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anti mouse pmk2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti mouse pmk2
    Anti Mouse Pmk2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 315 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pmk2+thr334/10__1074_slash_jbc__ra119__011633-193-84-86?v=Cell+Signaling+Technology+Inc
    Average 95 stars, based on 315 article reviews
    anti mouse pmk2 - by Bioz Stars, 2026-07
    95/100 stars

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    Cell Signaling Technology Inc pmk2 primary antibody
    (A,B) Representative images of primary breast lesions, n=53, and bone metastatic biopsies, n=33, Scale= 15 µm (Inset scale = 100µm). Serial sections were stained with antibodies against IL-6 (A) or phosphorylated MK2 <t>(pMK2)</t> (B), along with hematoxylin and eosin (H&E), E-cadherin, or pan-cytokeratin (C) IHC for IL-6 in tumor versus stroma on primary breast and patient-matched bone metastatic lesions. Semi-quantitative analysis using histoscore (H-score) system. Two-tailed Wilcoxon signed-rank test, **** p<0.0001. D) IL-6 expression across molecular subtypes of breast cancer. Two-way ANOVA, ***p≤ 0.001. (E) IL-6 expression in tumor stroma versus tumor epithelium (epi) in the pan-Breast cancer dataset. Boxplot, t-test, **** p< 2.2e-16. Below the boxplot is a list of p38MAPK-dependent stromal factors expressed in the three datasets analyzed. (F) GSVA analysis for enrichment of p38MAPK-dependent protumorigenic factors in stroma and epi from breast tumor samples (right). Gene list with overlapping genes (bottom left). Significance was determined by comparing the GSVA enrichment scores of stroma versus epi within each signature, one-way ANOVA with Tukey post-hoc test, ***p≤ 0.0001. All data are displayed as mean±SEM.
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    Cell Signaling Technology Inc immunohistochemistry for pmk2 thr334
    (A,B) Representative images of primary breast lesions, n=53, and bone metastatic biopsies, n=33, Scale= 15 µm (Inset scale = 100µm). Serial sections were stained with antibodies against IL-6 (A) or phosphorylated MK2 <t>(pMK2)</t> (B), along with hematoxylin and eosin (H&E), E-cadherin, or pan-cytokeratin (C) IHC for IL-6 in tumor versus stroma on primary breast and patient-matched bone metastatic lesions. Semi-quantitative analysis using histoscore (H-score) system. Two-tailed Wilcoxon signed-rank test, **** p<0.0001. D) IL-6 expression across molecular subtypes of breast cancer. Two-way ANOVA, ***p≤ 0.001. (E) IL-6 expression in tumor stroma versus tumor epithelium (epi) in the pan-Breast cancer dataset. Boxplot, t-test, **** p< 2.2e-16. Below the boxplot is a list of p38MAPK-dependent stromal factors expressed in the three datasets analyzed. (F) GSVA analysis for enrichment of p38MAPK-dependent protumorigenic factors in stroma and epi from breast tumor samples (right). Gene list with overlapping genes (bottom left). Significance was determined by comparing the GSVA enrichment scores of stroma versus epi within each signature, one-way ANOVA with Tukey post-hoc test, ***p≤ 0.0001. All data are displayed as mean±SEM.
    Immunohistochemistry For Pmk2 Thr334, 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
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    Cell Signaling Technology Inc pmk2 thr334
    A) MK2 is constitutively activated in CT26 cells. Serum-starvation (SS) reduces <t>pMK2,</t> but treatment with IL-1β, IL-6, or TNF-α induces MK2 phosphorylation. Intratumoral treatment with IL-1β, IL-6, and TNF-α at levels produced by vehicle tumors resulted in B) representative images of tumors with C) restored tumor size and D) weight. In organ culture supernatants, cytokine treatment increased the MK2i tumor production of E) IL-1β, F) IL-6, and G) TNF-α. Increases were seen in mRNA levels for H) IL-1β, I) IL-6, and J) TNF-α were also seen. N=10 *p < 0.05, **p<0.01, ***p < 0.005.
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    Cell Signaling Technology Inc rabbit anti pmk2
    A) MK2 is constitutively activated in CT26 cells. Serum-starvation (SS) reduces <t>pMK2,</t> but treatment with IL-1β, IL-6, or TNF-α induces MK2 phosphorylation. Intratumoral treatment with IL-1β, IL-6, and TNF-α at levels produced by vehicle tumors resulted in B) representative images of tumors with C) restored tumor size and D) weight. In organ culture supernatants, cytokine treatment increased the MK2i tumor production of E) IL-1β, F) IL-6, and G) TNF-α. Increases were seen in mRNA levels for H) IL-1β, I) IL-6, and J) TNF-α were also seen. N=10 *p < 0.05, **p<0.01, ***p < 0.005.
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    Image Search Results


