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Neuron (Cambridge, Mass.), 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
Cell host & microbe, ISSN 1931-3128, 2007, Volume 1, Issue 1, pp. 77 - 83
Many bacteria pathogenic for plants or animals, including Shigella spp., which is responsible for shigellosis in humans, use a type III secretion apparatus to inject effector proteins into host cells... 
PROTEINS | MICROBIO | SHIGELLA-FLEXNERI | IMMUNITY | MUTANTS | TRANSCRIPTION | MICROBIOLOGY | DIVERSITY | SACCHAROMYCES-CEREVISIAE | G-PROTEIN | EXPRESSION | APPARATUS | CELL-DEATH | Protein Kinases - metabolism | Protein Kinases - genetics | Shigella flexneri - genetics | Saccharomyces cerevisiae - genetics | Shigella flexneri - metabolism | Humans | Shigella flexneri - pathogenicity | Ubiquitin - metabolism | Antigens, Bacterial - genetics | Saccharomyces cerevisiae - metabolism | Mitogen-Activated Protein Kinase Kinases | Protein Kinase C - metabolism | Genes, Reporter | Protein Structure, Tertiary | Bacterial Proteins - genetics | Ubiquitin-Protein Ligases - metabolism | Pheromones - metabolism | Saccharomyces cerevisiae Proteins - genetics | Animals | Saccharomyces cerevisiae Proteins - metabolism | Bacterial Proteins - metabolism | Signal Transduction - physiology | Biological Transport - physiology | Proteasome Endopeptidase Complex - metabolism | Ubiquitin-Protein Ligases - genetics | Antigens, Bacterial - metabolism | Mitogen-Activated Protein Kinases - metabolism | Ubiquitin | Ligases | Mitogen-Activated Protein Kinases | Signal Transduction | Biochemistry, Molecular Biology | Shigella flexneri | Antigens, Bacterial | Pheromones | Proteasome Endopeptidase Complex | Bacterial Proteins | Ubiquitin-Protein Ligases | Life Sciences | Protein Kinases | Biological Transport | Saccharomyces cerevisiae Proteins | Saccharomyces cerevisiae | Protein Kinase C
Journal Article
2004, Methods in molecular biology, ISBN 1592594301, Volume 237., xii, 249
G proteins and G protein-coupled receptors are ubiquitously expressed proteins that regulate a wide range of physiological processes and are consequently the targets of many pharmaceuticals... 
Cellular signal transduction | G proteins | Laboratory manuals | Cytology | Cell Biology | Life Sciences
Book
2004, Molecular biology intelligence unit, ISBN 9780306479922, 235
Book
Cellular signalling, ISSN 0898-6568, 2006, Volume 18, Issue 9, pp. 1351 - 1359
... extracellular regulated kinases (ERKs), p38 mitogen-activated protein kinases (MAPKs), and phosphatidylinositol-3 kinase (PI3K... 
Protein kinase A | Mitogen-activated protein kinase | Follicle-stimulating hormone | Female reproduction | Hypoxia-induced factor 1 | Histone H3 | histone H3 | SIDE-CHAIN CLEAVAGE | follicle-stimulating hormone | ELEMENT-BINDING PROTEIN | HISTONE H3 PHOSPHORYLATION | hypoxia-induced factor 1 | STEROIDOGENIC FACTOR-I | female reproduction | P38 MAP KINASE | LUTEINIZING-HORMONE | CYCLIC ADENOSINE-3',5'-MONOPHOSPHATE | CELL BIOLOGY | mitogen-activated protein kinase | FOLLICLE-STIMULATING-HORMONE | protein kinase A | RAT INHIBIN | GROWTH-FACTOR-I | Cyclic AMP-Dependent Protein Kinases - metabolism | Follicle Stimulating Hormone - metabolism | Tumor Suppressor Proteins - metabolism | Granulosa Cells - physiology | Gene Expression Regulation | Protein Tyrosine Phosphatases - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Animals | Forkhead Transcription Factors - metabolism | Cyclic AMP Response Element-Binding Protein - metabolism | Female | Signal Transduction - physiology | p38 Mitogen-Activated Protein Kinases - metabolism | Enzyme Activation | Histones - metabolism | Tyrosine | Chromatin | Phosphatases | Corticosteroids | Peptides | Tuberous sclerosis | Glycoproteins | DNA binding proteins | Hormones | Gene expression | Phosphatidylinositol | Luteinizing hormone | Mitogens | Vascular endothelial growth factor | Protein kinases | Growth factors | Protein binding | GIOT-1, gonadotropin-inducible ovarian transcription factor-1 | p70S6K, p70 ribosomal S6 kinase | TGFβ, transforming growth factor β | EGF, epidermal growth factor | CREB, cAMP response element binding protein | PDE, phosphodiesterase | R, PKA regulatory subunits | GPCR, G-protein-coupled receptor | MAP2D, microtubule-associated protein 2D | Sp1 | Epac, exchange proteins activated by cAMP | PI3K, phosphatidylinositol 3-kinase | IGF, insulin-like growth factor | mTOR, mammalian target of rapamycin | AKAP, A kinase anchoring protein | Sp3, specific protein 1 | PKI, PKA inhibitor peptide | PKC, protein kinase C | SCC, P450 cholesterol side chain cleavage | VEGF, vascular endothelial growth factor | CBP, CREB binding protein | ERK, extracellular regulated kinase | MNK, MAPK-interacting kinase | Aromatase, P450 aromatase | ChIP, chromatin immunoprecipitation assay | HIF-1, hypoxia-induced factor-1 | Egr-1, early growth response protein-1 | LH, luteinizing hormone | MEK, mitogen- and extracellular-regulated kinase kinase | TSC, tuberous sclerosis complex tumor suppressor gene | SF-1, steroidogenic factor-1 | SGK, serum glucocorticoid kinase | RSK, p90 ribosomal S6 protein kinase | LRH-1, liver receptor homolog-1 | MAPK, mitogen-activated protein kinase | PKA, protein kinase A | PTP, protein tyrosine phosphatase | FSH, follicle-stimulating hormone | MK, MAPK-activated protein kinases
Journal Article
2005, ISBN 0121755517, xviii, 784
Book
Neuropsychopharmacology (New York, N.Y.), ISSN 0893-133X, 01/2014, Volume 39, Issue 1, pp. 131 - 155
There is serious interest in understanding the dynamics of the receptor-receptor and receptor-protein interactions in space and time and their integration in GPCR heteroreceptor complexes of the CNS... 
receptorreceptor interactions | moonlighting | neuropsychiatric disorders | G protein-coupled receptors | neurotherapeutic targets | heterodimerization | PSYCHIATRY | RESONANCE ENERGY-TRANSFER | FIBROBLAST-GROWTH-FACTOR | NEUROSCIENCES | INDUCED MOTOR COMPLICATIONS | receptor-receptor interactions | ADENOSINE A(2A) RECEPTORS | DOPAMINE D2 RECEPTORS | HIGHER-ORDER OLIGOMERS | ANTIPSYCHOTIC-DRUGS | PHARMACOLOGY & PHARMACY | CENTRAL-NERVOUS-SYSTEM | PARKINSONS-DISEASE | MOLECULAR-MECHANISMS | Schizophrenia - metabolism | Antiparkinson Agents - pharmacology | Receptors, G-Protein-Coupled - metabolism | Humans | Drug Discovery - methods | Parkinson Disease - drug therapy | Antidepressive Agents - therapeutic use | Antiparkinson Agents - therapeutic use | Cocaine - pharmacology | Depression - drug therapy | Protein Interaction Mapping - methods | Depression - metabolism | Animals | Cocaine-Related Disorders - metabolism | Antipsychotic Agents - therapeutic use | Antidepressive Agents - pharmacology | Cocaine-Related Disorders - drug therapy | Parkinson Disease - metabolism | Antipsychotic Agents - pharmacology | Schizophrenia - drug therapy | Cocaine - adverse effects | Molecular Targeted Therapy - methods | Allosteric properties | receptor–receptor interactions | Receptor Pharmacology | Dopamine | Development | Neuropharmacology | Drug Discovery | Neuropsychopharmacology Reviews
Journal Article
British journal of pharmacology, ISSN 0007-1188, 2009, Volume 147, Issue S1, pp. S46 - S55
Journal Article
Molecules (Basel, Switzerland), ISSN 1420-3049, 2017, Volume 22, Issue 12, p. 2045
.... The WEE kinase family consists of three proteins: WEE1, PKMYT1, and the less important WEE1B... 
