positive multinuclear cells was quantified in ( b ). ** p
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    Cell Signaling Technology Inc anti nfatc1
    A schematic model of osteoclastogenesis regulated by the Blimp1-Bcl6-osteoclastic gene axis. RANKL–RANK interaction results in Blimp1 induction, leading to Bcl6 down-regulation and dissociation of Bcl6 from osteoclastic gene promoters, an event critical for osteoclastogenesis. <t>NFATc1</t> activation is induced by various factors, such as ITAM, TRAF6, c-Fos, and Ca 2+ signaling, which are also activated by RANKL.
    Anti Nfatc1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 120 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology nfatc1
    A schematic model of osteoclastogenesis regulated by the Blimp1-Bcl6-osteoclastic gene axis. RANKL–RANK interaction results in Blimp1 induction, leading to Bcl6 down-regulation and dissociation of Bcl6 from osteoclastic gene promoters, an event critical for osteoclastogenesis. <t>NFATc1</t> activation is induced by various factors, such as ITAM, TRAF6, c-Fos, and Ca 2+ signaling, which are also activated by RANKL.
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    Cell Signaling Technology Inc nfatc1 nfat2 antibody
    A schematic model of osteoclastogenesis regulated by the Blimp1-Bcl6-osteoclastic gene axis. RANKL–RANK interaction results in Blimp1 induction, leading to Bcl6 down-regulation and dissociation of Bcl6 from osteoclastic gene promoters, an event critical for osteoclastogenesis. <t>NFATc1</t> activation is induced by various factors, such as ITAM, TRAF6, c-Fos, and Ca 2+ signaling, which are also activated by RANKL.
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    Cell Signaling Technology Inc nfatc inhibitor
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
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    Cell Signaling Technology Inc t cells nfatc 1 antibodies
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
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    Cell Signaling Technology Inc alexafluor 488 conjugated nfatc1
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
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    Cell Signaling Technology Inc anti phospho nfatc1 antibodies
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
    Anti Phospho Nfatc1 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc anti nfatc1 cat no 8032 antibody
    rBCG::PGL-I preferentially triggers <t>Syk/calcineurin/NFATc</t> through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P
    Anti Nfatc1 Cat No 8032 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc rabbit antibody against nfatc1
    Iguratimod blocks PPAR-γ/c-Fos signaling. Proteins were extracted, and the protein expression levels of PPAR-γ, c-Fos and <t>NFATc1</t> were detected (A) and quantified (B). The experiments were repeated 3 times independently. Data are presented as means ± SD. *P
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    GeneTex fbln2
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    GeneTex rabbit polyclonal anti agouti signaling protein asip
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    GeneTex antibodies against apoptosis signal regulating kinase 1
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    Cell Signaling Technology Inc anti rabbit
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    GeneTex β tubulin
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    GeneTex gapdh
    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified <t>Fbln2</t> as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P
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    GeneTex cd81
    Hepatitis C virus (HCV) E2 protein enhances Hippo activity and decreases yes-associated protein (Yap) in human hepatocellular carcinoma and primary human hepatocytes. A: HepaRG cells were treated with HCV E2 protein 10 μg/mL for 5 hours, and whole-cell lysates were analyzed by Western blot for <t>CD81,</t> MPS one binder kinase activator-like protein (Mob)-1, phosphorylated (p)-MOB1, serine/threonine-protein kinase LATS-1, p-LATS1, and YAP/tafazzin (Taz). B: Primary human hepatocytes were treated with 10 μg/mL HCV E2 protein for 5 hours, and total nuclear protein and cytoplasmic fraction were analyzed separately by Western blot for YAP, CD81, ezrin, and p-ezrin (Thr567) and cleaved (activated) p–mammalian STE20-like protein kinase (MST)-1.
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    GeneTex anti csa antibody
    Hepatitis C virus (HCV) E2 protein enhances Hippo activity and decreases yes-associated protein (Yap) in human hepatocellular carcinoma and primary human hepatocytes. A: HepaRG cells were treated with HCV E2 protein 10 μg/mL for 5 hours, and whole-cell lysates were analyzed by Western blot for <t>CD81,</t> MPS one binder kinase activator-like protein (Mob)-1, phosphorylated (p)-MOB1, serine/threonine-protein kinase LATS-1, p-LATS1, and YAP/tafazzin (Taz). B: Primary human hepatocytes were treated with 10 μg/mL HCV E2 protein for 5 hours, and total nuclear protein and cytoplasmic fraction were analyzed separately by Western blot for YAP, CD81, ezrin, and p-ezrin (Thr567) and cleaved (activated) p–mammalian STE20-like protein kinase (MST)-1.
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    GeneTex twf1
    miR-206 decreases invasion through regulating MKL1/SRF and IL-11 A. Realtime PCR of MKL1 expression in MDA-MB-231 cells transfected with either scramble, miR-206 or <t>TWF1</t> siRNA. *p
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    GeneTex ing4
    Loss of <t>ING4</t> expression is required for tumorigenesis
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    GeneTex trim3
    <t>TRIM3</t> attenuates the stem cell population in GBM neurosphere cultures
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    GeneTex phosph erk
    <t>TRIM3</t> attenuates the stem cell population in GBM neurosphere cultures
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    Image Search Results


