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antielk4 antibody  (Proteintech)


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    Structured Review

    Proteintech antielk4 antibody
    Antielk4 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/elk4/ELK4+Antibody/pm40205485-163-17-21
    Average 93 stars, based on 7 article reviews
    antielk4 antibody - by Bioz Stars, 2026-09
    93/100 stars

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    Related Articles

    Incubation:

    Article Title: Exosomes from Microvascular Endothelial Cells under Mechanical Unloading Inhibit Osteogenic Differentiation via miR-92b-3p/ELK4 Axis
    Article Snippet: Protein samples supplemented with loading buffer in equal proportions were electrophoresed on NuPAGETM Bis-Tris Protein Gels (Invitrogen, Waltham, MA, USA) and then transferred onto polyvinylidene fluoride (PVDF) membranes. .. After incubation with 5% skim milk (5% w / v ) for 2 h at room temperature, the membranes were co-incubated overnight at 4 °C with the following primary antibodies specific for GAPDH (1:1000; Cell Signaling Technology, USA), Runx2 (1:1000; Cell Signaling Technology, Danvers, MA, USA), Osx (1:1000; Abcam, Cambridge, UK), Ocn (1:2000; Abcam, UK), ELK4 (1:1000; Proteintech, Rosemont, IL, USA), GM130 (1:1000; Proteintech, USA), CD9 (1:1000; Proteintech, USA), and TSG101 (1:1000; Proteintech, USA). ..

    Article Title: Exosomes from Microvascular Endothelial Cells under Mechanical Unloading Inhibit Osteogenic Differentiation via miR-92b-3p/ELK4 Axis.
    Article Snippet: Protein samples supplemented with loading buffer in equal proportions were electrophoresed on NuPAGETM Bis-Tris Protein Gels (Invitrogen, Waltham, MA, USA) and then transferred onto polyvinylidene fluoride (PVDF) membranes. .. After incubation with 5% skim milk (5% w/v) for 2 h at room temperature, the membranes were co-incubated overnight at 4 ◦C with the following primary antibodies specific for GAPDH (1:1000; Cell Signaling Technology, USA), Runx2 (1:1000; Cell Signaling Technology, Danvers, MA, USA), Osx (1:1000; Abcam, Cambridge, UK), Ocn (1:2000; Abcam, UK), ELK4 (1:1000; Proteintech, Rosemont, IL, USA), GM130 (1:1000; Proteintech, USA), CD9 (1:1000; Proteintech, USA), and TSG101 (1:1000; Proteintech, USA). ..

    other:

    Article Title: tRNA-Derived Fragment tRF-Glu-TTC-027 Regulates the Progression of Gastric Carcinoma via MAPK Signaling Pathway
    Article Snippet: ELK4 , proteintech , 14666-1-AP , Rabbit , 1: 1000.



