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phosphorylated erk p erk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated erk p erk
    KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, <t>phosphorylated</t> Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).
    Phosphorylated Erk P Erk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 16851 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phosphorylated+erk+p+erk/Phospho-p44%2F42+MAPK+(Erk1%2F2)+(Thr202%2FTyr204)+Antibody/pmc13007551-66-63-67
    Average 99 stars, based on 16851 article reviews
    phosphorylated erk p erk - by Bioz Stars, 2026-11
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    Images

    1) Product Images from "Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation"

    Article Title: Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation

    Journal: ImmunoTargets and Therapy

    doi: 10.2147/ITT.S563951

    KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, phosphorylated Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).
    Figure Legend Snippet: KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, phosphorylated Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

    Techniques Used: Activation Assay, Recombinant, Western Blot, Quantitation Assay

    Related Articles

    Western Blot:

    Article Title: Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation
    Article Snippet: Differential ImmunoTargets and Therapy 2026:15 https://doi.org/10.2147/ITT.S563951 3 Powered by TCPDF (www.tcpdf.org) transcriptomic gene expression profiling and data analysis were conducted to identify genes regulated by CHI3L1 and KSM using Illumina’s next-generation sequencing, which detects coding and long non-coding RNAs (Standard RNA-Seq Service provided by Genewiz/Azenta Life Science, Waltham, MA). .. Western Blotting (Immunoblotting) Protein lysates (25 μg) from lung tissues or cells were subjected to SDS-PAGE, transferred to membranes, and immunoblotted with primary antibodies against CD163 (#PA5-109327, Thermo Fisher Scientific), CD206 (E6T5J, #24595S, Cell Signaling Technology), phosphorylated AKT (p-Akt) (193H12, #4058S, Cell Signaling Technology), and total Akt (11E7, #4685S, Cell Signaling Technology), phosphorylated EGFR (Tyr1068) (p-EGFR) (#44-788G, Thermo Fisher Scientific), EGFR (D38B1, #4267S, Cell Signaling Technology), phosphorylated Erk (p-Erk) (#9101S, Cell Signaling Technology), total Erk (#9102S, Cell Signaling Technology), phosphorylated STAT3 (Tyr705) (p-STAT3) (D3A7, #9145, Cell Signaling Technology), total STAT3 (79D7, #4904, Cell Signaling Technology) and b-actin (C4, #sc47778 HRP, Santa Cruz Biotechnology). .. HRP-conjugated anti-rabbit IgG secondary antibody (#7074S, Cell Signaling Technology) was used for detection.

    Incubation:

    Article Title: Neuroprotective effects of traditional Chinese medicine Naofucong on diabetic cognitive impairment: Mechanisms involving insulin-degrading enzyme-mediated degradation of Amyloid-β and inhibition of ERK/JNK/p38 MAPK signaling pathway.
    Article Snippet: Postdeparaffinization, the sections underwent antigen retrieval using TrisEDTA Antigen Retrieval Solution (Beyotime, P0084), followed by blocking with a 5% bovine serum albumin (BSA) (Solarbio, SW3015) solution to avoid non-specific binding. .. The tissue sections were incubated with specific primary antibodies at 4◦C overnight, including: IDE (1:200, Bioss, bs-0018M), amyloid precursor protein (APP) (1:200, Abcam, ab126732), phosphorylated Tau (p-Tau) (1:50, Abcam, ab92676), phosphorylated ERK (p-ERK) (1:100, Cell Signaling Technology, 89967SF), ERK (1:250, Abcam, ab184699), phosphorylated JNK (p-JNK) (1:200, Cell Signaling Technology, 9255s), JNK (1:1000, Abcam, ab208035), phosphorylated p38 (p-p38) (1:400, Cell Signaling Technology, 9216S), p38 (1:250, Abcam, ab32142). ..

    Article Title: Resveratrol combats Salmonella infection via liberating vacuole-enclosed bacteria for enhanced autophagic clearance and blocking HMGA2-mediated G2/M arrest.
    Article Snippet: The escalating crisis of antimicrobial resistance necessitates a paradigm shift toward host-directed therapies (HDTs) that circumvent pathogen evasion strategies.. Here we show that the natural polyphenol resveratrol clears intracellular Salmonella typhimurium (S. typhimurium) by orchestrating a multipronged strategy involving Salmonella-containing vacuole (SCV) disruption via ERK1/2 inhibition to liberate bacteria for enhanced autophagic clearance, concurrently reversing pathogen-induced G2/M cell cycle arrest.. We identify High Mobility Group ATHook 2 (HMGA2) as a critical, previously unrecognized host dependency factor essential for Salmonella-driven cell cycle manipulation, which resveratrol targets to restrict bacterial replication.