    TRAIL inhibits RANKL-induced osteoclast differentiation and activation of NFATc1. a Bone marrow-derived macrophages (BMMs) from wild type (WT) and TRAIL-R knockout ( Trail-r −/− ) mice were plated in 96-well plates and stimulated with the RANKL (50 ng/ml) + M-CSF (20 ng/ml), TRAIL (500 ng/ml), or RANKL + M-CSF + TRAIL as indicated in the figure. After 10 days, cells were analyzed for osteoclast differentiation. After incubation, cells were subjected to a tartrate-resistant acid phosphatase (TRAP) assay. Cell morphology was examined by light microscopy (Scale bars, 100 µm), and the number of TRAP-positive multinuclear cells was quantified in ( b ). ** p

    Journal: Cell Death & Disease

    Article Title: TRAIL inhibits RANK signaling and suppresses osteoclast activation via inhibiting lipid raft assembly and TRAF6 recruitment

    doi: 10.1038/s41419-019-1353-3

    Figure Lengend Snippet: TRAIL inhibits RANKL-induced osteoclast differentiation and activation of NFATc1. a Bone marrow-derived macrophages (BMMs) from wild type (WT) and TRAIL-R knockout ( Trail-r −/− ) mice were plated in 96-well plates and stimulated with the RANKL (50 ng/ml) + M-CSF (20 ng/ml), TRAIL (500 ng/ml), or RANKL + M-CSF + TRAIL as indicated in the figure. After 10 days, cells were analyzed for osteoclast differentiation. After incubation, cells were subjected to a tartrate-resistant acid phosphatase (TRAP) assay. Cell morphology was examined by light microscopy (Scale bars, 100 µm), and the number of TRAP-positive multinuclear cells was quantified in ( b ). ** p

    Article Snippet: To further confirm whether RANKL or TRAIL induces osteoclastogenesis signaling through nuclear translocation of NFATc1, the critical transcription factor of osteoclasts, we isolated nuclei to detect the translocation of NFATc1 when cells were treated with RANKL plus M-CSF in the presence or absence of TRAIL.

    Techniques: Activation Assay, Derivative Assay, Knock-Out, Mouse Assay, Incubation, TRAP Assay, Light Microscopy

    A schematic model of osteoclastogenesis regulated by the Blimp1-Bcl6-osteoclastic gene axis. RANKL–RANK interaction results in Blimp1 induction, leading to Bcl6 down-regulation and dissociation of Bcl6 from osteoclastic gene promoters, an event critical for osteoclastogenesis. NFATc1 activation is induced by various factors, such as ITAM, TRAF6, c-Fos, and Ca 2+ signaling, which are also activated by RANKL.

    Journal: The Journal of Experimental Medicine

    Article Title: The Blimp1-Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis

    doi: 10.1084/jem.20091957

    Figure Lengend Snippet: A schematic model of osteoclastogenesis regulated by the Blimp1-Bcl6-osteoclastic gene axis. RANKL–RANK interaction results in Blimp1 induction, leading to Bcl6 down-regulation and dissociation of Bcl6 from osteoclastic gene promoters, an event critical for osteoclastogenesis. NFATc1 activation is induced by various factors, such as ITAM, TRAF6, c-Fos, and Ca 2+ signaling, which are also activated by RANKL.

    Article Snippet: Immunoprecipitation was performed using anti-NFATc1 (7A6), anti-Bcl6 (N-3), and anti-Blimp1 (C14A4; Cell Signaling Technology).

    Techniques: Activation Assay

    Bcl6 suppresses osteoclast differentiation. (A) Total RNA was prepared from control (white bars) or Blimp1 cKO (shaded bars) cells treated with (+) or without (−) RANKL, and the expression of the osteoclastic genes NFATc1 , DC-STAMP , and Ctsk relative to β-actin was analyzed by a quantitative real-time PCR. Data are means ± SD of osteoclastic genes / β-actin . (**, P

    Journal: The Journal of Experimental Medicine

    Article Title: The Blimp1-Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis

    doi: 10.1084/jem.20091957

    Figure Lengend Snippet: Bcl6 suppresses osteoclast differentiation. (A) Total RNA was prepared from control (white bars) or Blimp1 cKO (shaded bars) cells treated with (+) or without (−) RANKL, and the expression of the osteoclastic genes NFATc1 , DC-STAMP , and Ctsk relative to β-actin was analyzed by a quantitative real-time PCR. Data are means ± SD of osteoclastic genes / β-actin . (**, P

    Article Snippet: Immunoprecipitation was performed using anti-NFATc1 (7A6), anti-Bcl6 (N-3), and anti-Blimp1 (C14A4; Cell Signaling Technology).

