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Clinical Cancer Research, ISSN 1078-0432, 09/2005, Volume 11, Issue 17, pp. 6139 - 6147
Journal Article
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2013, Volume 133, Issue 5, pp. 1332 - 1339.e3
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 58 - 71
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that... 
RAPAMYCIN | TARGET | FORKHEAD TRANSCRIPTION FACTOR | CELLS | INSULIN-RECEPTOR | ACTIVATION | ONCOLOGY | SIGNALING PATHWAY | PHOSPHORYLATION | UPSTREAM | HUMAN CANCER | CELL BIOLOGY | RNA, Small Interfering - genetics | Receptor, IGF Type 1 - metabolism | Protein Binding - genetics | Receptor, ErbB-3 - metabolism | Humans | Forkhead Transcription Factors - metabolism | Protein Binding - drug effects | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptor, ErbB-2 - antagonists & inhibitors | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Quinoxalines - therapeutic use | Carcinoma, Non-Small-Cell Lung - metabolism | Receptor, ErbB-3 - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Breast Neoplasms - drug therapy | Receptor, IGF Type 1 - genetics | Signal Transduction - drug effects | Mice, Nude | Models, Biological | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Feedback, Physiological - physiology | Quinazolines - pharmacology | Proteins - antagonists & inhibitors | Neoplasms - metabolism | Gene Expression - drug effects | Multiprotein Complexes | Receptor, ErbB-2 - metabolism | Promoter Regions, Genetic - genetics | Proto-Oncogene Proteins c-akt - genetics | Breast Neoplasms - metabolism | Mechanistic Target of Rapamycin Complex 1 | Quinoxalines - pharmacology | Receptor, Insulin - genetics | Female | Forkhead Transcription Factors - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Gene Expression Regulation, Neoplastic - physiology | Carcinoma, Non-Small-Cell Lung - pathology | Up-Regulation - genetics | Forkhead Transcription Factors - genetics | Xenograft Model Antitumor Assays | Animals | Receptor Protein-Tyrosine Kinases - genetics | Breast Neoplasms - pathology | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Feedback, Physiological - drug effects | Receptor, Insulin - metabolism | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Benzylamines - pharmacology | Benzylamines - therapeutic use | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2012, Volume 287, Issue 16, pp. 13371 - 13381
Journal Article
Cellular Physiology and Biochemistry, ISSN 1015-8987, 12/2017, Volume 43, Issue 6, pp. 2212 - 2225
Background/Aims: Little is known about the potential mechanism of action for androgen receptor (AR) targeting treatment in estrogen receptor (ER)-negative... 
Original Paper | Bicalutamide | Breast cancer | Prognosis | Antagonize | Estrogen receptor-negative | Androgen receptor-positive | PR | PHYSIOLOGY | SUBTYPES | TUMORS | ER | CELL BIOLOGY | AR | THERAPIES | OUTCOMES | PRACTICE GUIDELINE UPDATE | AMERICAN SOCIETY | ENZALUTAMIDE | Immunohistochemistry | Transcription, Genetic - drug effects | Anilides - therapeutic use | Receptors, Estrogen - metabolism | Androgen Receptor Antagonists - therapeutic use | Nitriles - pharmacology | Apoptosis - drug effects | Humans | Middle Aged | Receptors, Androgen - metabolism | Transplantation, Heterologous | Androgen Receptor Antagonists - pharmacology | Tosyl Compounds - pharmacology | Female | Receptors, Androgen - chemistry | Receptors, Estrogen - genetics | Kaplan-Meier Estimate | Down-Regulation - drug effects | Breast Neoplasms - drug therapy | Proto-Oncogene Proteins c-myc - metabolism | beta Catenin - metabolism | beta Catenin - genetics | Animals | Receptors, Androgen - genetics | Signal Transduction - drug effects | Breast Neoplasms - pathology | Mice, Nude | Tosyl Compounds - therapeutic use | Anilides - pharmacology | Cell Line, Tumor | Breast Neoplasms - mortality | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | Nitriles - therapeutic use | Androgens | Gene amplification | Biochemistry | Gene expression | Prostate | Patients | Cancer therapies | Tumors
Journal Article
Journal Article
Journal Article
Journal Article
Science, ISSN 0036-8075, 1/2002, Volume 295, Issue 5554, pp. 491 - 495
Protein-protein interactions and calcium entry through the N-methyl-D-aspartate (NMDA)-type glutamate receptor regulate synaptic development and plasticity in... 
