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anti dusp16  (Proteintech)


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    Proteintech anti dusp16
    Anti Dusp16, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+dusp16/DUSP16+Antibody/pmc12145754-92-34-35
    Average 93 stars, based on 5 article reviews
    anti dusp16 - by Bioz Stars, 2026-10
    93/100 stars

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    Incubation:

    Article Title: Deregulated JNK signaling enhances apoptosis during hyperthermia.
    Article Snippet: To assay cell death or apoptosis, the cells were left untreated or heated at 43 °C for 60 min, and assayed 24 h later by staining with either trypan blue or using a Mitochondrial Transmembrane Potential Apoptosis Detection Kit (Abcam, Cambridge), respectively. .. The blots were then incubated at 1:1000 dilution overnight at 4 °C with one of the following antibodies: anti-ASK1 (Santa Cruz Biotechnology, Santa Cruz, CA), anti-phospho-ASK1(Gene Tex, Irvine, CA), anti-MLK3 (Abcam, Cambridge), anti-phospho-MLK3 (Gene Tex), anti-SEK1/MKK4 (Cell Signaling Technology, Beverly, MA), anti-phospho-SEK1 (Cell Signaling Technology), anti-JNK (Cell Signaling Technology), anti-phospho-JNK (Cell Signaling Technology), anti-DUSP10 (Santa Cruz Biotechnology), anti-DUSP16 (Proteintech, Rosemont, IL), anti-CDK2 (Santa Cruz Biotechnology), anti-GAPDH (MBL), anti-cleaved Caspase-3 (Proteintech), anti-HSP90 (Cell Signaling Technology), or anti-β-actin (Sigma). .. Equivalent amounts of total cell lysates were separated by SDS-PAGE and then transferred onto Immobilon PVDF membranes (Millipore, Bedford, MA).

    Article Title: JNK signaling dominance in hyperthermia
    Article Snippet: .. The blots were then incubated with one of the following antibodies: anti-JNK (Cell Signaling Technology, Beverly, MA), antiphospho-JNK (Cell Signaling Technology), anti-ERK1/2 (Proteintech, Rosemont, IL), antiphospho-ERK1/2 (Proteintech), anti-DUSP1 (Merck, Darmstadt), anti-DUSP4 (Proteintech), anti-DUSP6 (Proteintech), anti-DUSP16 (Proteintech), and anti-Glyceraldehyde 3-phosphate dehydrogenase (MBL, Tokyo). .. The resulting signals were detected on X-ray films (GE Healthcare, Buckinghamshire) using an enhanced chemiluminescence detection system (GE Healthcare).

    Article Title: JNK Signaling Dominance in Hyperthermia.
    Article Snippet: .. The blots were then incubated with one of the following antibodies: anti-JNK (Cell Signaling Technology, Beverly, MA), anti-phospho-JNK (Cell Signaling Technology), anti-ERK1/2 (Proteintech, Rosemont, IL), anti-phospho-ERK1/2 (Proteintech), anti-DUSP1 (Merck, Darmstadt), anti-DUSP4 (Proteintech), anti-DUSP6 (Proteintech), anti-DUSP16 (Proteintech), and anti-GAPDH (MBL, Tokyo). .. The resulting signals were detected on X-ray films (GE Healthcare, Buckinghamshire) using an enhanced chemiluminescence detection system (GE Healthcare).



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    FBXL18 targeted <t>DUSP16</t> as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous interaction of FBXL18 and DUSP16. ( C-D ) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. ( E-F ) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. ( G-H ) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. ( I-J ) DUSP16 protein half-life in EC cells of LV-Control and LV-FBXL18 groups were evaluated by CHX chase assay. ( K-L ) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. ( M-N ) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001
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    FBXL18 targeted <t>DUSP16</t> as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous interaction of FBXL18 and DUSP16. ( C-D ) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. ( E-F ) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. ( G-H ) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. ( I-J ) DUSP16 protein half-life in EC cells of LV-Control and LV-FBXL18 groups were evaluated by CHX chase assay. ( K-L ) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. ( M-N ) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001
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    FBXL18 targeted DUSP16 as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous interaction of FBXL18 and DUSP16. ( C-D ) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. ( E-F ) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. ( G-H ) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. ( I-J ) DUSP16 protein half-life in EC cells of LV-Control and LV-FBXL18 groups were evaluated by CHX chase assay. ( K-L ) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. ( M-N ) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001