    Techniques: Expressing, Real-time Polymerase Chain Reaction

    Bcl6 is suppressed during osteoclastogenesis and inhibits osteoclast formation. (A) Bcl6 expression was examined by comparative microarray analysis between osteoclast precursors (M-CSF) and osteoclasts (M-CSF + RANKL) cultured for 6 d. (B) BMMs were cultured with or without RANKL for 8 d and subjected to immunofluorescence staining (left) and immunoblot (right) for Bcl6. Nuclei were visualized by DAPI. Bar, 25 µm. (C) Recruitment of NFATc1 and Bcl6 to the NFATc1 P1 distal promoter was detected by ChIP assay. RAW264.7 cells were stimulated with or without RANKL for 48 h and subjected to ChIP analysis. (D) RAW264.7 cells transduced with Bcl6-overexpressing (Bcl6) or mock (control) retrovirus were cultured in the presence (RANKL) or absence (control) of RANKL for 5 d and stained with TRAP. Left, TRAP staining. (right) Numbers are means ± SD of multinuclear TRAP-positive cells in control or Bcl6-overexpressing RAW264.7 cells cultured with RANKL (**, P

    Journal: The Journal of Experimental Medicine

    Article Title: The Blimp1-Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis

    doi: 10.1084/jem.20091957

    Figure Lengend Snippet: Bcl6 is suppressed during osteoclastogenesis and inhibits osteoclast formation. (A) Bcl6 expression was examined by comparative microarray analysis between osteoclast precursors (M-CSF) and osteoclasts (M-CSF + RANKL) cultured for 6 d. (B) BMMs were cultured with or without RANKL for 8 d and subjected to immunofluorescence staining (left) and immunoblot (right) for Bcl6. Nuclei were visualized by DAPI. Bar, 25 µm. (C) Recruitment of NFATc1 and Bcl6 to the NFATc1 P1 distal promoter was detected by ChIP assay. RAW264.7 cells were stimulated with or without RANKL for 48 h and subjected to ChIP analysis. (D) RAW264.7 cells transduced with Bcl6-overexpressing (Bcl6) or mock (control) retrovirus were cultured in the presence (RANKL) or absence (control) of RANKL for 5 d and stained with TRAP. Left, TRAP staining. (right) Numbers are means ± SD of multinuclear TRAP-positive cells in control or Bcl6-overexpressing RAW264.7 cells cultured with RANKL (**, P

    Article Snippet: Immunoprecipitation was performed using anti-NFATc1 (7A6), anti-Bcl6 (N-3), and anti-Blimp1 (C14A4; Cell Signaling Technology).

    Techniques: Expressing, Microarray, Cell Culture, Immunofluorescence, Staining, Chromatin Immunoprecipitation, Transduction

    Expression of osteoclast differentiation markers in RAW 264.7 cells decreases after culture with the conditioned media of 4T1 cells overexpressing NDRG2. (A–D) RAW 264.7 cells were seeded into 6-well plate (2×10 5 ) and differentiated in α-MEM (Control) and the CM of 4T1, 4T1-mock and 4T1-NDRG2 cells in the presence of RANKL (100 ng/ml) for 4 days. The media and RANKL were changed daily. The mRNA expression levels of Cathepsin K, MITF, NFATc1 and TRAP in RAW 264.7 cells were confirmed by quantitative real time PCR. The protein expression of NFATc1 and MITF was measured by Western blot analysis ( ** p

    Journal: Biomolecules & Therapeutics

    Article Title: NDRG2 Expression Decreases Tumor-Induced Osteoclast Differentiation by Down-regulating ICAM1 in Breast Cancer Cells

    doi: 10.4062/biomolther.2015.105

    Figure Lengend Snippet: Expression of osteoclast differentiation markers in RAW 264.7 cells decreases after culture with the conditioned media of 4T1 cells overexpressing NDRG2. (A–D) RAW 264.7 cells were seeded into 6-well plate (2×10 5 ) and differentiated in α-MEM (Control) and the CM of 4T1, 4T1-mock and 4T1-NDRG2 cells in the presence of RANKL (100 ng/ml) for 4 days. The media and RANKL were changed daily. The mRNA expression levels of Cathepsin K, MITF, NFATc1 and TRAP in RAW 264.7 cells were confirmed by quantitative real time PCR. The protein expression of NFATc1 and MITF was measured by Western blot analysis ( ** p

    Article Snippet: The antibodies against actin, α-actinin, NDRG2 and ICAM1 were purchased from Santa Cruz Biotechnology and the antibodies against NFATc1, MITF, STAT3, p-STAT3, JNK, p-JNK, ERK, p-ERK, p38, p-p38, AKT and p-AKT were obtained from Cell Signaling (Danvers, MA, USA).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

    Diagram of the proposed mechanism of AA-induced antitumoral activity. This mechanism includes the NFATc1-dependent down-regulation of GLI1 and its target genes ( BCL2 , BFL1/A1 , and 4-1BB ). ROS , reactive oxygen species.

    Journal: The Journal of Biological Chemistry

    Article Title: Nuclear Factor of Activated T Cells-dependent Down-regulation of the Transcription Factor Glioma-associated Protein 1 (GLI1) Underlies the Growth Inhibitory Properties of Arachidonic Acid *

    doi: 10.1074/jbc.M115.691972

    Figure Lengend Snippet: Diagram of the proposed mechanism of AA-induced antitumoral activity. This mechanism includes the NFATc1-dependent down-regulation of GLI1 and its target genes ( BCL2 , BFL1/A1 , and 4-1BB ). ROS , reactive oxygen species.

    Article Snippet: GLI1 and NFATc1 antibodies were obtained from Cell Signaling Technology (Danvers, MA).

    Techniques: Activity Assay

    NFATc1 mediates AA silencing of GLI1 expression. A , PANC1 cells were transfected with an expression construct encoding NFATc1-GFP for 48 h and then treated with AA (60 μg/ml) or vehicle for 15 or 30 min. Cells were fixed, stained with DAPI, and

    Journal: The Journal of Biological Chemistry

    Article Title: Nuclear Factor of Activated T Cells-dependent Down-regulation of the Transcription Factor Glioma-associated Protein 1 (GLI1) Underlies the Growth Inhibitory Properties of Arachidonic Acid *

    doi: 10.1074/jbc.M115.691972

    Figure Lengend Snippet: NFATc1 mediates AA silencing of GLI1 expression. A , PANC1 cells were transfected with an expression construct encoding NFATc1-GFP for 48 h and then treated with AA (60 μg/ml) or vehicle for 15 or 30 min. Cells were fixed, stained with DAPI, and

    Article Snippet: GLI1 and NFATc1 antibodies were obtained from Cell Signaling Technology (Danvers, MA).

    Techniques: Expressing, Transfection, Construct, Staining

    rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: rBCG::PGL-I preferentially triggers Syk/calcineurin/NFATc through CR3 to rewire innate cells (A) DCs or PMNs from WT or myd88 −/− mice were infected with the three rBCG strains at MOI of 5. WT cells were treated with GS-9973 to inhibit the Syk pathway, or CsA to block NFATc translocation 1 h before infection. After overnight incubation supernatants were harvested to measure by ELISA IL-2 produced by DCs and IL-10 produced by PMNs. (B) Before infection of DCs or PMNs with rBCG::noPGL or rBCG::PGL-I as in (A) , cells were either incubated for 1 h with anti-CD11b antibody M1/70 to block CR3-mediated entry, or exposed to CsA to block NFATc translocation as indicated. IL-2 produced by DCs and IL-10 by PMNs after overnight incubation were measured by ELISA. Data are presented as mean ± SEM ( n = 4). * P

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: Mouse Assay, Infection, Blocking Assay, Translocation Assay, Incubation, Enzyme-linked Immunosorbent Assay, Produced

    CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: CR3 triggers the Syk/calcineurin/NFATc pathway upon engagement by PGL-I-producing mycobacteria to rewire the innate response. rBCG::PGL-I targets the lectin domain of CR3 on the surface of DCs, PMNs, and MPs. Dectin-1 and CR3 cooperate to induce highly efficient entry of the bacilli. This triggers Syk for translocation of NFATc to the nucleus and initiates a transcriptional program to generate an NF-κB-independent mediator signature. This preferentially PGL-I-triggered pathway does not depend on MYD88 even though both cooperate to induce maximum levels of these mediators.

