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Neuron, ISSN 0896-6273, 02/2013, Volume 77, Issue 3, pp. 472 - 484
Major outputs of the neocortex are conveyed by corticothalamic axons (CTAs), which form reciprocal connections with thalamocortical axons, and... 
MUTANT MICE | CORTICAL AXONS | THALAMOCORTICAL AXONS | GROWTH | SEMAPHORIN 3E | CENTRAL-NERVOUS-SYSTEM | GUIDANCE | CHICK HINDLIMB | CAJAL-RETZIUS CELLS | NEUROSCIENCES | CEREBRAL-CORTEX | Thyroid Nuclear Factor 1 | Age Factors | Embryo, Mammalian | Leukocyte L1 Antigen Complex - metabolism | Gene Expression Regulation, Developmental - genetics | Axons - physiology | Cerebral Cortex - cytology | Neural Pathways - physiology | DNA-Binding Proteins - metabolism | POU Domain Factors - genetics | tau Proteins - genetics | Thalamus - physiology | Contactin 2 - metabolism | Repressor Proteins - metabolism | Glycoproteins - genetics | Tumor Suppressor Proteins - metabolism | Wnt3A Protein - genetics | Membrane Proteins - genetics | Mice, Inbred C57BL | Mice, Transgenic | Nuclear Proteins - metabolism | Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Homeodomain Proteins - genetics | Membrane Glycoproteins - genetics | Nerve Tissue Proteins - metabolism | S100 Calcium Binding Protein G - metabolism | Transcription Factors - metabolism | Animals | Calbindin 2 | Thalamus - cytology | Cerebral Cortex - physiology | Luminescent Proteins - genetics | Mice | Body Patterning - genetics | Luminescent Proteins - metabolism | Developmental biology | Neurons | Studies | Laboratories | Experiments | Repressor Proteins | Cerebral Cortex | Cellular Biology | Neural Pathways | tau Proteins | Life Sciences | Contactin 2 | Gene Expression Regulation, Developmental | Body Patterning | Thalamus | Membrane Glycoproteins | Luminescent Proteins | DNA-Binding Proteins | POU Domain Factors | Calcium-Binding Protein, Vitamin D-Dependent | Glycoproteins | Nerve Tissue Proteins | Nuclear Proteins | Membrane Proteins | Axons | Homeodomain Proteins | Leukocyte L1 Antigen Complex | Transcription Factors | Wnt3A Protein | Tumor Suppressor Proteins | reciprocal connections | handshake | waiting period | PlexinD1 | axon guidance | Sema3E | thalamocortical | corticothalamic
Journal Article
American journal of human genetics, ISSN 0002-9297, 2016, Volume 99, Issue 5, pp. 1190 - 1198
Uveal melanoma (UM) is a rare intraocular tumor that, similar to cutaneous melanoma, originates from melanocytes. To gain insights into its genetics, we... 
OCULAR MELANOMA | CELLS | COLORECTAL-CANCER | PROTEINS DLK1 | METASTASES | GENETICS & HEREDITY | RISK | EXPRESSION | RADIATION | SF3B1 | SOMATIC MUTATIONS | Melanoma - diagnosis | Exons | Humans | Middle Aged | Male | Phosphoproteins - metabolism | Case-Control Studies | RNA Splicing Factors - metabolism | DNA Copy Number Variations | Melanoma - genetics | Melanocytes - pathology | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Ubiquitin Thiolesterase - metabolism | Adult | Female | Membrane Proteins - metabolism | Eukaryotic Initiation Factor-1 - metabolism | GTP-Binding Protein alpha Subunits, Gq-G11 - metabolism | Tumor Suppressor p53-Binding Protein 1 - metabolism | GTP-Binding Protein alpha Subunits, Gq-G11 - genetics | Uveal Neoplasms - genetics | Genome-Wide Association Study | Tumor Suppressor Proteins - metabolism | GTP-Binding Protein alpha Subunits - metabolism | Tumor Suppressor p53-Binding Protein 1 - genetics | Membrane Proteins - genetics | Eukaryotic Initiation Factor-1 - genetics | Ubiquitin-Protein Ligases - metabolism | GTP-Binding Protein alpha Subunits - genetics | Phosphoproteins - genetics | RNA Splicing Factors - genetics | Ubiquitin Thiolesterase - genetics | Skin Neoplasms | Uveal Neoplasms - diagnosis | Aged | Mutation | Ubiquitin-Protein Ligases - genetics | Genetic aspects | Nucleotide sequencing | Methods | Melanoma | DNA sequencing | Report
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2008, Volume 283, Issue 9, pp. 5496 - 5509
... (protein kinase A /PK G /PK C ) kinases. It is a tumor suppressor gene originally isolated from Drosophila and recently isolated from mice and humans... 
