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erk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc erk
    BGB-15025 inhibits the cell cycle and the <t>MAPK/ERK</t> signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection <t>of</t> <t>cyclin</t> D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.
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    Images

    1) Product Images from "Hematopoietic progenitor kinase 1 inhibitor BGB-15025 induces apoptosis in acute myeloid leukemia cells through the cell cycle pathway and mitogen-activated protein kinase/extracellular signal-regulated kinase pathway signaling axis"

    Article Title: Hematopoietic progenitor kinase 1 inhibitor BGB-15025 induces apoptosis in acute myeloid leukemia cells through the cell cycle pathway and mitogen-activated protein kinase/extracellular signal-regulated kinase pathway signaling axis

    Journal: Anti-Cancer Drugs

    doi: 10.1097/CAD.0000000000001794

    BGB-15025 inhibits the cell cycle and the MAPK/ERK signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection of cyclin D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.
    Figure Legend Snippet: BGB-15025 inhibits the cell cycle and the MAPK/ERK signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection of cyclin D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.

    Techniques Used: Protein-Protein interactions, Control, Expressing, Quantitative RT-PCR, Western Blot, Derivative Assay, Knockdown, Real-time Polymerase Chain Reaction

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    Santa Cruz Biotechnology signal regulated kinase erk 1
    BGB-15025 inhibits the cell cycle and the <t>MAPK/ERK</t> signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection <t>of</t> <t>cyclin</t> D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.
    Signal Regulated Kinase Erk 1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    BGB-15025 inhibits the cell cycle and the MAPK/ERK signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection of cyclin D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.

    Journal: Anti-Cancer Drugs

    Article Title: Hematopoietic progenitor kinase 1 inhibitor BGB-15025 induces apoptosis in acute myeloid leukemia cells through the cell cycle pathway and mitogen-activated protein kinase/extracellular signal-regulated kinase pathway signaling axis

    doi: 10.1097/CAD.0000000000001794

    Figure Lengend Snippet: BGB-15025 inhibits the cell cycle and the MAPK/ERK signaling pathway in AML cells. (a) KEGG analysis revealed that differentially expressed genes were significantly enriched in relevant signaling pathways. (b) GSEA of differentially expressed genes in the treated group, compared with the control group, indicated a predominant enrichment in cell cycle-related pathways. (c) Two AML cell lines (KG1A and THP-1) were exposed to different concentrations of BGB-15025, and the expression levels of CCND1 , CDK4 , and P21 genes were quantified using qRT-PCR. (d) Various concentrations of BGB-15025 were administered to two AML cell lines (KG1A and THP-1), followed by the detection of cyclin D1, CDK4, and P21 protein expressions via Western blot analysis. (f) Different concentrations of BGB-15025 were administered to two AML cell lines, KG1A and THP-1. The expression levels of ERK, p-ERK, P38, and p-P38 proteins were assessed using Western blot analysis. Data presented are derived from at least three independent experiments. Statistical significance was determined as follows: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001 when compared with the control group. (e and g) The effect of HPK1 knockdown on the expression of the above-mentioned proteins was assessed in AML (THP-1) cells. AML, acute myeloid leukemia; GSEA, Gene Set Enrichment Analysis; HPK1, hematopoietic progenitor kinase 1; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK/ERK, mitogen-activated protein kinase/extracellular signal-regulated kinase; qRT-PCR, quantitative real-time PCR.

    Article Snippet: Membranes were subsequently incubated overnight at 4 °C with specific primary antibodies: β-actin (#4970; 1 : 1000), HPK1 (#46510; 1 : 1000), cyclin D1 (#55506; 1 : 1000), P21 (#2947; 1 : 1000), ERK (#4696; 1 : 1000), phosphorylated ERK (p-ERK, #4370; 1 : 1000), P38 MAPK (#8690; 1 : 1000), and phosphorylated P38 MAPK (p-P38, #9211; 1 : 1000) (all from Cell Signaling Technology, Danvers, Massachusetts, USA).

    Techniques: Protein-Protein interactions, Control, Expressing, Quantitative RT-PCR, Western Blot, Derivative Assay, Knockdown, Real-time Polymerase Chain Reaction