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    Identification of transcription factors regulating HOMER3 expression in glioma. ( A ) Prediction of transcription factor binding sites in the HOMER3 promoter using JASPAR, highlighting <t>ELK4,</t> SP1, and CREB1 as potential regulators. ( B ) Association of expression levels of SP1, CREB1, and ELK4 with the overall survival of glioma patients from TCGA datasets. ( C ) Expression patterns of SP1 and ELK4 in LGG and GBM tissues compared to normal tissues. ( D ) ELK4 binding site predictions on the HOMER3 promoter illustrated. ( E ) Chromatin immunoprecipitation (ChIP) analysis confirming ELK4 binding to the HOMER3 promoter. ( F ) Luciferase reporter assays demonstrating increased luciferase activity in the presence of wild-type ELK4 binding sites in U251 and U87 glioma cells. ( G ) Elevated expression levels of ELK4 in glioma cell lines compared to normal cells as assessed by RT-PCR and western blot analysis. ( H ) Knockdown of ELK4 via shRNAs, which was confirmed by RT-PCR and western bot. ( I and J ) The effect of ELK4 knockdown on glioma cell proliferation assessed by CCK-8 and clonogenic assays. ( K and L ) In vivo analysis of ELK4 knockdown effects on tumor growth. Each group contained n = 6 mice, and the experiment was repeated three times independently. ( M ) Western blot for the expression of CDK4 and CDK6 after ELK4 knockdown. ( N ) The effects of ELK4 knockdown on the migration and invasion of U251 and U87 cells. ( O ) The effects of ELK4 knockdown on the expression of EMT-related proteins by western blot. All experiments were performed in three independent biological replicates ( n = 3) to ensure the reproducibility and reliability of the results
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    Novus Biologicals novus nbp1 87092 hsp70 mouse
    Identification of transcription factors regulating HOMER3 expression in glioma. ( A ) Prediction of transcription factor binding sites in the HOMER3 promoter using JASPAR, highlighting <t>ELK4,</t> SP1, and CREB1 as potential regulators. ( B ) Association of expression levels of SP1, CREB1, and ELK4 with the overall survival of glioma patients from TCGA datasets. ( C ) Expression patterns of SP1 and ELK4 in LGG and GBM tissues compared to normal tissues. ( D ) ELK4 binding site predictions on the HOMER3 promoter illustrated. ( E ) Chromatin immunoprecipitation (ChIP) analysis confirming ELK4 binding to the HOMER3 promoter. ( F ) Luciferase reporter assays demonstrating increased luciferase activity in the presence of wild-type ELK4 binding sites in U251 and U87 glioma cells. ( G ) Elevated expression levels of ELK4 in glioma cell lines compared to normal cells as assessed by RT-PCR and western blot analysis. ( H ) Knockdown of ELK4 via shRNAs, which was confirmed by RT-PCR and western bot. ( I and J ) The effect of ELK4 knockdown on glioma cell proliferation assessed by CCK-8 and clonogenic assays. ( K and L ) In vivo analysis of ELK4 knockdown effects on tumor growth. Each group contained n = 6 mice, and the experiment was repeated three times independently. ( M ) Western blot for the expression of CDK4 and CDK6 after ELK4 knockdown. ( N ) The effects of ELK4 knockdown on the migration and invasion of U251 and U87 cells. ( O ) The effects of ELK4 knockdown on the expression of EMT-related proteins by western blot. All experiments were performed in three independent biological replicates ( n = 3) to ensure the reproducibility and reliability of the results
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    Santa Cruz Biotechnology anti elk4
    Identification of transcription factors regulating HOMER3 expression in glioma. ( A ) Prediction of transcription factor binding sites in the HOMER3 promoter using JASPAR, highlighting <t>ELK4,</t> SP1, and CREB1 as potential regulators. ( B ) Association of expression levels of SP1, CREB1, and ELK4 with the overall survival of glioma patients from TCGA datasets. ( C ) Expression patterns of SP1 and ELK4 in LGG and GBM tissues compared to normal tissues. ( D ) ELK4 binding site predictions on the HOMER3 promoter illustrated. ( E ) Chromatin immunoprecipitation (ChIP) analysis confirming ELK4 binding to the HOMER3 promoter. ( F ) Luciferase reporter assays demonstrating increased luciferase activity in the presence of wild-type ELK4 binding sites in U251 and U87 glioma cells. ( G ) Elevated expression levels of ELK4 in glioma cell lines compared to normal cells as assessed by RT-PCR and western blot analysis. ( H ) Knockdown of ELK4 via shRNAs, which was confirmed by RT-PCR and western bot. ( I and J ) The effect of ELK4 knockdown on glioma cell proliferation assessed by CCK-8 and clonogenic assays. ( K and L ) In vivo analysis of ELK4 knockdown effects on tumor growth. Each group contained n = 6 mice, and the experiment was repeated three times independently. ( M ) Western blot for the expression of CDK4 and CDK6 after ELK4 knockdown. ( N ) The effects of ELK4 knockdown on the migration and invasion of U251 and U87 cells. ( O ) The effects of ELK4 knockdown on the expression of EMT-related proteins by western blot. All experiments were performed in three independent biological replicates ( n = 3) to ensure the reproducibility and reliability of the results
    Anti Elk4, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    Identification of transcription factors regulating HOMER3 expression in glioma. ( A ) Prediction of transcription factor binding sites in the HOMER3 promoter using JASPAR, highlighting ELK4, SP1, and CREB1 as potential regulators. ( B ) Association of expression levels of SP1, CREB1, and ELK4 with the overall survival of glioma patients from TCGA datasets. ( C ) Expression patterns of SP1 and ELK4 in LGG and GBM tissues compared to normal tissues. ( D ) ELK4 binding site predictions on the HOMER3 promoter illustrated. ( E ) Chromatin immunoprecipitation (ChIP) analysis confirming ELK4 binding to the HOMER3 promoter. ( F ) Luciferase reporter assays demonstrating increased luciferase activity in the presence of wild-type ELK4 binding sites in U251 and U87 glioma cells. ( G ) Elevated expression levels of ELK4 in glioma cell lines compared to normal cells as assessed by RT-PCR and western blot analysis. ( H ) Knockdown of ELK4 via shRNAs, which was confirmed by RT-PCR and western bot. ( I and J ) The effect of ELK4 knockdown on glioma cell proliferation assessed by CCK-8 and clonogenic assays. ( K and L ) In vivo analysis of ELK4 knockdown effects on tumor growth. Each group contained n = 6 mice, and the experiment was repeated three times independently. ( M ) Western blot for the expression of CDK4 and CDK6 after ELK4 knockdown. ( N ) The effects of ELK4 knockdown on the migration and invasion of U251 and U87 cells. ( O ) The effects of ELK4 knockdown on the expression of EMT-related proteins by western blot. All experiments were performed in three independent biological replicates ( n = 3) to ensure the reproducibility and reliability of the results

