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p-mk2 thr 334  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p-mk2 thr 334
    (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an <t>MK2</t> inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.
    P Mk2 Thr 334, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p-mk2+thr+334/anti+p+mk2/pmc04640462-369-27-62
    Average 90 stars, based on 1 article reviews
    p-mk2 thr 334 - by Bioz Stars, 2026-10
    90/100 stars

    Images

    1) Product Images from "Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis"

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis

    Journal: Science signaling

    doi: 10.1126/scisignal.aaa2147

    (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an MK2 inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.
    Figure Legend Snippet: (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an MK2 inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.

    Techniques Used: Isolation, Cell Culture, Incubation, Real-time Polymerase Chain Reaction, Western Blot

    Related Articles

    Western Blot:

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis
    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).

    Isolation:

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis
    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).

    Cell Culture:

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis
    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).

    Incubation:

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis
    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).

    Real-time Polymerase Chain Reaction:

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis
    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).



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    p-mk2 thr 334  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc p-mk2 thr 334
    (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an <t>MK2</t> inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.
    P Mk2 Thr 334, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p-mk2+thr+334/anti+p+mk2/pmc04640462-369-27-62
    Average 90 stars, based on 1 article reviews
    p-mk2 thr 334 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier
    primary antibodies against p-mk2 (thr 334  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc primary antibodies against p-mk2 (thr 334
    (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an <t>MK2</t> inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.
    Primary Antibodies Against P Mk2 (Thr 334, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p-mk2+thr+334/anti+p+mk2/pm21471309-149-20-29
    Average 90 stars, based on 1 article reviews
    primary antibodies against p-mk2 (thr 334 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an MK2 inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.

    Journal: Science signaling

    Article Title: Control of IL-17 receptor signaling and tissue inflammation by the p38α–MKP-1 signaling axis in a mouse model of multiple sclerosis

    doi: 10.1126/scisignal.aaa2147

    Figure Lengend Snippet: (A) MEFs isolated from WT or p38αCreER mice were treated with 4-OHT, and were left untreated or treated with IL-17 or TNF-α alone or in combination for 24 hours. Cell culture medium was then analyzed to determine the amounts of CXCL1 protein secreted by the cells. Data are means ± SEM of six mice per group. (B) Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for 5 hours. Cells were subjected to real-time PCR analysis to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of three to seven mice per group. (C) Left: Astrocytes isolated from WT or p38αCreER mice were treated with 4-OHT, and were then incubated in the absence or presence of IL-17 for the indicated times. Samples were then analyzed by Western blotting with antibodies specific for the indicated proteins. Blots are representative of five mice per group from two independent experiments. Right: Relative band intensities were determined by densitometry and are shown as means ± SEM of five mice per group. (D) Astrocytes from WT mice were treated with vehicle or an MK2 inhibitor before being stimulated with IL-17 for 5 hours. Cells were analyzed by real-time PCR to determine the relative abundances of the indicated mRNAs. Data are means ± SEM of seven mice per group. NS, not significant; *P < 0.05; **P < 0.01; ***P < 0.001. Data are representative of two to three independent experiments.

    Article Snippet: Western blotting analysis was performed as described previously ( 50 ) with antibodies specific for phosphorylated p38 (p-p38) at Thr 180 /Tyr 182 (9211), total p38 (9212), p-MK2 at Thr 334 (27B7), p-CREB at Ser 133 (87G3), p-IκBα (inhibitor of κB α) at Ser 32 (2859), p-ERK at Thr 202 /Tyr 204 (9101), p-JNK at Thr 183 /Tyr 185 (9251, all from Cell Signaling Technology), and β-actin (AC-15, Sigma).

    Techniques: Isolation, Cell Culture, Incubation, Real-time Polymerase Chain Reaction, Western Blot