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mitogen activated protein kinase kinase mek inhibitor  (MedChemExpress)


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    MedChemExpress mitogen activated protein kinase kinase mek inhibitor
    Mitogen Activated Protein Kinase Kinase Mek Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 188 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mitogen+activated+protein+kinase+kinase+mek+inhibitor/Mirdametinib/pmc13116222-41-4-13
    Average 96 stars, based on 188 article reviews
    mitogen activated protein kinase kinase mek inhibitor - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    Functional Assay:

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
    Article Snippet: MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. Hepatic artery ligation (HAL) and orthotopic liver implantation A 100-μl cell suspension (MHCC-97/SVIL-shRNA, containing 5 × 106 cells) in PBS was subcutaneously injected into the flanks of male BALB/c nude mice (n = 5) at the age of 6 weeks. ..

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway
    Article Snippet: The RNAi targeting sequences and their corresponding target exons in the supervillin gene are shown in Additional file : Table S . MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. ..

    Expressing:

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
    Article Snippet: MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. Hepatic artery ligation (HAL) and orthotopic liver implantation A 100-μl cell suspension (MHCC-97/SVIL-shRNA, containing 5 × 106 cells) in PBS was subcutaneously injected into the flanks of male BALB/c nude mice (n = 5) at the age of 6 weeks. ..

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway
    Article Snippet: The RNAi targeting sequences and their corresponding target exons in the supervillin gene are shown in Additional file : Table S . MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. ..

    Ligation:

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
    Article Snippet: MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. Hepatic artery ligation (HAL) and orthotopic liver implantation A 100-μl cell suspension (MHCC-97/SVIL-shRNA, containing 5 × 106 cells) in PBS was subcutaneously injected into the flanks of male BALB/c nude mice (n = 5) at the age of 6 weeks. ..

    Suspension:

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
    Article Snippet: MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. Hepatic artery ligation (HAL) and orthotopic liver implantation A 100-μl cell suspension (MHCC-97/SVIL-shRNA, containing 5 × 106 cells) in PBS was subcutaneously injected into the flanks of male BALB/c nude mice (n = 5) at the age of 6 weeks. ..

    Injection:

    Article Title: Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.
    Article Snippet: MHCC-97H supervillin knockdown stable clones were constructed using pLVshRNA-EGFP (2A) Puro (Invivogen, Shanghai, China) lentiviral shRNA vector targeting supervillin (5′-AGGTGATGAAGCCAGATGA-3′). .. To determine the functional crosstalk between RhoA/ ROCK and ERK/p38 signaling, HCC cells were pretreated with the specific mitogen-activated protein kinase kinase (MEK) inhibitor (PD0325901, 10 μM; MedChemExpress, Monmouth Junction, NJ, USA), p38 MAPK inhibitor (SB239063, 10 μM; MedChemExpress), or ROCK inhibitor (Y27632 2HCl, 10 μM; MedChemExpress) for 1 h. To investigate the functional crosstalk between supervillin expression and HIF1α, we used the HIF inhibitor (2-Methoxyestradiol; 2-MeOE2, 10 μM; MedChemExpress) for 8 h. Hepatic artery ligation (HAL) and orthotopic liver implantation A 100-μl cell suspension (MHCC-97/SVIL-shRNA, containing 5 × 106 cells) in PBS was subcutaneously injected into the flanks of male BALB/c nude mice (n = 5) at the age of 6 weeks. ..



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    Fig. 4 The effect of AKR1C3, MEK, or AKT inhibition on colony formation of KYSE170R cells. KYSE170R cells were treated with the inhibitor of AKR1C3 (AKR1C3-IN-1, 20 μM), MEK <t>(PD98059,</t> 20 μM), AKT (MK-2206, 20 μM), or JNK (SP600125, 20 μM) for 24 h, followed by exposure to different doses of 6 MV X-rays (0, 2, 4, and 8 Gy). The irradiated cells were collected, seeded in 6-well plates at 500 (0 Gy group), 1000 (2 and 4 Gy groups), or 2000 (8 Gy group) cells/well, and cultured for 7–10 days. The numbers of colonies were counted. The surviving fraction was calculated. Representative images are shown. Magnification 100 ×. Data are expressed as the mean ± SD
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    Image Search Results


    Fig. 4 The effect of AKR1C3, MEK, or AKT inhibition on colony formation of KYSE170R cells. KYSE170R cells were treated with the inhibitor of AKR1C3 (AKR1C3-IN-1, 20 μM), MEK (PD98059, 20 μM), AKT (MK-2206, 20 μM), or JNK (SP600125, 20 μM) for 24 h, followed by exposure to different doses of 6 MV X-rays (0, 2, 4, and 8 Gy). The irradiated cells were collected, seeded in 6-well plates at 500 (0 Gy group), 1000 (2 and 4 Gy groups), or 2000 (8 Gy group) cells/well, and cultured for 7–10 days. The numbers of colonies were counted. The surviving fraction was calculated. Representative images are shown. Magnification 100 ×. Data are expressed as the mean ± SD