PKMYT1 | WEE1 | G2/M transition | CANCER-CELLS | CELL-CYCLE REGULATION | PROTEIN-KINASE | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MATURATION-PROMOTING FACTOR | MITOTIC CATASTROPHE | M transition | TUMOR-CELLS | G CHECKPOINT | PHOSPHORYLATES CDC2 | CHEMISTRY, MULTIDISCIPLINARY | DNA-DAMAGING AGENTS | Neoplasms - metabolism | Multigene Family | Protein-Tyrosine Kinases - metabolism | Humans | Antineoplastic Agents - therapeutic use | Structure-Activity Relationship | Molecular Targeted Therapy | Cell Cycle Proteins - antagonists & inhibitors | Cell Cycle Proteins - chemistry | Protein-Tyrosine Kinases - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | Neoplasms - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Protein-Tyrosine Kinases - chemistry | Cell Cycle Proteins - genetics | Antineoplastic Agents - pharmacology | Membrane Proteins - metabolism | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Membrane Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Enzyme Activation - drug effects | Nuclear Proteins - chemistry | Neoplasms - drug therapy | Animals | Membrane Proteins - antagonists & inhibitors | Membrane Proteins - chemistry | Protein Kinase Inhibitors - therapeutic use | Nuclear Proteins - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - chemistry | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Phosphorylation | Mitosis | Cyclin B | Cell cycle | Inhibition | Kinases | DNA repair | Deoxyribonucleic acid--DNA | Cancer
Journal Article
Nature communications, ISSN 2041-1723, 2018, Volume 9, Issue 1, pp. 2280 - 14
Defects in DNA repair can cause various genetic diseases with severe pathological phenotypes. Fanconi anemia ( FA) is a rare disease characterized by bone... 
UBIQUITINATION | DAMAGE RESPONSE | CHROMATIN | CROSS-LINK REPAIR | HUMAN-CELLS | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | BRCA1 | ENRICHMENT ANALYSIS | ASSOCIATION | NUCLEASE | Genetic Therapy | Ubiquitin-Specific Proteases - genetics | Fanconi Anemia Complementation Group D2 Protein - genetics | Fanconi Anemia - metabolism | Humans | DNA Repair - physiology | DNA Repair - genetics | Fanconi Anemia Complementation Group C Protein - genetics | Fanconi Anemia Complementation Group A Protein - genetics | Fanconi Anemia Complementation Group D2 Protein - deficiency | Fanconi Anemia Complementation Group A Protein - metabolism | Fanconi Anemia Complementation Group Proteins - metabolism | Ubiquitination | Fanconi Anemia Complementation Group G Protein - genetics | Ubiquitin-Specific Proteases - deficiency | Fanconi Anemia Complementation Group G Protein - deficiency | BRCA1 Protein - metabolism | Fanconi Anemia - genetics | Ubiquitin-Specific Proteases - metabolism | Chromosomal Instability | Rad51 Recombinase - metabolism | Cell Line | Fanconi Anemia Complementation Group Proteins - deficiency | Fanconi Anemia Complementation Group Proteins - genetics | Fanconi Anemia Complementation Group G Protein - metabolism | Gene Knockout Techniques | Fanconi Anemia Complementation Group C Protein - metabolism | Fanconi Anemia Complementation Group D2 Protein - metabolism | Fanconi Anemia Complementation Group A Protein - deficiency | CRISPR-Cas Systems | Fanconi Anemia Complementation Group C Protein - deficiency | Fanconi Anemia - therapy | DNA Damage | Histones - metabolism | Mutation | Phenotypes | Stability | Deactivation | BRCA1 protein | Anemia | Abnormalities | DNA damage | Genotoxicity | Health risks | Crosslinking | Breast cancer | Genomes | Inactivation | Fanconi syndrome | DNA repair | Screens | Genomic instability | FANCC protein | Bone cancer | Bone marrow | Repair | Deoxyribonucleic acid--DNA | Cancer
Journal Article