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met kinase inhibitor pha-665752  (Promega)

 
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    Promega met kinase inhibitor pha-665752
    Met Kinase Inhibitor Pha 665752, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/met+kinase+inhibitor+pha-665752/pha+665752/pmc05355264-206-1-8
    Average 90 stars, based on 1 article reviews
    met kinase inhibitor pha-665752 - by Bioz Stars, 2026-11
    90/100 stars

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    Related Articles

    other:

    Article Title: MET receptor variant R970C favors calpain-dependent generation of a fragment promoting epithelial cell scattering
    Article Snippet: The MET kinase inhibitor PHA-665752 was purchased from Promega (Madison, WI, USA).

    Article Title: PEA3 transcription factors are downstream effectors of Met signaling involved in migration and invasiveness of Met‐addicted tumor cells
    Article Snippet: The Met kinase inhibitor PHA‐665752 and MEK inhibitor U0126 were purchased from Promega (Madison, WI, USA), the PI3K inhibitor LY294002 from BioMol (Germany), Anisomycin, DMSO, Hoechst‐33258 dye and mitomycin‐c were obtained from Sigma (St Louis, MO, USA), DilC12 fluorescent dye was purchased from BD and Gefitinib from Santa cruz.



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    Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor <t>PHA665752</t> (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).
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    Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor <t>PHA665752</t> (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).
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    Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor <t>PHA665752</t> (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).
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    MV‐DN30 overcomes resistance induced by small kinase inhibitors and synergizes with MET <t>TKIs.</t> (A, B) Sensitivity to MV‐DN30 treatment of (A) cells resistant to PHA 50 nM (EBC1 RPHA 50) and (B) GTL16 cells resistant to PHA 150 nM ...
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    Image Search Results


    Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor PHA665752 (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).

    Journal: Scientific Reports

    Article Title: Proteomic analysis reveals a protective role of specific macrophage subsets in liver repair

    doi: 10.1038/s41598-019-39007-6

    Figure Lengend Snippet: Ly6C lo CX 3 CR1 hi macrophages directly accelerate hepatocyte proliferation in vitro . ( A ) Schematic of the experimental design. Normal hepatocytes (HCs) were co-cultured with the CM from 24 h Ly6C hi CX 3 CR1 lo macrophages or 72 h Ly6C lo CX 3 CR1 hi macrophages. ( B ) Representative images of hepatocytes pulsed with EdU and the quantification of hepatocyte proliferation are shown. Scale bar, 50 μm. ( C ) Differential expression of the indicated genes measured by qPCR in 24 h Ly6C hi CX 3 CR1 lo macrophages and 72 h Ly6C lo CX 3 CR1 hi macrophages, presented relative to Gapdh . ( D ) Hepatocytes were co-cultured with the CM from 72 h Ly6C lo CX 3 CR1 hi macrophages or supplemented with the c-Met kinase inhibitor PHA665752 (2.5 μM). Representative images of hepatocytes pulsed with EdU (left panel) and the quantification of hepatocyte proliferation (right panel) are shown. Scale bar, 50 μm. The data shown are representative of at least two independent experiments (n = 3/group). The results represent means ± SEM (*p < 0.05, **p < 0.01, ***p < 0.001).

    Article Snippet: Hepatocytes were treated with macrophage-derived CM or HGF (50 ng/ml, Peprotech) for 12 h, followed by EdU (5-ethynyl-2′-deoxyuridine, 20 μM) pulsing for an additional 36 h. In another series of experiments, isolated hepatocytes were treated with Ly6C lo CX 3 CR1 hi macrophage-derived CM supplemented with or without the c-Met kinase inhibitor PHA665752 (2.5 μM, R&D systems).

    Techniques: In Vitro, Cell Culture, Quantitative Proteomics

    MV‐DN30 overcomes resistance induced by small kinase inhibitors and synergizes with MET TKIs. (A, B) Sensitivity to MV‐DN30 treatment of (A) cells resistant to PHA 50 nM (EBC1 RPHA 50) and (B) GTL16 cells resistant to PHA 150 nM ...

    Journal: Molecular Oncology

    Article Title: Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence

    doi: 10.1016/j.molonc.2014.06.010

    Figure Lengend Snippet: MV‐DN30 overcomes resistance induced by small kinase inhibitors and synergizes with MET TKIs. (A, B) Sensitivity to MV‐DN30 treatment of (A) cells resistant to PHA 50 nM (EBC1 RPHA 50) and (B) GTL16 cells resistant to PHA 150 nM ...

    Article Snippet: We used the following small‐molecules: the ATP‐competitive MET Tyrosine Kinase Inhibitors PHA‐665752 (Tocris Bioscience) and JNJ‐38877605 (Johnson & Johnson) and the p38 MAP kinase inhibitor SB203580 (Merck).

    Techniques: