TPL2 enforces RAS-induced inflammatory signaling and is activated by point mutations

Keyphrases

• Inflammatory Pathways 100%
• Point mutation 100%
• TPL2 100%
• IRAK4 55%
• NF-B 44%
• MAP3K8 44%
• Pancreatic Ductal Adenocarcinoma 33%
• KRAS mutant 22%
• Mitogen-activated Protein Kinase 11%
• RNA Sequencing (RNA-seq) 11%
• Transcription Factor 11%
• Cell Growth 11%
• Therapeutic Target 11%
• Protein Degradation 11%
• Chemotherapy 11%
• KRAS mutation 11%
• Human Cells 11%
• Ablation 11%
• RNA-protein Complex 11%
• Cancer Cell Lines 11%
• Mutant Cells 11%
• K-ras 11%
• Murine Cells 11%
• Treatment Resistance 11%
• Chemotherapy-induced 11%
• Pro-survival 11%
• Site-directed mutation 11%
• Factor-driven 11%
• Genotoxic Stress 11%
• IL-1 Signaling 11%
• Pancreatic Duct Cells 11%
• Toll-like Receptor 9 (TLR9) 11%
• Curb 11%
• MAPK Activation 11%
• Reverse Phase Protein Array 11%
• Induced Transformations 11%

Biochemistry, Genetics and Molecular Biology

• Mitogen-Activated Protein Kinase 100%
• Point Mutation 100%
• IRAK4 100%
• KRAS 80%
• RNA Sequence 20%
• Cancer Cell 20%
• Cell Growth 20%
• Kinase 20%
• Phosphotransferase 20%
• Transcription Factors 20%
• Interleukin-1 20%
• Clinical Study 20%
• Protein Catabolism 20%
• Cell Mutant 20%
• Protein Microarray 20%
• TLR9 20%

Immunology and Microbiology

• Point Mutation 100%
• Transcription Factors 50%
• Interleukin-1 50%
• Cell Growth 50%
• RNA Sequence 50%
• Cell Mutant 50%
• Protein Degradation 50%
• TLR9 50%
• Cancer Cell Line 50%