YES-ASSOCIATED PROTEIN | APOPTOSIS | SIGNALING PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | KINASE | HIPPO PATHWAY | CELL-PROLIFERATION | DROSOPHILA LATS | PROMOTES | HUMAN HOMOLOG | Oncogene Proteins - genetics | Phosphorylation | Cell Proliferation | Oligonucleotide Array Sequence Analysis | Humans | Gene Expression Profiling | Intracellular Signaling Peptides and Proteins - metabolism | Drosophila Proteins - metabolism | Phosphoproteins - metabolism | Cell Nucleus - metabolism | Cell Transformation, Neoplastic - genetics | Tumor Suppressor Proteins - genetics | Nuclear Proteins - genetics | Active Transport, Cell Nucleus - genetics | Intracellular Signaling Peptides and Proteins - genetics | Gene Expression Regulation, Neoplastic - genetics | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | Drosophila | Oncogene Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Phosphoproteins - genetics | Transcription Factors - genetics | Cell Transformation, Neoplastic - metabolism | Transcription Factors - metabolism | Animals | Cell Nucleus - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice | Drosophila Proteins - genetics | HeLa Cells | Transcription, Genetic - genetics | Adaptor Proteins, Signal Transducing - metabolism | Amino Acid Motifs - genetics
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2009, Volume 119, Issue 12, pp. 3626 - 3636
The polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog (Bmi-1) is dysregulated in various cancers, and its upregulation strongly correlates... 
MEDICINE, RESEARCH & EXPERIMENTAL | BREAST-CANCER CELLS | DEVELOPMENTAL REGULATORS | CELLULAR MEMORY | E-CADHERIN EXPRESSION | HEMATOPOIETIC STEM-CELLS | PROSTATE-CANCER | MYC TRANSGENIC MICE | SELF-RENEWAL | NF-KAPPA-B | TRANSCRIPTION FACTOR | Nasopharyngeal Neoplasms - genetics | Neoplasm Transplantation | Nasopharyngeal Neoplasms - metabolism | Epithelial Cells - metabolism | Cadherins - metabolism | Humans | Glycogen Synthase Kinase 3 beta | Transplantation, Heterologous | Phosphatidylinositol 3-Kinases - metabolism | Mesoderm - cytology | Repressor Proteins - antagonists & inhibitors | Nasopharyngeal Neoplasms - pathology | Cadherins - genetics | Epithelial Cells - cytology | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Nasopharyngeal Neoplasms - etiology | Snail Family Transcription Factors | Nasopharynx - metabolism | Repressor Proteins - metabolism | Proto-Oncogene Proteins - metabolism | PTEN Phosphohydrolase - genetics | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Neoplasm Invasiveness | Down-Regulation | Gene Silencing | PTEN Phosphohydrolase - metabolism | Repressor Proteins - genetics | Nuclear Proteins - metabolism | Proto-Oncogene Proteins - genetics | Glycogen Synthase Kinase 3 - metabolism | Transcription Factors - metabolism | Animals | Polycomb Repressive Complex 1 | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mesoderm - metabolism | Mice | Nasopharynx - cytology | Chromatin | Care and treatment | Lymphomas | Research | Analysis | Cancer
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2014, Volume 124, Issue 6, pp. 2640 - 2650
Journal Article
Nature, ISSN 0028-0836, 08/2009, Volume 460, Issue 7257, pp. 904 - 908
.... aUPD is associated not only with loss-of-function mutations of tumour suppressor genes... 
TRANSFORMATION | PROTEIN | RETROVIRAL VECTOR GCDNSAP | NEGATIVE REGULATION | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | V-CBL | MUTATIONS | UBIQUITIN LIGASES | MYELODYSPLASTIC SYNDROMES | P53 | NIH 3T3 Cells | Neoplasm Transplantation | ras Proteins - genetics | Phosphorylation | Proto-Oncogene Proteins c-cbl - metabolism | Humans | Leukemia, Myeloid - genetics | Molecular Sequence Data | ras Proteins - metabolism | Male | Leukemia, Myeloid - pathology | Allelic Imbalance | Ubiquitination | Base Sequence | Female | Proto-Oncogene Proteins c-cbl - deficiency | Genes, Tumor Suppressor | Proto-Oncogene Proteins c-cbl - genetics | Amino Acid Sequence | Oncogenes - genetics | Mutant Proteins - genetics | Models, Molecular | Mutant Proteins - metabolism | Chromosomes, Human, Pair 11 - genetics | Proto-Oncogene Proteins c-cbl - chemistry | Mice, Knockout | Animals | Uniparental Disomy - genetics | Leukemia, Myeloid - metabolism | Mice, Nude | Mutant Proteins - chemistry | Proto-Oncogene Proteins c-cbl - antagonists & inhibitors | Protein Conformation | Mice | Mutation | Gene mutations | Myelocytic leukemia | Physiological aspects | Tumor suppressor genes | Development and progression | Genetic aspects | Nonlymphoid leukemia | Research | Protein kinases | Proteins | Genes | Amino acids | Kinases | Cells | Clinical outcomes | Crystal structure | cytokine sensitivity | tumor suppressor | myelodysplasia | 490 | LOH | ubiquitination
Journal Article
Nature cell biology, ISSN 1476-4679, 2018, Volume 20, Issue 8, pp. 954 - 965
.... We identified two previously uncharacterized proteins, C2Oorf196 and FAM35A, whose inactivation confers strong PARP-inhibitor resistance... 
PATHWAY CHOICE | STRAND BREAK REPAIR | RESECTION | DAMAGE-RESPONSE | 53BP1 | CLASS-SWITCH RECOMBINATION | FANCONI-ANEMIA | DIFFERENTIAL EXPRESSION ANALYSIS | POLYMERASE-ZETA | TELOMERES | CELL BIOLOGY | Osteosarcoma - drug therapy | Mad2 Proteins - metabolism | Humans | Multiprotein Complexes | Ovarian Neoplasms - pathology | Bone Neoplasms - pathology | DNA Breaks, Double-Stranded | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Ovarian Neoplasms - genetics | Telomere-Binding Proteins - genetics | DNA End-Joining Repair | HEK293 Cells | Female | Bone Neoplasms - genetics | Ovarian Neoplasms - metabolism | Bone Neoplasms - drug therapy | BRCA1 Protein - deficiency | Telomere-Binding Proteins - metabolism | Ovarian Neoplasms - drug therapy | Osteosarcoma - metabolism | DNA-Binding Proteins | Tumor Suppressor p53-Binding Protein 1 - metabolism | Recombinational DNA Repair | Tumor Suppressor p53-Binding Protein 1 - genetics | Cisplatin - pharmacology | Breast Neoplasms - drug therapy | Proteins - genetics | Xenograft Model Antitumor Assays | BRCA1 Protein - genetics | Poly(ADP-ribose) Polymerase Inhibitors - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Breast Neoplasms - genetics | Proteins - metabolism | Breast Neoplasms - pathology | Mad2 Proteins - genetics | Cell Line, Tumor | Mice | Osteosarcoma - genetics | Cell Cycle Proteins | Osteosarcoma - pathology | Care and treatment | DNA | Cancer cells | Breast cancer | Genetic aspects | Research | Gene expression | Single-stranded DNA | DNA damage | Homologous recombination | Poly(ADP-ribose) | Homology | Genomes | Inactivation | Proteins | Ribose | Null cells | Deoxyribonucleic acid--DNA | BRCA2 protein | CRISPR | Deactivation | BRCA1 protein | Poly(ADP-ribose) polymerase | Adenosine diphosphate | Oligosaccharides | Double-strand break repair | Screens | Cisplatin | Polymerase | Inhibitors | Prostate | Viability | Tumors | Telomere-Binding Proteins / metabolism | Osteosarcoma / genetics | Telomere-Binding Proteins / genetics | BRCA1 Protein / genetics | Cellular Biology | Genetics | Proteins / genetics | Osteosarcoma / drug therapy | Ovarian Neoplasms / genetics | Mad2 Proteins / genetics | Proteins / metabolism | Breast Neoplasms / drug therapy | Breast Neoplasms / metabolism | Tumor Suppressor p53-Binding Protein 1 / genetics | BRCA1 Protein / deficiency | Ovarian Neoplasms / metabolism | Mad2 Proteins / metabolism | Breast Neoplasms / pathology | Bone Neoplasms / genetics | Ovarian Neoplasms / pathology | Bone Neoplasms / pathology | Life Sciences | Bone Neoplasms / drug therapy | Ovarian Neoplasms / drug therapy | Osteosarcoma / metabolism | Biochemistry, Molecular Biology | Breast Neoplasms / genetics | Drug Resistance, Neoplasm / genetics | Osteosarcoma / pathology | Bone Neoplasms / metabolism | Poly(ADP-ribose) Polymerase Inhibitors / pharmacology | Cisplatin / pharmacology | Molecular biology | Tumor Suppressor p53-Binding Protein 1 / metabolism | Cancer
Journal Article
Nature medicine, ISSN 1546-170X, 2018, Volume 25, Issue 1, pp. 130 - 140
In T lymphocytes, the Wiskott-Aldrich Syndrome protein (WASP) and WASP-interacting-protein (WIP... 
ALK | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | ACTIN POLYMERIZATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | RHOA | DEFICIENCY | CELL BIOLOGY | CDC42 | MUTATIONS | RAC1 | WIP | Wiskott-Aldrich Syndrome Protein - deficiency | Cell Proliferation | Humans | cdc42 GTP-Binding Protein - metabolism | Guanosine Triphosphate - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Lymphoma, T-Cell - metabolism | MAP Kinase Signaling System | Lymphoma, T-Cell - enzymology | Wiskott-Aldrich Syndrome Protein - metabolism | Anaplastic Lymphoma Kinase - metabolism | Cytoskeletal Proteins - metabolism | STAT3 Transcription Factor - metabolism | Tumor Suppressor Proteins - metabolism | Cell Survival | Down-Regulation | Kaplan-Meier Estimate | CCAAT-Enhancer-Binding Protein-beta - metabolism | Animals | Lymphoma, T-Cell - pathology | Cell Line, Tumor | Protein Binding | T-Lymphocytes - immunology | Mice | Enzyme Activation | Research | B cells | T cells | Protein kinases | Cdc42 protein | GTP | Stat3 protein | MAP kinase | Lymphocytes T | CCAAT/enhancer-binding protein | Kinases | Lymphoma | Suppressors | Proteins | T-cell receptor | Inhibitors | Clonal deletion | Protein kinase | Lymphocytes | Tumor suppressor genes | Lymphomas | Anaplastic large-cell lymphoma | Protein-tyrosine kinase | T-cell lymphoma | Tumors
Journal Article