    Journal: Biology Direct

    Article Title: ELK4 induced upregulation of HOMER3 promotes the proliferation and metastasis in glioma via Wnt/β-catenin/EMT signaling pathway

    doi: 10.1186/s13062-025-00643-w

    Figure Lengend Snippet: Identification of transcription factors regulating HOMER3 expression in glioma. ( A ) Prediction of transcription factor binding sites in the HOMER3 promoter using JASPAR, highlighting ELK4, SP1, and CREB1 as potential regulators. ( B ) Association of expression levels of SP1, CREB1, and ELK4 with the overall survival of glioma patients from TCGA datasets. ( C ) Expression patterns of SP1 and ELK4 in LGG and GBM tissues compared to normal tissues. ( D ) ELK4 binding site predictions on the HOMER3 promoter illustrated. ( E ) Chromatin immunoprecipitation (ChIP) analysis confirming ELK4 binding to the HOMER3 promoter. ( F ) Luciferase reporter assays demonstrating increased luciferase activity in the presence of wild-type ELK4 binding sites in U251 and U87 glioma cells. ( G ) Elevated expression levels of ELK4 in glioma cell lines compared to normal cells as assessed by RT-PCR and western blot analysis. ( H ) Knockdown of ELK4 via shRNAs, which was confirmed by RT-PCR and western bot. ( I and J ) The effect of ELK4 knockdown on glioma cell proliferation assessed by CCK-8 and clonogenic assays. ( K and L ) In vivo analysis of ELK4 knockdown effects on tumor growth. Each group contained n = 6 mice, and the experiment was repeated three times independently. ( M ) Western blot for the expression of CDK4 and CDK6 after ELK4 knockdown. ( N ) The effects of ELK4 knockdown on the migration and invasion of U251 and U87 cells. ( O ) The effects of ELK4 knockdown on the expression of EMT-related proteins by western blot. All experiments were performed in three independent biological replicates ( n = 3) to ensure the reproducibility and reliability of the results

    Article Snippet: The following step was to extract the DNA fragments linked to ELK4 from the lysate using an anti-ELK4 antibody(Cat no: 14666-1-AP, Proteintech, Wuhan, China).

    Techniques: Expressing, Binding Assay, Chromatin Immunoprecipitation, Luciferase, Activity Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot, Knockdown, CCK-8 Assay, In Vivo, Migration