MEK1 (dn) Adenovirus
Mitogen-activated protein kinases (MAPK), including ERK1/2, p38, and JNK1/2, are important regulators of cell function. The ERK MAPKs are most frequently activated by mitogenes, whereas the JNK and p38 MAPKs are strongly responsive to stress and inflammatory signals. The MAPKs are activated through multiple intracellular phosphorylation cascade events. The core unit includes MAPKKKs and MAPKKs. MEK1 and MEK2 are dual-specificity proteins kinases. MEKs activates ERK1 and ERK2 by phosphorylating both threonine and tyrosine residues at sites located within the activation loop of kinase subdomain VIII.
1165
Ad-CMV-MEK1(dn)
Ready-to-use MEK1 (dn) Adenovirus. 1165
Related Citations
- Insulin-like growth factor 1 attenuates antiestrogen- and antiprogestin-induced apoptosis in ER+ breast cancer cells by MEK1 regulation of the BH3-only pro-apoptotic protein Bim. Sudharsan Periyasamy-Thandavan, etc, (2012), Breast Cancer Research
- Inhibition of Multiple Protective Signaling Pathways and Ad. 5/3 Delivery Enhances mda-7/IL-24 Therapy of Malignant Glioma. Hossein A Hamed, (2010), Molecular Therapy
- 17-Allylamino-17-Demethoxygeldanamycin and MEK1/2 Inhibitors Kill GI Tumor Cells via Ca2+-Dependent Suppression of GRP78/BiP and Induction of Ceramide and Reactive Oxygen Species. Teneille Walker, (2010), Mol Cancer Ther
- Cisplatin Enhances Protein Kinase R-Like Endoplasmic Reticulum Kinase- and CD95-Dependent Melanoma Differentiation-Associated Gene-7/Interleukin-24¿Induced Killing in Ovarian Carcinoma Cells. Adly Yacoub, (2009), Molecular Pharmacology
- Bcl-2 Family Inhibitors Enhance Histone Deacetylase Inhibitor And Sorafenib Lethality Via Autophagy And Overcome Blockade Of The Extrinsic Pathway To Facilitate Killing. Martin, AP. etc, (2009), Mol Pharmacol
- Sorafenib And Vorinostat Kill Colon Cancer Cells By Cd95-Dependent And -Independent Mechanisms. Walker T, etc, (2009), Mol Pharmacol
- Erk1 And Erk2 Play Essential Roles In Osteoblast Differentiation And In Supporting Osteoclastogenesis. Matsushita T,, (2009), Molecular and Cellular Biology
- Mek1/2 Inhibitors And 17AAG Synergize To Kill Human Gi Tumor Cells In Vitro Via Suppression Of C-Flip-S Levels And Activation Of Cd95. Park MA, etc, (2009), Mol Cancer Ther
- Extracellular Signal-Regulated Kinase 1 (Erk1) And Erk2 Play Essential Roles In Osteoblast Differentiation And In Supporting Osteoclastogenesis. Matsushita, T, etc, (2009), Molecular and Cellular Biology
- PERK-dependent regulation of ceramide synthase 6 and thioredoxin play a key role in mda-7/IL-24-induced killing of primary human glioblastoma multiforme cells. Adly Yacoub, (2009), Cancer Research
- Sphingosine Kinases And Sphingosine-1-Phosphate Are Critical For Tgf{Beta}-Induced Erk1/2 Activation And Promotion Of Migration And Invasion Of Esophageal Cancer Cells. Miller, A., etc., (2008), Mol Cell Biol
- Mitogen-Activated Protein Kinase Kinase 1/2 Inhibitors And 17-Allylamino-17-Demethoxygeldanamycin Synergize To Kill Human Gastrointestinal Tumor Cells In Vitro Via Suppression Of C-Flip-S Levels And Activation Of Cd95. Park, M., etc., (2008), Molecular Cancer Therapeutics
- Regulation Of Gst-Mda-7 Toxicity In Human Glioblastoma Cells By Erbb1, Erk1/2, Pi3k, And Jnk1-3 Pathway Signaling. Yacoub, A., etc., (2008), Molecular Cancer Therapeutics
- Vorinostat And Sorafenib Increase Er Stress, Autophagy And Apoptosis Via Ceramide-Dependent Cd95 And Perk Activation. Park MA, etc, (2008), Cancer Biol Ther
- Osu-03012 Stimulates Pkr-Like Endoplasmic Reticulum-Dependent Increases In 70-Kda Heat Shock Protein Expression, Attenuating Its Lethal Actions In Transformed Cells. Park, M., etc., (2008), Mol Pharmacol
- Caspase-, cathepsin-, and PERK-dependent regulation of MDA-7/IL-24-induced cell killing in primary human glioma cells. Yacoub, A. etc, (2008), Molecular Cancer Therapeutics
- Vorinostat And Sorafenib Synergistically Kill Tumor Cells Via Flip Suppression And Cd95 Activation. Zhang, G., etc., (2008), Clinical Cancer Research
- Extrinsic Pathway- And Cathepsin-Dependent Induction Of Mitochondrial Dysfunction Are Essential For Synergistic Flavopiridol And Vorinostat Lethality In Breast Cancer Cells. Mitchell, C. etc, (2007), Molecular Cancer Therapeutics
- Osu-03012 Promotes Caspase-Independent But Perk-, Cathepsin B-, Bid-, And Aif-Dependent Killing Of Transformed Cells. Yacoub, A., (2006), Pharmacol
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About Storage Conditions
All our viral products should be kept at -80°C. At this temperature, the virus will remain stable for 6-12 months (and in some cases, up to 2 years). Once thawed, the product can be stored at 4°C for 2-3 weeks without significant loss of biological activity.
We recommend aliquoting your vectors into low protein binding tubes upon receipt. This helps avoid repeated freeze-thaw cycles, as well as prevent loss of virus. To maintain accurate titer, aliquot in at least 20ul per tube.