    Journal: Cancer Cell International

    Article Title: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway

    doi: 10.1186/s12935-025-03808-9

    Figure Lengend Snippet: FBXL18 targeted DUSP16 as a ubiquitination substrate. ( A-B ) The results of Co-IP and western blotting assays revealed the endogenous and exogenous interaction of FBXL18 and DUSP16. ( C-D ) qRT-PCR analysis of DUSP16 mRNA levels after silencing or overexpressing FBXL18 in KLE and Ishikawa cells. ( E-F ) Western blot analysis of DUSP16 protein level in EC cells of shNC and shFBXL18 groups, and quantitative analysis. ( G-H ) Western blot analysis of DUSP16 protein level in EC cells after overexpressing FBXL18, and quantitative analysis. ( I-J ) DUSP16 protein half-life in EC cells of LV-Control and LV-FBXL18 groups were evaluated by CHX chase assay. ( K-L ) Comparison of DUSP16 protein half-life in EC cells stably knockdown of FBXL18 and control cells. ( M-N ) The ubiquitination status of endogenous DUSP16 after silencing or overexpressing FBXL18 in EC cells were determined by immunoprecipitation and western blotting. * P < 0.05; ** P < 0.01; *** P < 0.001

    Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

    Techniques: Ubiquitin Proteomics, Co-Immunoprecipitation Assay, Western Blot, Quantitative RT-PCR, Control, Comparison, Stable Transfection, Knockdown, Immunoprecipitation

    FBXL18 promoted EC cell malignancy via DUSP16-mediated activation of JNK signaling. ( A-C ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells of siNeg and siDUSP16 groups, and quantitative analysis. ( D-F ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells after overexpressing DUSP16, and quantitative analysis. ( G-I ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with LV-Ctrl + Vector, LV-Ctrl + DUSP16, LV-FBXL18 + Vector, LV-FBXL18 + DUSP16, and quantitative analysis. ( J-L ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with shNC + siNeg, shNC + siDUSP16, shFBXL18 + siNeg, shFBXL18 + siDUSP16, and quantitative analysis. * P < 0.05; ** P < 0.01; *** P < 0.001

    Journal: Cancer Cell International

    Article Title: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway

    doi: 10.1186/s12935-025-03808-9

    Figure Lengend Snippet: FBXL18 promoted EC cell malignancy via DUSP16-mediated activation of JNK signaling. ( A-C ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells of siNeg and siDUSP16 groups, and quantitative analysis. ( D-F ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells after overexpressing DUSP16, and quantitative analysis. ( G-I ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with LV-Ctrl + Vector, LV-Ctrl + DUSP16, LV-FBXL18 + Vector, LV-FBXL18 + DUSP16, and quantitative analysis. ( J-L ) Western blot analysis of DUSP16, JNK, p-JNK, c-JUN, and p-c-JUN levels in EC cells transfected with shNC + siNeg, shNC + siDUSP16, shFBXL18 + siNeg, shFBXL18 + siDUSP16, and quantitative analysis. * P < 0.05; ** P < 0.01; *** P < 0.001

    Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

    Techniques: Activation Assay, Western Blot, Transfection, Plasmid Preparation

    Silence of FBXL18 inhibited EC growth in vivo. ( A ) Tumor volumes of shNC and shFBXL18 groups were determined at different defined time points. ( B ) Representative images of xenograft tumors in shNC and shFBXL18 groups. ( C ) Tumor weights of shNC and shFBXL18 groups were measured at the end point. ( E ) Western blot analysis of FBXL18, DUSP16, JNK, p-JNK, c-JUN, p-c-JUN, and EMT-related markers in tumor samples of shNC and shFBXL18 groups, and quantitative analysis. ( F ) qRT-PCR analysis of FBXL18 and DUSP16 in tumor samples of shNC and shFBXL18 groups. * P < 0.05; ** P < 0.01; *** P < 0.001

    Journal: Cancer Cell International

    Article Title: FBXL18 promotes endometrial carcinoma progression via destabilizing DUSP16 and thus activating JNK signaling pathway

    doi: 10.1186/s12935-025-03808-9

    Figure Lengend Snippet: Silence of FBXL18 inhibited EC growth in vivo. ( A ) Tumor volumes of shNC and shFBXL18 groups were determined at different defined time points. ( B ) Representative images of xenograft tumors in shNC and shFBXL18 groups. ( C ) Tumor weights of shNC and shFBXL18 groups were measured at the end point. ( E ) Western blot analysis of FBXL18, DUSP16, JNK, p-JNK, c-JUN, p-c-JUN, and EMT-related markers in tumor samples of shNC and shFBXL18 groups, and quantitative analysis. ( F ) qRT-PCR analysis of FBXL18 and DUSP16 in tumor samples of shNC and shFBXL18 groups. * P < 0.05; ** P < 0.01; *** P < 0.001

    Article Snippet: The primary antibodies included FBXL18 (sc-100738, Santa Cruz, USA), DUSP16 (#5523, CST, USA), FLAG (#14793, CST, USA), HA (#3724, CST, USA).

    Techniques: In Vivo, Western Blot, Quantitative RT-PCR