Phosphorylation | Receptors | Calcium | Neurons | N methyl D aspartate receptors | Developmental biology | Antibodies | Reports | Gene expression | Family members | Synapses | SUBUNIT 2B | INCREASES TYROSINE PHOSPHORYLATION | ACTIVATION | MULTIDISCIPLINARY SCIENCES | GROWTH | SITES | LONG-TERM POTENTIATION | D-ASPARTATE RECEPTOR | HIPPOCAMPAL-NEURONS | CELL-CONTACT | KINASES | Receptors, Eph Family | Recombinant Fusion Proteins - pharmacology | Calcium - metabolism | Humans | Proto-Oncogene Proteins c-fyn | Receptors, N-Methyl-D-Aspartate - metabolism | Membrane Proteins - pharmacology | Cerebral Cortex - cytology | Recombinant Fusion Proteins - metabolism | Phosphotyrosine - metabolism | Receptors, N-Methyl-D-Aspartate - genetics | Brain-Derived Neurotrophic Factor - pharmacology | Synapses - metabolism | src-Family Kinases - metabolism | Transcription, Genetic | Membrane Proteins - metabolism | Neurons - metabolism | Genes, Reporter | Proto-Oncogene Proteins - metabolism | Receptor, EphB4 | Cell Line | Ephrin-B2 | Signal Transduction | Immunoglobulin Fc Fragments | Cells, Cultured | Gene Expression Regulation | Rats | Receptor Protein-Tyrosine Kinases - metabolism | Animals | Cerebral Cortex - embryology | Receptor Protein-Tyrosine Kinases - genetics | Cyclic AMP Response Element-Binding Protein - metabolism | Glutamic Acid - metabolism | Models, Neurological | Mutation | Receptor Protein-Tyrosine Kinases - chemistry | Glutamate | Methyl aspartate | Research
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2014, Volume 289, Issue 29, pp. 20102 - 20119
Endoplasmic reticulum (ER) stress and ER stress-associated unfolded protein response (UPR) can promote cancer cell survival, but it remains unclear whether... 
CELLS | CARCINOGENESIS | INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SIGNALING NETWORK | TRANSCRIPTION | INDUCED SKIN TUMORIGENESIS | DIFFERENTIATION | EXPRESSION | CANCER | LIGAND ACTIVATION | RNA, Small Interfering - genetics | Colonic Neoplasms - genetics | TOR Serine-Threonine Kinases - metabolism | Adenoma - genetics | Humans | Colonic Neoplasms - metabolism | Adenoma - metabolism | Gene Knockdown Techniques | Heat-Shock Proteins - genetics | Genes, p53 | Cell Transformation, Neoplastic - genetics | Proto-Oncogene Proteins c-akt - metabolism | PPAR delta - genetics | Skin Neoplasms - pathology | Cellular Senescence - genetics | Gene Expression | PPAR delta - deficiency | PPAR-beta - metabolism | Signal Transduction | Cells, Cultured | Activating Transcription Factor 4 - genetics | Cellular Senescence - physiology | Keratinocytes - cytology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | PPAR-beta - genetics | Unfolded Protein Response | Cell Transformation, Neoplastic - metabolism | PPAR-beta - deficiency | Regulatory Factor X Transcription Factors | Skin Neoplasms - metabolism | Animals | Keratinocytes - metabolism | Models, Biological | Colonic Neoplasms - pathology | Endoplasmic Reticulum Stress | Skin Neoplasms - genetics | Adenoma - pathology | Mice | PPAR delta - metabolism | Genes, ras | Index Medicus | Molecular Bases of Disease | Cancer Therapy | Keratinocyte | Cancer Biology | H-RAS-induced Senescence | Tumor Suppressor Gene | Peroxisome Proliferator-activated Receptor β | Cancer | Oncogene-induced Endoplasmic Reticulum Stress
Journal Article
Cellular and Molecular Life Sciences, ISSN 1420-682X, 6/2014, Volume 71, Issue 11, pp. 2179 - 2192
Journal Article