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Molecular Cancer Therapeutics, ISSN 1535-7163, 10/2019, Volume 18, Issue 10, pp. 1682 - 1683
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2001, Volume 98, Issue 24, pp. 13681 - 13686
Jun N-terminal kinase (JNK) is a stress-activated protein kinase that can be induced by inflammatory cytokines, bacterial endotoxin, osmotic shock, UV... 
T lymphocytes | Enzymes | Biological Sciences | Phosphorylation | Cell growth | Nervous system diseases | Messenger RNA | Cytokines | Thymocytes | Inhibitory concentration 50 | Apoptosis | SIGNAL-TRANSDUCTION | TUMOR-NECROSIS-FACTOR | MESSENGER-RNA | ANTICANCER AGENTS | MULTIDISCIPLINARY SCIENCES | C-JUN | CELL-DIFFERENTIATION | TRANSCRIPTION FACTOR | EXPRESSION | AP-1 | T-CELLS | Gene Expression - drug effects | Monocytes - cytology | Humans | Monocytes - metabolism | Structure-Activity Relationship | Pyrazolones | CD4-Positive T-Lymphocytes - immunology | Adenosine Triphosphate - metabolism | Enzyme Inhibitors - chemistry | JNK Mitogen-Activated Protein Kinases | Female | Molecular Structure | Binding, Competitive | Cytokines - metabolism | Enzyme Inhibitors - metabolism | Anthracenes - chemistry | Jurkat Cells | Pyrazoles | CD4-Positive T-Lymphocytes - cytology | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Anthracenes - pharmacology | Protein Kinase Inhibitors | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Anthraquinones | Cell Differentiation - drug effects | Lymphocyte Activation - drug effects | Anthracenes - metabolism | Mice | Tumor Necrosis Factor-alpha - biosynthesis | CD4-Positive T-Lymphocytes - drug effects | Physiological aspects | Protein kinases | Enzyme inhibitors
Journal Article
Nature, ISSN 0028-0836, 03/2015, Volume 519, Issue 7541, pp. 102 - 105
The BCR-ABL1 fusion gene is a driver oncogene in chronic myeloid leukaemia and 30-50% of cases of adult acute lymphoblastic leukaemia(1). Introduction of ABL1... 
CELLS | PONATINIB | MECHANISM | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | RESISTANCE | FOLLOW-UP | PATIENTS RECEIVING IMATINIB | BCR-ABL INHIBITOR | CHRONIC MYELOID-LEUKEMIA | T315I MUTANT | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Molecular Conformation | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors | Protein Kinase Inhibitors - chemistry | Angiogenesis Inhibitors - therapeutic use | Imidazoles - therapeutic use | Phosphorylation - drug effects | Fusion Proteins, bcr-abl - chemistry | Cell Line | Proto-Oncogene Proteins c-abl - genetics | Indazoles - chemistry | Crystallization | Proto-Oncogene Proteins c-abl - chemistry | Angiogenesis Inhibitors - pharmacology | Models, Molecular | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Imidazoles - pharmacology | Drug Repositioning | Indazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Fusion Proteins, bcr-abl - genetics | Vascular Endothelial Growth Factor Receptor-2 - chemistry | Protein Kinase Inhibitors - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Protein Binding | Proto-Oncogene Proteins c-abl - metabolism | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Kidney Neoplasms - drug therapy | Fusion Proteins, bcr-abl - metabolism | Indazoles - therapeutic use | Angiogenesis Inhibitors - chemistry | Drug Screening Assays, Antitumor | Axitinib | Genetic aspects | Research | Gene mutations | Drug resistance | Analysis | Phosphorylation | Inhibitor drugs | Leukemia | Bone marrow | Mutation | Kinases | Drug dosages | Patients | Index Medicus
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2010, Volume 107, Issue 20, pp. 9446 - 9451
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2015, Volume 10, Issue 9, pp. e0138616 - e0138616
Cell cycle checkpoint intervention is an effective therapeutic strategy for cancer when applied to patients predisposed to respond and the treatment is... 
CELLS | KINETOCHORES | THERAPY | MICROTUBULES | MULTIDISCIPLINARY SCIENCES | CDK4/6 INHIBITION | MECHANISMS | GENE-PRODUCT | SPINDLE-ASSEMBLY CHECKPOINT | NEGATIVE BREAST-CANCER | CHROMOSOMAL INSTABILITY | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Phosphorylation | Intestine, Small - pathology | Apoptosis - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Transplantation, Heterologous | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - genetics | RNA Interference | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Bone Marrow Cells - drug effects | Female | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Cell Survival - drug effects | Bone Marrow Cells - cytology | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Rats | Cyclin-Dependent Kinase 6 - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Mice, SCID | Breast Neoplasms - drug therapy | Piperazines - pharmacology | Animals | Mitosis - drug effects | Breast Neoplasms - pathology | Protein Kinase Inhibitors - therapeutic use | Cell Line, Tumor | Protein Kinase Inhibitors - toxicity | Breast Neoplasms - diagnosis | Cell Proliferation - drug effects | Mice | Pyridines - pharmacology | Histones - metabolism | G1 Phase Cell Cycle Checkpoints - drug effects | Bone Marrow Cells - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | RNA, Small Interfering - metabolism | Physiological aspects | Genetic aspects | Research | Mitosis | Protein kinases | Toxicity | Body weight | Cytotoxicity | Oncology | Body weight loss | Catalytic activity | Kinases | Cancer therapies | Cyclin-dependent kinase 4 | Genomic instability | Proteins | Cyclin-dependent kinase | Metaphase | Cell cycle | Bone marrow | Physiology | Bioindicators | Inhibition | Pretreatment | Catalysis | Drug therapy | Product safety | Chromosomes | Pharmaceutical sciences | Neutropenia | Stability | Research & development--R&D | Tumor cells | Cell division | Breast cancer | Pharmacology | Hypotheses | Inhibitors | Biomarkers | Safety research | Viability | Anaphase | Apoptosis | Tumors | Cancer | Index Medicus | Research & development | R&D
Journal Article
Methods in Molecular Biology, ISSN 1064-3745, 2015, Volume 1248, pp. 267 - 276
Peptide-based molecules are known to have therapeutic utility, but the generation of phage-focused libraries to optimize peptide properties and functionality... 
Peptide phage display library | Codon-corrected trinucleotide cassettes | Conjugation | Maleimide | Peptide extension | Receptor, Epidermal Growth Factor - genetics | Animals | Humans | Cysteine - chemistry | Peptide Library | Maleimides - chemistry | Receptor, Epidermal Growth Factor - chemistry
Journal Article
Science, ISSN 0036-8075, 10/1997, Volume 278, Issue 5339, pp. 860 - 866
Activation of the transcription factor nuclear factor kappa B (NF-κB) is controlled by sequential phosphorylation, ubiquitination, and degradation of its... 
Phosphorylation | Human umbilical vein endothelial cells | Databases | Transfection | Gels | Cell lines | HeLa cells | Antibodies | Amino acids | Reports | Cellular immunity | TRANSCRIPTION FACTORS | UBIQUITINATION | SIGNAL | ALPHA PROTEOLYSIS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | DEGRADATION | K RO MULTIDISCIPLINARY SCIENCES | PROTEINS | IDENTIFICATION | MASS-SPECTROMETRY | FAMILY
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 11/2012, Volume 109, Issue 45, pp. 18281 - 18289
Journal Article
Journal Article