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1. Full Text RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth
by Alvarado, Ryan and Yen, Ivana and Stokoe, David and Liu, Bonnie and Aliagas, Ignacio and Ludlam, Mary J. C and Morales, Tony and Jaiswal, Bijay S and Brandhuber, Barbara J and Gloor, Susan L and Hoeflich, Klaus P and Malek, Shiva and Vigers, Guy and Belvin, Marcia and Hatzivassiliou, Georgia and Anderson, Daniel J and Sideris, Steve and Seshagiri, Somasekar and Song, Kyung and Friedman, Lori S and Koeppen, Hartmut
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | C-RAF | HETERODIMERIZATION | B-RAF | PROTEIN-KINASE KINASE | CANCER | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Index Medicus | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
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2. Full Text The Hippo effector YAP promotes resistance to RAF- and MEK-targeted cancer therapies
by Lin, Luping and Sabnis, Amit J and Chan, Elton and Olivas, Victor and Cade, Lindsay and Pazarentzos, Evangelos and Asthana, Saurabh and Neel, Dana and Yan, Jenny Jiacheng and Lu, Xinyuan and Pham, Luu and Wang, Mingxue M and Karachaliou, Niki and Cao, Maria Gonzalez and Manzano, Jose Luis and Ramirez, Jose Luis and Torres, Jose Miguel Sanchez and Buttitta, Fiamma and Rudin, Charles M and Collisson, Eric A and Algazi, Alain and Robinson, Eric and Osman, Iman and Muñoz-Couselo, Eva and Cortes, Javier and Frederick, Dennie T and Cooper, Zachary A and Mcmahon, Martin and Marchetti, Antonio and Rosell, Rafael and Flaherty, Keith T and Wargo, Jennifer A and Bivona, Trever G
Nature Genetics, ISSN 1061-4036, 02/2015, Volume 47, Issue 3, pp. 250 - 256
Resistance to RAF-and MEK-targeted therapy is a major clinical challenge(1-4). RAF and MEK inhibitors are initially but only transiently effective in some but... 
COLON-CANCER | SURVIVAL | LUNG | ACTIVATION | INHIBITION | MELANOMA | SIGNALING PATHWAY | TRANSCRIPTION | GENETICS & HEREDITY | BRAF | KRAS | Humans | Molecular Targeted Therapy | Phosphoproteins - metabolism | Gene Knockdown Techniques | Heterografts | MAP Kinase Signaling System - genetics | HEK293 Cells | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins B-raf - metabolism | MAP Kinase Kinase Kinases - genetics | Protein-Serine-Threonine Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Phosphoproteins - genetics | Mice, SCID | HT29 Cells | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Mice, Inbred NOD | Biomarkers, Tumor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Genes, ras | Antimitotic agents | Gene mutations | Genetic aspects | Research | Antineoplastic agents | Drug resistance | Health aspects | Thyroid cancer | Lung cancer | Colorectal cancer | Melanoma | Kinases | Charitable foundations | Cancer therapies | Design of experiments | Tumors | Index Medicus
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3. Full Text Smyd3 links lysine methylation of map3k2 to ras-driven cancer
by Mazur, P.K and Reynoird, N and Khatri, P and Jansen, P. W and Wilkinson, A.W and Liu, S and Barbash, O and Aller, G.S. Van and Huddleston, M and Dhanak, D and Tummino, P.J and Kruger, R.G and Garcia, B.A and Butte, A.J and Vermeulen, M and Sage, J and Gozani, O
Nature, ISSN 0028-0836, 2014, Volume 510, Issue 7504, pp. 283 - 287
Deregulation of lysine methylation signalling has emerged as a common aetiological factor in cancer pathogenesis, with inhibitors of several histone lysine... 
