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mouse anti phospho atf2  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology mouse anti phospho atf2
    Mouse Anti Phospho Atf2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 573 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+phospho+atf2/pmc12395842-80-19-22?v=Santa+Cruz+Biotechnology
    Average 94 stars, based on 573 article reviews
    mouse anti phospho atf2 - by Bioz Stars, 2026-07
    94/100 stars

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    ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and <t>ATF2</t> phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).
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    ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and <t>ATF2</t> phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).
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    ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and <t>ATF2</t> phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).
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    Santa Cruz Biotechnology antibody cocktail containing 0.2 ug/ml mouse anti-phospho atf2 (santa cruz biotechnology sc-8398)
    ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and <t>ATF2</t> phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).
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    ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and ATF2 phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).

    Journal: bioRxiv

    Article Title: Lack of p38 activation in T cells increases IL-35 production and protects against obesity by promoting thermogenesis

    doi: 10.1101/2023.08.04.551982

    Figure Lengend Snippet: ( A ) mRNA expression of p35 subunit of IL-35 in human visceral fat isolated from lean (N=12) and obese patients (N=52). ( C ) C57BL6 mice were treated with recombinant IL-35 i.v. (300ng per mouse) and BAT temperature was measured 4h later (mean ± SEM; PBS n = 7; IL-35 treated mice n = 9). ( D ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 48h and UCP1 and FGF21 levels were analysed by immunoblot. Loading control for UCP1 was run on different gel and not presented. (n=4 for each condition, technical replicates). ( E ) Immortalized brown preadipocytes were differentiated in vitro . Once differentiated, cells were stimulated in the presence or absence of IL-35 (100 ng/ml) for 0-120 minutes and ATF2 phosphorylation was analysed by immunoblot. ( F ) Differentiated adipocytes were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of Ucp1 level was measured by qRT-PCR and relativized to b-actin . ( G ) Primary white preadipocytes were isolated from C57BL6 mice and differentiated in vitro. Once differentiated, cells were stimulated with IL-35 (100 ng/ml) for 48h in the presence or absence of SB203580 inhibitor (10 uM). The expression of principal adipogenic markers ( Pparg, Adipoq, Leptin, Perlinipin ) level was measured by qRT-PCR and relativized to b-actin . Data are mean ± SEM, *p < 0.05, ** p < 0.01, ***p<0.001. Analysis by t test (A, C, E, F), 2-way ANOVA (B) or 1-way ANOVA (G).

    Article Snippet: Primary antibodies used in the study: anti-mouse MKK3 (Cat# 9238, Cell Signaling Technology), anti-mouse MKK6 (Cat# ADI-KAP-MA014-E, Enzo Life Sciences), anti-mouse UCP1 (Cat# AB10983, Abcam), anti-mouse FGF21 (Cat# RD281108100, BioVendor), anti-mouse p-ATF2 T69/71 (Cat# 9225S, Cell Signaling Technology), anti-mouse ATF2 (Cat# 9226S, Cell Signaling Technology), anti-mouse p-s6 S240/244 (Cat# 5364S, Cell Signaling Technology), anti-mouse p-p38 T180/Y182 (Cat# 9211S, Cell Signaling Technology), anti-mouse b-actin (Cat# sc-47778, Santa Cruz Technology), anti-mouse vinculin (Cat# V9131, Sigma) and secondary antibodies used in the study: goat anti-mouse (Cat# 31430, ThermoFisher) and goat anti-rabbit (Cat# 31460, ThermoFisher).

    Techniques: Expressing, Isolation, Recombinant, In Vitro, Western Blot, Control, Phospho-proteomics, Quantitative RT-PCR

    T cell expression of stress kinases MKK3 and MKK6 contributes to obesity and inflammation in AT through a compromised metabolic profile characterized by reduced browning and thermogenesis, as well as worsened liver steatosis. When T cells lack p38 activation, it enhances the expansion of adipose tissue Tregs and increases Treg IL35 expression via the mTOR pathway. IL35 induces phosphorylation of ATF-2, leading to the upregulation of UCP1 and FGF21 levels in adipocytes, which in turn promotes browning. Additionally, IL35 limits the infiltration and inflammation of CD8 + T cells in adipose tissue, thereby providing protection against obesity.

    Journal: bioRxiv

    Article Title: Lack of p38 activation in T cells increases IL-35 production and protects against obesity by promoting thermogenesis

    doi: 10.1101/2023.08.04.551982

    Figure Lengend Snippet: T cell expression of stress kinases MKK3 and MKK6 contributes to obesity and inflammation in AT through a compromised metabolic profile characterized by reduced browning and thermogenesis, as well as worsened liver steatosis. When T cells lack p38 activation, it enhances the expansion of adipose tissue Tregs and increases Treg IL35 expression via the mTOR pathway. IL35 induces phosphorylation of ATF-2, leading to the upregulation of UCP1 and FGF21 levels in adipocytes, which in turn promotes browning. Additionally, IL35 limits the infiltration and inflammation of CD8 + T cells in adipose tissue, thereby providing protection against obesity.

    Article Snippet: Primary antibodies used in the study: anti-mouse MKK3 (Cat# 9238, Cell Signaling Technology), anti-mouse MKK6 (Cat# ADI-KAP-MA014-E, Enzo Life Sciences), anti-mouse UCP1 (Cat# AB10983, Abcam), anti-mouse FGF21 (Cat# RD281108100, BioVendor), anti-mouse p-ATF2 T69/71 (Cat# 9225S, Cell Signaling Technology), anti-mouse ATF2 (Cat# 9226S, Cell Signaling Technology), anti-mouse p-s6 S240/244 (Cat# 5364S, Cell Signaling Technology), anti-mouse p-p38 T180/Y182 (Cat# 9211S, Cell Signaling Technology), anti-mouse b-actin (Cat# sc-47778, Santa Cruz Technology), anti-mouse vinculin (Cat# V9131, Sigma) and secondary antibodies used in the study: goat anti-mouse (Cat# 31430, ThermoFisher) and goat anti-rabbit (Cat# 31460, ThermoFisher).

    Techniques: Expressing, Activation Assay, Phospho-proteomics