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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/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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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).

Article Title: Deficiency of smooth muscle cell ILF3 alleviates intimal hyperplasia via HMGB1 mRNA degradation-mediated regulation of the STAT3/DUSP16 axis.
Article Snippet: Intimal hyperplasia is a complicated pathophysiological phenomenon attributable to in-stent restenosis, and the underlying mechanism remains unclear.. Interleukin enhancer-binding factor 3 (ILF3), a double-stranded RNAbinding protein involved in regulating mRNA stability, has been recently demonstrated to assume a crucial role in cardiovascular disease; nevertheless, its impact on intimal hyperplasia remains unknown.. In current study, we used samples of human restenotic arteries and rodent models of intimal hyperplasia, we found that vascular smooth muscle cell (VSMC) ILF3 expression was markedly elevated in human restenotic arteries and murine ligated carotid arteries.

Derivative Assay:

Article Title: NR4A1 enhances MKP7 expression to diminish JNK activation induced by ROS or ER-stress in pancreatic β cells for surviving
Article Snippet: .. The antibodies used in the experiment were as follows: cleaved caspase-3 Antibody (9661) and rabbit anti-pJNK antibody (4668) were purchased from CST; mouse anti-GAPDH (10494-1-AP), rabbit anti-MKP2 antibody (10739-1-AP), and rabbit anti-MKP7 antibody (14237-1-AP) were derived from Proteintech Group (Wuhan, China); rabbit anti-NR4A1 antibody (ab13851 and DF7850) was purchased from Abcam and Affinity; mouse anti-β-Actin (BS6007M) and rabbit anti-tubulin α (BS1699) were purchased from Bioworld Technology. .. Data were expressed as the mean ± SD (standard deviation). t -test or analysis of variance (ANOVA) in GraphPad Prism 5.0.

Image Search Results

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

Fig. 5 FBXL18 targeted DUSP16 as a ubiquitination substrate. (A-B) The results of Co-IP and western blotting assays revealed the endogenous and exog enous 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: Fig. 5 FBXL18 targeted DUSP16 as a ubiquitination substrate. (A-B) The results of Co-IP and western blotting assays revealed the endogenous and exog enous 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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

Fig. 7 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: Fig. 7 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: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

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

Article Snippet: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

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

Article Snippet: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

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

Article Snippet: SiRNA specifically targeting DUSP16 or negative control siRNA (siNeg) were obtained from Sangon Biotech (Shanghai, China).

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

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