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: Translocation Assay

    rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P

    Journal: Frontiers in Immunology

    Article Title: CR3 Engaged by PGL-I Triggers Syk-Calcineurin-NFATc to Rewire the Innate Immune Response in Leprosy

    doi: 10.3389/fimmu.2019.02913

    Figure Lengend Snippet: rBCG::PGL-I targeting CR3 triggers Syk and NFATc in vivo . (A,B) WT and itgam −/− mice were nasally infected with 5 × 10 6 CFUs of fluorescent rBCG::PGL-I or rBCG::noPGL, and received two nasal doses of Syk inhibitor GS-9973 administered 1 h before and after bacteria. BAL and lung tissues were harvested 24 h later to analyze cells by flow cytometry. (A,B) Numbers of Ly-6G + , CD11c − PMNs and Ly-6G − , CD11c + MPs harboring BCG-EGFP + recovered from the lung parenchyma from 11 individuals (A) or BAL from 12 individuals pooled per 2 (B) . (C) IL-10 produced in situ by lung cells was analyzed by ELISA in the first BAL from 12 individuals pooled per 2. (D) WT mice received two nasal doses of CsA 1 h before and 1 h after rBCG::PGL-I or rBCG::noPGL inhalation, to block NFATc translocation. IL-10 produced in situ by lung cells was analyzed as in (C) . Data are represented as individual values from n = 11 (A) or n = 6 (B–D) from two independent experiments. ** P

    Article Snippet: Mice received 40 μL of vehicle (DMSO 2%), or 1 μM Syk inhibitor (GS-9973, ApexBio Technology), or 50 ng/ml NFATc inhibitor (Cyclosporin A, Cell signaling Technology) via the nasal route 1 h before and 1 h after BCG infection.

    Techniques: In Vivo, Mouse Assay, Infection, Flow Cytometry, Cytometry, Produced, In Situ, Enzyme-linked Immunosorbent Assay, Blocking Assay, Translocation Assay

    Iguratimod blocks PPAR-γ/c-Fos signaling. Proteins were extracted, and the protein expression levels of PPAR-γ, c-Fos and NFATc1 were detected (A) and quantified (B). The experiments were repeated 3 times independently. Data are presented as means ± SD. *P

    Journal: Molecular Medicine Reports

    Article Title: Iguratimod prevents ovariectomy-induced bone loss and suppresses osteoclastogenesis via inhibition of peroxisome proliferator-activated receptor-γ

    doi: 10.3892/mmr.2017.7648

    Figure Lengend Snippet: Iguratimod blocks PPAR-γ/c-Fos signaling. Proteins were extracted, and the protein expression levels of PPAR-γ, c-Fos and NFATc1 were detected (A) and quantified (B). The experiments were repeated 3 times independently. Data are presented as means ± SD. *P

    Article Snippet: Rabbit antibody against NFATc1 (no. 8032, dilution 1:1,000) was purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA).

    Techniques: Expressing

    Iguratimod inhibits the expression of c-Fos, NFATc1 and osteoclast marker genes. (A) The mRNA levels of c-Fos, NFATc1 and osteoclast marker genes were detected using RT-qPCR. Data are presented as means ± SD. (B and C) Proteins were extracted at indicated times and protein expression levels of c-Fos and NFATc1 were detected by western blotting (B) and quantified (C). The experiments were repeated 3 times independently. Data are presented as means ± SD. **P

    Journal: Molecular Medicine Reports

    Article Title: Iguratimod prevents ovariectomy-induced bone loss and suppresses osteoclastogenesis via inhibition of peroxisome proliferator-activated receptor-γ

    doi: 10.3892/mmr.2017.7648

    Figure Lengend Snippet: Iguratimod inhibits the expression of c-Fos, NFATc1 and osteoclast marker genes. (A) The mRNA levels of c-Fos, NFATc1 and osteoclast marker genes were detected using RT-qPCR. Data are presented as means ± SD. (B and C) Proteins were extracted at indicated times and protein expression levels of c-Fos and NFATc1 were detected by western blotting (B) and quantified (C). The experiments were repeated 3 times independently. Data are presented as means ± SD. **P

    Article Snippet: Rabbit antibody against NFATc1 (no. 8032, dilution 1:1,000) was purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA).

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

    Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified Fbln2 as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Therapeutic Cardiac-Targeted Delivery of miR‐1 Reverses Pressure Overload-Induced Cardiac Hypertrophy and Attenuates Pathological Remodeling

    doi: 10.1161/JAHA.113.000078

    Figure Lengend Snippet: Identification and validation of the miR‐1 direct target genes. A, Bioinformatics analysis identified Fbln2 as a putative target gene of miR‐1 . The mRNA sequence of Fbln2 is predicted to contain a conserved “seed” sequence complimentary to miR‐1 in the 3′‐untranslated region (3′‐UTR). B, Luciferase reporter assays performed by cotransfection of miR‐1 “mimics” (pre– miR‐1 ) with a luciferase vector linked to the Fbln2 or Ncx1 3′‐UTR or deleted 3′‐UTR complementary site (No 3′‐UTR); a control nontargeting “mimic” (pre–miR‐control) was also included. Data represent mean±SE of n=6 experiments per condition, $ P