LUNG-CANCER | ACTIVATION | PROTEIN | K-RAS | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | KINASE | PANCREATIC INTRAEPITHELIAL NEOPLASIA | GROWTH-FACTOR | HISTONE METHYLTRANSFERASE | PROGRESSION | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Adenocarcinoma of Lung | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Oncogene Protein p21(ras) - metabolism | MAP Kinase Kinase Kinases - chemistry | Adenocarcinoma - metabolism | Cell Transformation, Neoplastic - genetics | MAP Kinase Kinase Kinase 2 - chemistry | Adenocarcinoma - genetics | Lysine - metabolism | Disease Models, Animal | Lung Neoplasms - genetics | MAP Kinase Kinase Kinase 2 - metabolism | Lung Neoplasms - enzymology | Protein Phosphatase 2 - antagonists & inhibitors | Signal Transduction | Pancreatic Neoplasms - pathology | Adenocarcinoma - enzymology | Pancreatic Neoplasms - enzymology | Pancreatic Neoplasms - genetics | MAP Kinase Kinase Kinases - metabolism | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins A-raf - metabolism | Animals | Histone-Lysine N-Methyltransferase - metabolism | Protein Phosphatase 2 - metabolism | Cell Line, Tumor | Mice | Cell Transformation, Neoplastic - pathology | Methylation | Mitogen-Activated Protein Kinases - metabolism | Oncogene Protein p21(ras) - genetics | Physiological aspects | Research | Lysine | Oncology, Experimental | Cancer | DNA methylation | Peptides | Kinases | Rodents | Tumors | Index Medicus
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4. Full Text COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
by Emery, Caroline M and Hieronymus, Haley and Zhao, Jean J and Boehm, Jesse S and Golub, Todd and Yang, Xiaoping and Root, David E and Roberts, Thomas M and Hahn, William C and Hill, David E and Wilson, Christopher J and Weber, Barbara L and Garraway, Levi A and Johnson, Laura A and Kim, Sungjoon and Harris, Jennifer L and Kim, So Young and Vidal, Marc and Finan, Peter M and Myer, Vic E and Sellers, William R and Barretina, Jordi and Alkan, Ozan and Thomas, Sapana R and Wardwell, Leslie and Cogdill, Alexandria P and Dummer, Reinhard and Schlegel, Robert and Stransky, Nicolas and Flaherty, Keith T and Wargo, Jennifer A and Murray, Ryan R and Johannessen, Cory M and Salehi-Ashtiani, Kourosh and Caponigro, Giordano
Nature, ISSN 0028-0836, 12/2010, Volume 468, Issue 7326, pp. 968 - 972
Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas. Pre-clinical studies have... 
TRANSFORMATION | CELLS | TUMOR PROGRESSION | GENE | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | BRAF | B-RAF | KAPPA-B | MUTATIONS | CANCER | Allosteric Regulation | Humans | Gene Expression Regulation, Neoplastic | Melanoma - enzymology | Gene Expression Profiling | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Indoles - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Gene Library | Proto-Oncogene Proteins c-raf - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Open Reading Frames - genetics | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinases - metabolism | Protein research | Research | Properties | Protein kinases | Cancer cells | Cell lines | Biochemistry | Mutation | Kinases | Genes | Cancer | Index Medicus
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5. Full Text RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF
by Shokat, Kevan M and Rosen, Neal and Zhang, Chao and Bollag, Gideon and Poulikakos, Poulikos I
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 427 - 430
Tumours with mutant BRAF are dependent on the RAF–MEK–ERK signalling pathway for their growth. We found that ATP-competitive RAF inhibitors inhibit ERK... 
SELECTIVE INHIBITOR | ACTIVATION | MELANOMA | MECHANISM | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | HETERODIMERIZATION | KINASE INHIBITOR | B-RAF | CRAF | ONCOGENIC BRAF | Neoplasms - metabolism | ras Proteins - genetics | Phosphorylation | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | Transcriptional Activation - drug effects | ras Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Neoplasms - genetics | Adenosine Triphosphate - metabolism | Indoles - pharmacology | raf Kinases - genetics | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Cell Line | raf Kinases - chemistry | Catalytic Domain | Neoplasms - enzymology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Models, Biological | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Protein Binding | Mice | Protein Kinase Inhibitors - pharmacology | Protein Kinase Inhibitors - metabolism | Care and treatment | Enzyme inhibitors | Gene mutations | Cellular signal transduction | Genetic aspects | Research | Health aspects | Cancer | Proteins | Competition | Drugs | Mutation | Kinases | Tumors | Index Medicus
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6. Full Text PAK signalling drives acquired drug resistance to MAPK inhibitors in BRAF-mutant melanomas
by Lu, Hezhe and Liu, Shujing and Zhang, Gao and Wu, Bin and Zhu, Yueyao and Frederick, Dennie T and Hu, Yi and Zhong, Wenqun and Randell, Sergio and Sadek, Norah and Zhang, Wei and Chen, Gang and Cheng, Chaoran and Zeng, Jingwen and Wu, Lawrence W and Zhang, Jie and Liu, Xiaoming and Xu, Wei and Krepler, Clemens and Sproesser, Katrin and Xiao, Min and Miao, Benchun and Liu, Jianglan and Song, Claire D and Liu, Jephrey Y and Karakousis, Giorgos C and Schuchter, Lynn M and Lu, Yiling and Mills, Gordon and Cong, Yusheng and Chernoff, Jonathan and Guo, Jun and Boland, Genevieve M and Sullivan, Ryan J and Wei, Zhi and Field, Jeffrey and Amaravadi, Ravi K and Flaherty, Keith T and Herlyn, Meenhard and Xu, Xiaowei and Guo, Wei
Nature, ISSN 0028-0836, 10/2017, Volume 550, Issue 7674, pp. 133 - 136
Targeted BRAF inhibition (BRAFi) and combined BRAF and MEK inhibition (BRAFi and MEKi) therapies have markedly improved the clinical outcomes of patients with... 
METASTATIC MELANOMA | MEK | EPITHELIAL-CELLS | PHOSPHORYLATION | PATHWAY | RAF | P21-ACTIVATED-KINASE-1 | MULTIDISCIPLINARY SCIENCES | KINASE | MECHANISMS | THERAPIES | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Humans | p21-Activated Kinases - antagonists & inhibitors | Melanoma - enzymology | JNK Mitogen-Activated Protein Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Proto-Oncogene Proteins c-raf - chemistry | Female | beta Catenin - chemistry | Phosphorylation - drug effects | p21-Activated Kinases - genetics | JNK Mitogen-Activated Protein Kinases - chemistry | Enzyme Activation - drug effects | p21-Activated Kinases - metabolism | beta Catenin - metabolism | Proto-Oncogene Proteins c-raf - metabolism | Mitogen-Activated Protein Kinase Kinases - chemistry | Drug Resistance, Neoplasm - genetics | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Mutation | Drug Resistance, Neoplasm - drug effects | Melanoma | Physiological aspects | Cellular signal transduction | Drug resistance | Observations | Health aspects | Mitogen-activated protein kinases | TOR protein | Therapy | Phosphorylation | Activation | Metastasis | Drug development | Kinases | Cancer therapies | Metastases | Proteins | β-catenin | Signal transduction | Inhibition | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Patients | Signaling | Protein arrays | Molecular modelling | Biopsy | Cell lines | Apoptosis | Index Medicus
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7. Full Text BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis
by Wilhelm, Scott M and Carter, Christopher and Tang, LiYa and Wilkie, Dean and McNabola, Angela and Rong, Hong and Chen, Charles and Zhang, Xiaomei and Vincent, Patrick and McHugh, Mark and Cao, Yichen and Shujath, Jaleel and Gawlak, Susan and Eveleigh, Deepa and Rowley, Bruce and Liu, Li and Adnane, Lila and Lynch, Mark and Auclair, Daniel and Taylor, Ian and Gedrich, Rich and Voznesensky, Andrei and Riedl, Bernd and Post, Leonard E and Bollag, Gideon and Trail, Pamela A
Cancer Research, ISSN 0008-5472, 10/2004, Volume 64, Issue 19, pp. 7099 - 7109
The RAS/RAF signaling pathway is an important mediator of tumor cell proliferation and angiogenesis. The novel bi-aryl urea BAY 43-9006 is a potent inhibitor... 