    Journal: BMC cancer

    Article Title: Aldo-keto reductase family 1 member C3 mediates radioresistance of esophageal cancer cells through suppressing MAPK and AKT signaling.

    doi: 10.1186/s12885-024-13012-z

    Figure Lengend Snippet: Fig. 4 The effect of AKR1C3, MEK, or AKT inhibition on colony formation of KYSE170R cells. KYSE170R cells were treated with the inhibitor of AKR1C3 (AKR1C3-IN-1, 20 μM), MEK (PD98059, 20 μM), AKT (MK-2206, 20 μM), or JNK (SP600125, 20 μM) for 24 h, followed by exposure to different doses of 6 MV X-rays (0, 2, 4, and 8 Gy). The irradiated cells were collected, seeded in 6-well plates at 500 (0 Gy group), 1000 (2 and 4 Gy groups), or 2000 (8 Gy group) cells/well, and cultured for 7–10 days. The numbers of colonies were counted. The surviving fraction was calculated. Representative images are shown. Magnification 100 ×. Data are expressed as the mean ± SD

    Article Snippet: To investigate the roles of MAPK and AKT signaling in AKR1C3-regulated radiosensitivity of KYSE170R cells, we treated KYSE170R cells with AKR1C3 inhibitor AKR1C3-IN-1 (20 μM; MedChemExpress, Monmouth Junction, NJ, USA), mitogen-activated protein kinase kinase (MEK) inhibitor PD98059 (20 μM; MedChemExpress), AKT inhibitor MK-2206 (20 μM; MedChemExpress), or JNK inhibitor SP600125 (20 μM; MedChemExpress) for 24 h, followed by exposure to different doses of 6 MV X-rays.

    Techniques: Inhibition, Irradiation, Cell Culture

    Fig. 5 The effect of MEK or AKT inhibition on colony formation of KYSE170R-shAKR1C3 cells. KYSE170R-shAKR1C3 cells were treated with the inhibitor of MEK (PD98059, 20 μM), AKT (MK-2206, 20 μM), or JNK (SP600125, 20 μM) for 24 h, followed by exposure to different doses of 6 MV X-rays (0, 2, 4, and 8 Gy). The irradiated cells were collected, seeded in 6-well plates at 500 (0 Gy group), 1000 (2 and 4 Gy groups), or 2000 (8 Gy group) cells/well, and cultured for 7–10 days. The numbers of colonies were counted. The surviving fraction was calculated. Representative images are shown. Magnification 100×. Data are expressed as the mean ± SD

    Journal: BMC cancer

    Article Title: Aldo-keto reductase family 1 member C3 mediates radioresistance of esophageal cancer cells through suppressing MAPK and AKT signaling.

    doi: 10.1186/s12885-024-13012-z

    Figure Lengend Snippet: Fig. 5 The effect of MEK or AKT inhibition on colony formation of KYSE170R-shAKR1C3 cells. KYSE170R-shAKR1C3 cells were treated with the inhibitor of MEK (PD98059, 20 μM), AKT (MK-2206, 20 μM), or JNK (SP600125, 20 μM) for 24 h, followed by exposure to different doses of 6 MV X-rays (0, 2, 4, and 8 Gy). The irradiated cells were collected, seeded in 6-well plates at 500 (0 Gy group), 1000 (2 and 4 Gy groups), or 2000 (8 Gy group) cells/well, and cultured for 7–10 days. The numbers of colonies were counted. The surviving fraction was calculated. Representative images are shown. Magnification 100×. Data are expressed as the mean ± SD

    Article Snippet: To investigate the roles of MAPK and AKT signaling in AKR1C3-regulated radiosensitivity of KYSE170R cells, we treated KYSE170R cells with AKR1C3 inhibitor AKR1C3-IN-1 (20 μM; MedChemExpress, Monmouth Junction, NJ, USA), mitogen-activated protein kinase kinase (MEK) inhibitor PD98059 (20 μM; MedChemExpress), AKT inhibitor MK-2206 (20 μM; MedChemExpress), or JNK inhibitor SP600125 (20 μM; MedChemExpress) for 24 h, followed by exposure to different doses of 6 MV X-rays.

    Techniques: Inhibition, Irradiation, Cell Culture

    Kinase inhibitors used in the study.

    Journal: Cells

    Article Title: Cyclophilin E (CypE) Functions as a Positive Regulator in Osteoblast Differentiation by Regulating the Transcriptional Activity of Runx2

    doi: 10.3390/cells12212549

    Figure Lengend Snippet: Kinase inhibitors used in the study.

    Article Snippet: Mitogen-activated protein kinase (MEK) inhibitor (U1026) , 662005 , Calbiochem (San Diego, CA, USA).

    Techniques: