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Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 55 - 62
Somatic mutations have been extensively characterized in breast cancer, but the effects of these genetic alterations on the proteomic landscape remain poorly understood... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors
Journal Article
Cell Cycle, ISSN 1551-4005, 2014, Volume 3, Issue 10, pp. 1221 - 1224
Journal Article
Nature communications, ISSN 2041-1723, 2015, Volume 6, Issue 1, p. 6118
Journal Article
The Journal of pediatrics, ISSN 0022-3476, 2015, Volume 166, Issue 4, pp. 1048 - 1054.e5
Journal Article
Lung cancer (Amsterdam, Netherlands), ISSN 0169-5002, 2017, Volume 106, pp. 17 - 21
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 2/2008, Volume 105, Issue 7, pp. 2652 - 2657
.... The most prominent of these mutants, represented by single amino acid substitutions in the helical or kinase domain, show a gain of enzymatic function, activate AKT signaling, and induce oncogenic transformation... 
Proteins | Phosphorylation | Cell growth | Genetic vectors | B lymphocytes | Epithelial cells | Mathematical functions | Biochemistry | Genetic mutation | Phosphatidylinositols | AKT | p85 | RAS | Molecular mechanisms | Cancer | CATALYTIC SUBUNIT | ACTIVATION | MULTIDISCIPLINARY SCIENCES | ONCOGENIC PI3K | PHOSPHOINOSITIDE 3-KINASE | molecular mechanisms | PIK3CA GENE | CANCER-SPECIFIC MUTATIONS | HIGH-FREQUENCY | OVARIAN | TARGETS | cancer | Biological Sciences
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Journal Article