CELLS | ACTIVATION | GENE | ONCOLOGY | SIGNALING PATHWAY | PROTEIN-KINASE | MAP KINASE | B-RAF | INHIBITORS | CANCER | ENDOTHELIAL GROWTH-FACTOR | Niacinamide - analogs & derivatives | Humans | Phenylurea Compounds | Neovascularization, Pathologic - enzymology | Benzenesulfonates - pharmacology | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Administration, Oral | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Neoplasms - enzymology | Neoplasms - blood supply | MAP Kinase Kinase Kinases - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | Disease Progression | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mice, Nude | Neovascularization, Pathologic - drug therapy | Cell Line, Tumor | Mice | Proto-Oncogene Proteins c-raf - antagonists & inhibitors | Pyridines - pharmacology | MAP Kinase Kinase Kinase 1 | Mitogen-Activated Protein Kinase 3 | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Index Medicus
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8. Full Text The clinical effect of the dual-targeting strategy involving PI3K/AKT/mTOR and RAS/MEK/ERK pathways in patients with advanced cancer
by Shimizu, Toshio and Tolcher, Anthony W and Papadopoulos, Kyriakos P and Beeram, Muralidhar and Rasco, Drew W and Smith, Lon S and Gunn, Shelly and Smetzer, Leslie and Mays, Theresa A and Kaiser, Brianne and Wick, Michael J and Alvarez, Cathy and Cavazos, Aracely and Mangold, Gina L and Patnaik, Amita
Clinical Cancer Research, ISSN 1078-0432, 04/2012, Volume 18, Issue 8, pp. 2316 - 2325
Purpose: This study evaluated the clinical relevance of the dual-targeting strategy involving PI3K/AKT/mTOR and RAF/MEK/ERK pathways. Experimental Design: We... 
COLON-CANCER | METASTATIC MELANOMA | PIK3CA MUTATIONS | PI3K | ONCOLOGY | COLORECTAL-CANCER | RESISTANCE | BRAF | ANTITUMOR-ACTIVITY | MEK INHIBITORS | TUMORS | Neoplasms - metabolism | Extracellular Signal-Regulated MAP Kinases - drug effects | TOR Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Middle Aged | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | Young Adult | MAP Kinase Signaling System - genetics | TOR Serine-Threonine Kinases - genetics | Neoplasms - genetics | Aged, 80 and over | Adult | Female | Proto-Oncogene Proteins c-akt - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Neoplasms - drug therapy | Phosphatidylinositol 3-Kinases - genetics | MAP Kinase Signaling System - drug effects | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins p21(ras) - antagonists & inhibitors | Adolescent | Aged | Mutation | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
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9. Full Text A unique inhibitor binding site in ERK1/2 is associated with slow binding kinetics
by Chaikuad, Apirat and Chaikuad, Apirat and Tacconi, Eliana M. C and Zimmer, Jutta and Liang, Yanke and Gray, Nathanael S and Tarsounas, Madalena and Knapp, Stefan
Nature chemical biology, ISSN 1552-4450, 10/2014, Volume 10, Issue 10, pp. 853 - 860
Activation of the ERK pathway is a hallmark of cancer, and targeting of upstream signaling partners led to the development of approved drugs. Recently,... 
POLY(ADP-RIBOSE) POLYMERASE | RAF INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ACQUIRED-RESISTANCE | MAP KINASE ERK2 | BRAF | CONFORMATION | MEK INHIBITORS | SELECTIVITY | DISCOVERY | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Intracellular Signaling Peptides and Proteins - metabolism | Piperazines - chemistry | Mitogen-Activated Protein Kinase 1 - chemistry | Enzyme Inhibitors - chemistry | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Antineoplastic Agents - pharmacology | Mitogen-Activated Protein Kinase 3 - chemistry | Binding Sites | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Gene Expression | Indazoles - chemistry | Mitogen-Activated Protein Kinase 3 - genetics | Protein Structure, Secondary | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - chemistry | Mitogen-Activated Protein Kinase 8 - metabolism | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Antineoplastic Agents - chemistry | Piperazines - pharmacology | Indazoles - pharmacology | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Cell Line, Tumor | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | Kinetics | Mitogen-Activated Protein Kinase 1 - metabolism | Signal transduction | Binding sites | Pharmaceutical sciences | Cancer | Index Medicus
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