    (A,B) Representative images of primary breast lesions, n=53, and bone metastatic biopsies, n=33, Scale= 15 µm (Inset scale = 100µm). Serial sections were stained with antibodies against IL-6 (A) or phosphorylated MK2 (pMK2) (B), along with hematoxylin and eosin (H&E), E-cadherin, or pan-cytokeratin (C) IHC for IL-6 in tumor versus stroma on primary breast and patient-matched bone metastatic lesions. Semi-quantitative analysis using histoscore (H-score) system. Two-tailed Wilcoxon signed-rank test, **** p<0.0001. D) IL-6 expression across molecular subtypes of breast cancer. Two-way ANOVA, ***p≤ 0.001. (E) IL-6 expression in tumor stroma versus tumor epithelium (epi) in the pan-Breast cancer dataset. Boxplot, t-test, **** p< 2.2e-16. Below the boxplot is a list of p38MAPK-dependent stromal factors expressed in the three datasets analyzed. (F) GSVA analysis for enrichment of p38MAPK-dependent protumorigenic factors in stroma and epi from breast tumor samples (right). Gene list with overlapping genes (bottom left). Significance was determined by comparing the GSVA enrichment scores of stroma versus epi within each signature, one-way ANOVA with Tukey post-hoc test, ***p≤ 0.0001. All data are displayed as mean±SEM.

    Journal: Cancer research

    Article Title: Inhibition of the stromal p38MAPK/MK2 pathway limits breast cancer metastases and chemotherapy-induced bone loss

    doi: 10.1158/0008-5472.CAN-18-0234

    Figure Lengend Snippet: (A,B) Representative images of primary breast lesions, n=53, and bone metastatic biopsies, n=33, Scale= 15 µm (Inset scale = 100µm). Serial sections were stained with antibodies against IL-6 (A) or phosphorylated MK2 (pMK2) (B), along with hematoxylin and eosin (H&E), E-cadherin, or pan-cytokeratin (C) IHC for IL-6 in tumor versus stroma on primary breast and patient-matched bone metastatic lesions. Semi-quantitative analysis using histoscore (H-score) system. Two-tailed Wilcoxon signed-rank test, **** p<0.0001. D) IL-6 expression across molecular subtypes of breast cancer. Two-way ANOVA, ***p≤ 0.001. (E) IL-6 expression in tumor stroma versus tumor epithelium (epi) in the pan-Breast cancer dataset. Boxplot, t-test, **** p< 2.2e-16. Below the boxplot is a list of p38MAPK-dependent stromal factors expressed in the three datasets analyzed. (F) GSVA analysis for enrichment of p38MAPK-dependent protumorigenic factors in stroma and epi from breast tumor samples (right). Gene list with overlapping genes (bottom left). Significance was determined by comparing the GSVA enrichment scores of stroma versus epi within each signature, one-way ANOVA with Tukey post-hoc test, ***p≤ 0.0001. All data are displayed as mean±SEM.

    Article Snippet: Slides were stained with the following antibodies: anti-IL-6 primary antibody (ab6672, 1:100, AbCam), pMK2 primary antibody (3007, 1:50, Cell Signaling), Total p38 primary antibody (9212, 1:100, Cell Signaling), Biotinylated Donkey anti-Rabbit IgG (H+L) cross-adsorbed secondary antibody (Cat#:31821, 1:500, 2.2μg/ml, Thermofisher).

    Techniques: Staining, Two Tailed Test, Expressing

    A) MK2 is constitutively activated in CT26 cells. Serum-starvation (SS) reduces pMK2, but treatment with IL-1β, IL-6, or TNF-α induces MK2 phosphorylation. Intratumoral treatment with IL-1β, IL-6, and TNF-α at levels produced by vehicle tumors resulted in B) representative images of tumors with C) restored tumor size and D) weight. In organ culture supernatants, cytokine treatment increased the MK2i tumor production of E) IL-1β, F) IL-6, and G) TNF-α. Increases were seen in mRNA levels for H) IL-1β, I) IL-6, and J) TNF-α were also seen. N=10 *p < 0.05, **p<0.01, ***p < 0.005.

    Journal: International journal of cancer

    Article Title: Inhibition of MK2 suppresses IL-1β, IL-6, and TNF-α dependent colorectal cancer growth

    doi: 10.1002/ijc.31191

    Figure Lengend Snippet: A) MK2 is constitutively activated in CT26 cells. Serum-starvation (SS) reduces pMK2, but treatment with IL-1β, IL-6, or TNF-α induces MK2 phosphorylation. Intratumoral treatment with IL-1β, IL-6, and TNF-α at levels produced by vehicle tumors resulted in B) representative images of tumors with C) restored tumor size and D) weight. In organ culture supernatants, cytokine treatment increased the MK2i tumor production of E) IL-1β, F) IL-6, and G) TNF-α. Increases were seen in mRNA levels for H) IL-1β, I) IL-6, and J) TNF-α were also seen. N=10 *p < 0.05, **p<0.01, ***p < 0.005.

    Article Snippet: Tumor samples were labeled by immunohistochemistry for pMK2 Thr334 (Cell Signaling Technology, Danvers, MA).

    Techniques: Produced, Organ Culture