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C-Jun N-Terminal Kinase Inhibitor Favors Transforming Growth Factor-Β to Antagonize Hepatitis B Virus X Protein-Induced Cell Growth Promotion in Hepatocellular Carcinoma
Molecular Medicine Reports
Oncology
Genetics
Molecular Biology
Biochemistry
Cancer Research
Molecular Medicine
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Constitutive Activation of C-Jun N-Terminal Kinase by a Mutant Epidermal Growth Factor Receptor
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Growth Differentiation Factor 15 Is Induced by Hepatitis C Virus Infection and Regulates Hepatocellular Carcinoma-Related Genes
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Activation of the Hematopoietic Progenitor Kinase-1 (HPK1)-dependent, Stress-Activated C-Jun N-Terminal Kinase (JNK) Pathway by Transforming Growth Factor Β (TGF-β)-activated Kinase (TAK1), a Kinase Mediator of TGF Β Signal Transduction
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GqProtein-induced Apoptosis Is Mediated by AKT Kinase Inhibition That Leads to Protein Kinase C-Induced C-Jun N-Terminal Kinase Activation
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Platelet-Derived Growth Factor (PDGF) Receptor-Α Activates C-Jun NH2-terminal Kinase-1 and Antagonizes PDGF Receptor-Β-Induced Phenotypic Transformation
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