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    GA effects <t>on</t> <t>ERK1/2</t> phosphorylation in invasive ductal carcinoma-derived KAIMRC1 stem-like cells. Representative western blot analyses showed p-ERK1/2 in KAIMRC1 stem-like cells treated with 100 µg/ml GA for (A) 30 to 120 min and with (B) 50–100 µg/ml GA or unglycated BSA for 90 min of incubation. Bar graphs show the relative expression level of p-ERK1/2 normalized to total ERK1/2. GAPDH served as the loading control. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to the untreated control is indicated as *P < 0.05 and **P < 0.01. C, control; GA, glycated albumin; p-ERK1/2, phosphorylated-ERK1/2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.
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    KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, <t>phosphorylated</t> Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).
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    Image Search Results


    GA effects on ERK1/2 phosphorylation in invasive ductal carcinoma-derived KAIMRC1 stem-like cells. Representative western blot analyses showed p-ERK1/2 in KAIMRC1 stem-like cells treated with 100 µg/ml GA for (A) 30 to 120 min and with (B) 50–100 µg/ml GA or unglycated BSA for 90 min of incubation. Bar graphs show the relative expression level of p-ERK1/2 normalized to total ERK1/2. GAPDH served as the loading control. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to the untreated control is indicated as *P < 0.05 and **P < 0.01. C, control; GA, glycated albumin; p-ERK1/2, phosphorylated-ERK1/2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Journal: Oncology Letters

    Article Title: Methylglyoxal-derived glycated albumin enhances the stemness potential of invasive ductal carcinoma-derived breast cancer stem-like cell line KAIMRC1

    doi: 10.3892/ol.2026.15541

    Figure Lengend Snippet: GA effects on ERK1/2 phosphorylation in invasive ductal carcinoma-derived KAIMRC1 stem-like cells. Representative western blot analyses showed p-ERK1/2 in KAIMRC1 stem-like cells treated with 100 µg/ml GA for (A) 30 to 120 min and with (B) 50–100 µg/ml GA or unglycated BSA for 90 min of incubation. Bar graphs show the relative expression level of p-ERK1/2 normalized to total ERK1/2. GAPDH served as the loading control. Data are presented as the mean ± SD from three independent experiments. Statistical significance relative to the untreated control is indicated as *P < 0.05 and **P < 0.01. C, control; GA, glycated albumin; p-ERK1/2, phosphorylated-ERK1/2; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.

    Article Snippet: Mouse primary monoclonal antibodies directed against extracellular signal-regulated kinase (ERK)1 (clone G-8; cat. no. sc-271269), phosphorylated-ERK1/2 (p-ERK1/2; clone E-4; Tyr204 of ERK1; cat. no. sc-7383), OCT3/4 (clone A-9; cat. no. sc-365509) and RAGE (clone E-1; cat. no. sc-74473) were obtained from Santa Cruz Biotechnology, Inc.

    Techniques: Phospho-proteomics, Derivative Assay, Western Blot, Incubation, Expressing, Control

    KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, phosphorylated Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

    Journal: ImmunoTargets and Therapy

    Article Title: Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation

    doi: 10.2147/ITT.S563951

    Figure Lengend Snippet: KSM inhibits CHI3L1-stimulated Erk and Akt activation and the antiapoptotic effect of CHI3L1 in macrophages. ( A ) AMJ-C11 mouse lung macrophages were stimulated with recombinant (r) CHI3L1 overnight, and the activation of Erk and Akt was detected by Western blot evaluations. pErk, phosphorylated Erk; T-Erk, total Erk; pAkt, phosphorylated Akt, T-Akt, total Akt. Right panel, densitometric quantitation on the blots of pErk and pAkt. ( B ) After exposure of AMJ-C11 cells with H 2 O 2 (1 mM, 24 hours) with and without rCHI3L1 and KSM treatment, cellular apoptosis (% of Annexin V+ cells) was measured by FACS evaluations. ( A and B ) are representatives of 3 independent experiments. Right panel, the values of Annexin 5 (+) cells (%) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

    Article Snippet: Protein lysates (25 μg) from lung tissues or cells were subjected to SDS-PAGE, transferred to membranes, and immunoblotted with primary antibodies against CD163 (#PA5-109327, Thermo Fisher Scientific), CD206 (E6T5J, #24595S, Cell Signaling Technology), phosphorylated AKT (p-Akt) (193H12, #4058S, Cell Signaling Technology), and total Akt (11E7, #4685S, Cell Signaling Technology), phosphorylated EGFR (Tyr1068) (p-EGFR) (#44-788G, Thermo Fisher Scientific), EGFR (D38B1, #4267S, Cell Signaling Technology), phosphorylated Erk (p-Erk) (#9101S, Cell Signaling Technology), total Erk (#9102S, Cell Signaling Technology), phosphorylated STAT3 (Tyr705) (p-STAT3) (D3A7, #9145, Cell Signaling Technology), total STAT3 (79D7, #4904, Cell Signaling Technology) and b-actin (C4, #sc-47778 HRP, Santa Cruz Biotechnology).

    Techniques: Activation Assay, Recombinant, Western Blot, Quantitation Assay