Breast cancer-specific mutations in CK1ε inhibit Wnt/β-catenin and activate the Wnt/Rac1/JNK and NFAT pathways to decrease cell adhesion and promote cell migration

Keyphrases

• Breast Cancer 100%
• JNK Pathway 100%
• Rac1 100%
• Catenin 100%
• Specific mutation 100%
• Casein Kinase 2 100%
• NFAT Pathway 100%
• Cell Adhesion 100%
• Cell Migration 100%
• Cancer-specific 100%
• Wnt Signaling Pathway 11%
• Phosphorylation 11%
• Point mutation 11%
• Autophosphorylation 11%
• Terminal Lobes 11%
• Mammalian Cells 5%
• Molecular Mechanism 5%
• Most Common Form 5%
• In Silico Modeling 5%
• E-cadherin Expression 5%
• Small GTPase 5%
• Cell-to-cell 5%
• Breast Cancer Cell Lines 5%
• Loss Function 5%
• Pharmacological Inhibitors 5%
• Breast Cancer Progression 5%
• DVL2 5%
• MCF-7 5%
• Positive Regulation 5%
• Cell Migration Assays 5%
• Cancer Types 5%
• Canonical Wnt Signaling 5%
• Through Effect 5%
• MCF-7 Cells 5%
• Intracellular Localization 5%
• Kinase Activity 5%
• Silico 5%
• Wnt Signaling Cascade 5%
• In Vivo Data 5%

Biochemistry, Genetics and Molecular Biology

• Cell Adhesion 100%
• Cell Migration 100%
• NFAT 100%
• Catenin 100%
• Casein Kinase 100%
• Casein Kinase 1 100%
• Wnt Signaling Pathway 16%
• N-Terminus 11%
• Autophosphorylation 11%
• Point Mutation 11%
• Mammalian Cell 5%
• Transcription 5%
• Small GTPase 5%
• Cancer Cell 5%
• Kinase 5%
• Phosphotransferase 5%
• Cadherin 5%