    Article Snippet: Western Blotting Analysis Protein expression was evaluated in LV lysates by Western blot analysis according to standard procedures with antibodies against phospholamban (Pln) (Badrilla, UK), Serca2a (custom made in our laboratory), extracellular signal‐regulated protein kinase (ERK1/2), phospho‐ERK1/2 (Thr202/Tyr204), phospho‐p38 (Thr180/Tyr182), p38, phospho–c‐jun NH2 ‐terminal kinase (JNK) (Thr183/Tyr185), JNK, Bcl‐2, and Bax (Cell Signaling Technology), Fbln2 (Genetex), Ncx1 (Abcam), and Gapdh (Sigma‐Aldrich).

    Techniques: Sequencing, Luciferase, Cotransfection, Plasmid Preparation

    Hepatitis C virus (HCV) E2 protein enhances Hippo activity and decreases yes-associated protein (Yap) in human hepatocellular carcinoma and primary human hepatocytes. A: HepaRG cells were treated with HCV E2 protein 10 μg/mL for 5 hours, and whole-cell lysates were analyzed by Western blot for CD81, MPS one binder kinase activator-like protein (Mob)-1, phosphorylated (p)-MOB1, serine/threonine-protein kinase LATS-1, p-LATS1, and YAP/tafazzin (Taz). B: Primary human hepatocytes were treated with 10 μg/mL HCV E2 protein for 5 hours, and total nuclear protein and cytoplasmic fraction were analyzed separately by Western blot for YAP, CD81, ezrin, and p-ezrin (Thr567) and cleaved (activated) p–mammalian STE20-like protein kinase (MST)-1.

    Journal: The American Journal of Pathology

    Article Title: Hepatitis C Virus Mimics Effects of Glypican-3 on CD81 and Promotes Development of Hepatocellular Carcinomas via Activation of Hippo Pathway in Hepatocytes

    doi: 10.1016/j.ajpath.2018.02.013

    Figure Lengend Snippet: Hepatitis C virus (HCV) E2 protein enhances Hippo activity and decreases yes-associated protein (Yap) in human hepatocellular carcinoma and primary human hepatocytes. A: HepaRG cells were treated with HCV E2 protein 10 μg/mL for 5 hours, and whole-cell lysates were analyzed by Western blot for CD81, MPS one binder kinase activator-like protein (Mob)-1, phosphorylated (p)-MOB1, serine/threonine-protein kinase LATS-1, p-LATS1, and YAP/tafazzin (Taz). B: Primary human hepatocytes were treated with 10 μg/mL HCV E2 protein for 5 hours, and total nuclear protein and cytoplasmic fraction were analyzed separately by Western blot for YAP, CD81, ezrin, and p-ezrin (Thr567) and cleaved (activated) p–mammalian STE20-like protein kinase (MST)-1.

    Article Snippet: Signaling functions of CD81 were first demonstrated by treatment with the specific agonistic antibody 5A6.

    Techniques: Activity Assay, Western Blot, Microscale Thermophoresis

    Forced expression of CD81 in glypican (Gpc)-3–expressing JM2 hepatoma cells results in activation of the Hippo pathway, a decrease in nuclear Yap, and a decrease in the percentage of bromodeoxyuridine (BrdU)-positive nuclei. JM2 cells were transiently transfected with pCMV6-CD81 plasmid, and after 12 hours, total cell lysates were collected for protein expression analysis. A: Expression of CD81, Gpc3, ezrin, and phosphorylated (p)-ezrin (Thr567). B: Cleaved (activated) p-mammalian STE20-like protein kinase (Mst)-1, yes-associated protein (Yap), and p-Yap. In both A and B , each band represents a separate cell culture. Results are representative of four experiments. C: JM2 cells in sparse density (50%) after 24 hours of transfection and 24 hours of BrdU incorporation. Positive ratio indicates the fraction of cells whose nuclei were positive for BrdU by IHC analysis. Data are expressed as means ± SEM, derived from four separate cultures for each category ( C ). P = 0.0078.

    Journal: The American Journal of Pathology

    Article Title: Hepatitis C Virus Mimics Effects of Glypican-3 on CD81 and Promotes Development of Hepatocellular Carcinomas via Activation of Hippo Pathway in Hepatocytes

    doi: 10.1016/j.ajpath.2018.02.013

    Figure Lengend Snippet: Forced expression of CD81 in glypican (Gpc)-3–expressing JM2 hepatoma cells results in activation of the Hippo pathway, a decrease in nuclear Yap, and a decrease in the percentage of bromodeoxyuridine (BrdU)-positive nuclei. JM2 cells were transiently transfected with pCMV6-CD81 plasmid, and after 12 hours, total cell lysates were collected for protein expression analysis. A: Expression of CD81, Gpc3, ezrin, and phosphorylated (p)-ezrin (Thr567). B: Cleaved (activated) p-mammalian STE20-like protein kinase (Mst)-1, yes-associated protein (Yap), and p-Yap. In both A and B , each band represents a separate cell culture. Results are representative of four experiments. C: JM2 cells in sparse density (50%) after 24 hours of transfection and 24 hours of BrdU incorporation. Positive ratio indicates the fraction of cells whose nuclei were positive for BrdU by IHC analysis. Data are expressed as means ± SEM, derived from four separate cultures for each category ( C ). P = 0.0078.

    Article Snippet: Signaling functions of CD81 were first demonstrated by treatment with the specific agonistic antibody 5A6.

    Techniques: Expressing, Gel Permeation Chromatography, Activation Assay, Transfection, Plasmid Preparation, Microscale Thermophoresis, Cell Culture, BrdU Incorporation Assay, Immunohistochemistry, Derivative Assay

    Inhibition of CD81-associated tyrosine-protein kinase SYK (Syk) results in decrease in yes-associated protein (Yap) expression and ezrin phosphorylation. A: JM2 rat hepatocellular carcinoma cells were treated with Syk inhibitor at 0.1 and 0.4 μg/mL for 5 hours, and total proteins were analyzed by Western blot for Yap, ezrin, and phosphorylated (p)-ezrin (Thr567). B: JM2 cells were transiently transfected with pCMV6-Syk plasmid, and after 12 hours, total cell lysates were collected for protein expression analysis of Syk, ezrin, and p-ezrin (Thr567), cleaved p–mammalian STE20-like protein kinase (Mst)-1, Yap/tafazzin (Taz), and p-Yap. Red indicates high saturation of the band. C: Quantitative analysis of relative percentage of p-Yap and Yap expression from C .

    Journal: The American Journal of Pathology

    Article Title: Hepatitis C Virus Mimics Effects of Glypican-3 on CD81 and Promotes Development of Hepatocellular Carcinomas via Activation of Hippo Pathway in Hepatocytes

    doi: 10.1016/j.ajpath.2018.02.013

    Figure Lengend Snippet: Inhibition of CD81-associated tyrosine-protein kinase SYK (Syk) results in decrease in yes-associated protein (Yap) expression and ezrin phosphorylation. A: JM2 rat hepatocellular carcinoma cells were treated with Syk inhibitor at 0.1 and 0.4 μg/mL for 5 hours, and total proteins were analyzed by Western blot for Yap, ezrin, and phosphorylated (p)-ezrin (Thr567). B: JM2 cells were transiently transfected with pCMV6-Syk plasmid, and after 12 hours, total cell lysates were collected for protein expression analysis of Syk, ezrin, and p-ezrin (Thr567), cleaved p–mammalian STE20-like protein kinase (Mst)-1, Yap/tafazzin (Taz), and p-Yap. Red indicates high saturation of the band. C: Quantitative analysis of relative percentage of p-Yap and Yap expression from C .

    Article Snippet: Signaling functions of CD81 were first demonstrated by treatment with the specific agonistic antibody 5A6.

    Techniques: Inhibition, Expressing, Western Blot, Transfection, Plasmid Preparation, Microscale Thermophoresis

    Effects of the CD81 agonistic antibody 5A6 on hepatocyte proliferation. Rat hepatocytes at day 6 in primary culture were stimulated with 1 μg/mL of 5A6 or inactivated control for 5 hours. Yes-associated protein (Yap) and tafazzin (Taz) expression levels in nuclear extracts ( left panels ), total ezrin and phosphorylated (p)-ezrin (Thr567) expression levels in cytoplasm ( right panels ) were detected by Western blot analysis. Each bar indicates the ratio between the intensity of the relative band divided by the intensity of the Ponceau stain. The bars in the graphs in the bottom panels correspond to the labels and conditions shown in the corresponding top panels for the Western gels ( white bars , control medium; black bars , inactivated 5A6 agonistic antibody; red bars , 5A6 agonistic antibody; blue bars , 5A6 agonistic antibody+HGF). Data are expressed as means ± SEM of four separate cultures. ∗ P

    Journal: The American Journal of Pathology

    Article Title: Hepatitis C Virus Mimics Effects of Glypican-3 on CD81 and Promotes Development of Hepatocellular Carcinomas via Activation of Hippo Pathway in Hepatocytes

    doi: 10.1016/j.ajpath.2018.02.013

    Figure Lengend Snippet: Effects of the CD81 agonistic antibody 5A6 on hepatocyte proliferation. Rat hepatocytes at day 6 in primary culture were stimulated with 1 μg/mL of 5A6 or inactivated control for 5 hours. Yes-associated protein (Yap) and tafazzin (Taz) expression levels in nuclear extracts ( left panels ), total ezrin and phosphorylated (p)-ezrin (Thr567) expression levels in cytoplasm ( right panels ) were detected by Western blot analysis. Each bar indicates the ratio between the intensity of the relative band divided by the intensity of the Ponceau stain. The bars in the graphs in the bottom panels correspond to the labels and conditions shown in the corresponding top panels for the Western gels ( white bars , control medium; black bars , inactivated 5A6 agonistic antibody; red bars , 5A6 agonistic antibody; blue bars , 5A6 agonistic antibody+HGF). Data are expressed as means ± SEM of four separate cultures. ∗ P

    Article Snippet: Signaling functions of CD81 were first demonstrated by treatment with the specific agonistic antibody 5A6.

    Techniques: Expressing, Western Blot, Staining

    miR-206 decreases invasion through regulating MKL1/SRF and IL-11 A. Realtime PCR of MKL1 expression in MDA-MB-231 cells transfected with either scramble, miR-206 or TWF1 siRNA. *p

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    Article Title: MicroRNA-206 inhibits stemness and metastasis of breast cancer by targeting MKL1/IL11 pathway

    doi: 10.1158/1078-0432.CCR-16-0943

    Figure Lengend Snippet: miR-206 decreases invasion through regulating MKL1/SRF and IL-11 A. Realtime PCR of MKL1 expression in MDA-MB-231 cells transfected with either scramble, miR-206 or TWF1 siRNA. *p

    Article Snippet: RT-PCR results also demonstrated that in MCF7 cells miR-206 overexpression led to a comparable reduction of TWF1, MKL1, and IL-11 expression levels and signaling from TWF1 to MKL1 and IL-11 as in other breast cancer cells ( ).

    Techniques: Polymerase Chain Reaction, Expressing, Multiple Displacement Amplification, Transfection

    Loss of ING4 expression is required for tumorigenesis

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: Loss of ING4 expression is required for tumorigenesis

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques: Expressing

    Pten-mediated loss of ING4 and altered differentiation in tumorigenic cells

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: Pten-mediated loss of ING4 and altered differentiation in tumorigenic cells

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques:

    Myc-induced ING4 expression is required for differentiation

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: Myc-induced ING4 expression is required for differentiation

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques: Expressing

    Constitutive Myc and ING4 expression leads to cell death

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: Constitutive Myc and ING4 expression leads to cell death

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques: Expressing

    ING4 expression is lost in prostate cancer patients

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: ING4 expression is lost in prostate cancer patients

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques: Expressing

    ING4 is transiently expressed in differentiated immortalized prostate epithelial cells

    Journal: Cancer research

    Article Title: Transient Induction of ING4 by MYC Drives Prostate Epithelial Cell Differentiation and its Disruption Drives Prostate Tumorigenesis

    doi: 10.1158/0008-5472.CAN-13-3076

    Figure Lengend Snippet: ING4 is transiently expressed in differentiated immortalized prostate epithelial cells

    Article Snippet: Immunoblotting: Myc (o6-340) was purchased from Millipore, Erg (C-20) from Santa Cruz, Pten (138G6) and p27 (Kip1) from Cell Signaling, and ING4 (EP3804) from GeneTex.

    Techniques:

    TRIM3 attenuates the stem cell population in GBM neurosphere cultures

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 attenuates the stem cell population in GBM neurosphere cultures

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques:

    TRIM3 regulates Musashi/Numb signaling

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 regulates Musashi/Numb signaling

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques:

    TRIM3 expression is reduced in human GBMs

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 expression is reduced in human GBMs

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques: Expressing

    TRIM3 expression reduces cell proliferation and glioma growth

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 expression reduces cell proliferation and glioma growth

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques: Expressing

    TRIM3 regulates the stem cell population in GBM neurosphere cultures

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 regulates the stem cell population in GBM neurosphere cultures

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques:

    TRIM3 suppresses c-Myc expression

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 suppresses c-Myc expression

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques: Expressing

    TRIM3 , the human homolog of Drosophila brat is deleted in GBMs

    Journal: Cancer research

    Article Title: Human Brat ortholog TRIM3 is a tumor suppressor that regulates asymmetric cell division in glioblastoma

    doi: 10.1158/0008-5472.CAN-13-3703

    Figure Lengend Snippet: TRIM3 , the human homolog of Drosophila brat is deleted in GBMs

    Article Snippet: We further probed these cultures for signaling pathways regulated by TRIM3 that might explain the discrepancy between c-Myc expression and its target genes.

    Techniques: