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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
The FEBS journal, ISSN 1742-464X, 10/2017, Volume 284, Issue 19, pp. 3218 - 3229
.... 1H, 15N spectra showed that the C‐terminal SH3 domain of BIN1 isoform 1 (BIN1Iso1) is not mobile in solution but locked with the core of the protein... 
SH3 domain | nuclear magnetic resonance spectroscopy | protein–protein interaction | Tau | BIN1 | Alzheimer's disease | ALZHEIMERS-DISEASE | NMR-SPECTROSCOPY | BIOCHEMISTRY & MOLECULAR BIOLOGY | PATHOLOGY | MODEL | IDENTIFIES VARIANTS | AMPHIPHYSIN | MEMBRANE CURVATURE | protein-protein interaction | BINDING | EXPRESSION | GENOME-WIDE ASSOCIATION | Adaptor Proteins, Signal Transducing - chemistry | Humans | Peptides - genetics | tau Proteins - metabolism | tau Proteins - chemistry | Peptides - metabolism | Protein Isoforms - metabolism | tau Proteins - genetics | Protein Isoforms - chemistry | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Cloning, Molecular | Escherichia coli - metabolism | Nuclear Magnetic Resonance, Biomolecular | Neurons - metabolism | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Binding Sites | Recombinant Proteins - metabolism | Protein Conformation, alpha-Helical | Gene Expression | Tumor Suppressor Proteins - metabolism | Neurons - chemistry | Peptides - chemistry | Models, Molecular | Recombinant Proteins - chemistry | Nuclear Proteins - metabolism | Recombinant Proteins - genetics | Nuclear Proteins - chemistry | Amino Acid Motifs | Sequence Homology, Amino Acid | Sequence Alignment | Protein Conformation, beta-Strand | Escherichia coli - genetics | Adaptor Proteins, Signal Transducing - genetics | Protein Binding | Kinetics | Adaptor Proteins, Signal Transducing - metabolism | Protein Isoforms - genetics | Nuclear magnetic resonance spectroscopy | Neurons | Protein-protein interactions | Spectroscopy | Clathrin | Nuclear magnetic resonance--NMR | Peptides | Neurodegenerative diseases | Pathogenesis | Complexity | Proteins | Magnetic resonance spectroscopy | Tau protein | Spectrum analysis | Isoforms | Alzheimers disease | Binding sites | tau Proteins/metabolism | Nuclear Proteins/chemistry | Protein Isoforms/chemistry | Protein Isoforms/genetics | Adaptor Proteins, Signal Transducing/genetics | Recombinant Proteins/metabolism | Peptides/metabolism | Life Sciences | Recombinant Proteins/chemistry | Adaptor Proteins, Signal Transducing/chemistry | Nuclear Proteins/metabolism | Tumor Suppressor Proteins/chemistry | Nuclear Proteins/genetics | Tumor Suppressor Proteins/metabolism | Protein Isoforms/metabolism | Peptides/chemistry | Recombinant Proteins/genetics | Biochemistry, Molecular Biology | Escherichia coli/genetics | Escherichia coli/metabolism | Adaptor Proteins, Signal Transducing/metabolism | Neurons/chemistry | Tumor Suppressor Proteins/genetics | tau Proteins/genetics | Neurons/metabolism | Peptides/genetics | tau Proteins/chemistry
Journal Article
Nature structural & molecular biology, ISSN 1545-9985, 2010, Volume 17, Issue 10, pp. 1247 - 1254
... of genome stability after mutations in proteins that carry out repair through homologous recombination, such as BRCA2 (refs. 2,3). In mammalian cells, homologous... 
POLY(ADP-RIBOSE) POLYMERASE | COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | HISTONE H2AX | FANCONI-ANEMIA | CELL BIOLOGY | RAD51 | BIOPHYSICS | IN-VIVO | SUSCEPTIBILITY GENE | D-LOOP FORMATION | DNA-REPAIR | Recombination, Genetic - physiology | DNA, Neoplasm - metabolism | Humans | Neoplasm Proteins - physiology | DNA Repair - physiology | Molecular Sequence Data | Structure-Activity Relationship | DNA Breaks, Double-Stranded | BRCA2 Protein - physiology | Breast Neoplasms - metabolism | Base Sequence | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Female | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Nucleic Acid Conformation | Fanconi Anemia Complementation Group N Protein | Peptide Fragments - metabolism | Neoplasm Proteins - chemistry | Nuclear Proteins - chemistry | Poly(ADP-ribose) Polymerase Inhibitors | Protein Interaction Mapping | Tumor Suppressor Proteins - physiology | Peptide Fragments - chemistry | Apoptosis Regulatory Proteins | Models, Biological | Rad51 Recombinase - chemistry | Rad51 Recombinase - physiology | BRCA2 Protein - chemistry | Nuclear Proteins - physiology | Poly (ADP-Ribose) Polymerase-1 | Breast cancer | Genetic aspects | Research | BRCA mutations | Ovarian cancer | Proteins | Mutation | Molecular biology | Prostate cancer | homologous recombination | BRCA2 | PALB2
Journal Article
Cancer research (Chicago, Ill.), ISSN 1538-7445, 2017, Volume 77, Issue 17, pp. 4602 - 4612
Identifying critical factors involved in the metastatic progression of hepatocellular carcinoma (HCC) may offer important therapeutic opportunities. Here, we... 
TUMOR-PROTEIN-53-INDUCED-NUCLEAR-PROTEIN-1 | NUCLEAR-PROTEIN 1 | ONCOLOGY | MAP KINASE | PROSTATE-CANCER | KINASE PHOSPHATASES MKPS | GENE-EXPRESSION | TUMOR-SUPPRESSOR | STRESS | P53-INDUCED NUCLEAR-PROTEIN-1 | CELL-DEATH | Prognosis | Humans | Lung Neoplasms - metabolism | Tumor Protein p73 - genetics | Gene Expression Profiling | Tumor Protein p73 - metabolism | Heat-Shock Proteins - genetics | Neoplasm Metastasis | Lung Neoplasms - secondary | Carcinoma, Hepatocellular - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Dual-Specificity Phosphatases - genetics | Liver Neoplasms - pathology | Tumor Cells, Cultured | Lung Neoplasms - genetics | Liver Neoplasms - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Dual-Specificity Phosphatases - metabolism | Heat-Shock Proteins - metabolism | Mitogen-Activated Protein Kinase Phosphatases - genetics | Xenograft Model Antitumor Assays | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Mice, Nude | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Protein Array Analysis | Mice | Mice, Inbred BALB C | Carcinoma, Hepatocellular - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinase Phosphatases - metabolism | Liver | Extracellular signal-regulated kinase | Hepatocellular carcinoma | Metastasis | Metastases | Liver cancer | Signal transduction | Signaling | Stress response | Binding sites | Cellular stress response | Tumors | Apoptosis | Cancer | Liver Neoplasms | Lung Neoplasms | Life Sciences | Tumor Protein p73 | Heat-Shock Proteins | Mitogen-Activated Protein Kinase Phosphatases | Carcinoma, Hepatocellular | Dual-Specificity Phosphatases | Mitogen-Activated Protein Kinase 1 | Mitogen-Activated Protein Kinase 3 | Carrier Proteins
Journal Article
by Chu, Y and Yang, X
Oncogene, ISSN 1476-5594, 2010, Volume 30, Issue 9, pp. 1108 - 1116
.... Despite increasing recognition of the importance of this process, an extremely limited number of small ubiquitin-like modifier (SUMO) protein ligases (E3s... 
Mdm2 | TRIM proteins | sumoylation | SUMOE3 ligase | PML | p53 | BIOCHEMISTRY & MOLECULAR BIOLOGY | PML NUCLEAR-BODIES | DNA-DAMAGE | REGULATES P53 | FAMILY PROTEINS | SUMO E3 ligase | UBIQUITIN LIGASES | CELL BIOLOGY | RET FINGER PROTEIN | ONCOLOGY | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | C-JUN | Immunoprecipitation | Transcription Factors - chemistry | Humans | Tumor Suppressor Protein p53 - genetics | DNA-Binding Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - genetics | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Protein Interaction Domains and Motifs | Nuclear Proteins - genetics | Proto-Oncogene Proteins c-mdm2 - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | Small Ubiquitin-Related Modifier Proteins - metabolism | Tumor Suppressor Protein p53 - metabolism | Ubiquitin-Protein Ligases - metabolism | Nuclear Proteins - metabolism | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Nuclear Proteins - chemistry | DNA-Binding Proteins - chemistry | Transcription Factors - metabolism | Animals | Small Ubiquitin-Related Modifier Proteins - chemistry | Ubiquitin-Conjugating Enzymes - metabolism | Protein Binding | Sumoylation | RNA, Small Interfering | Ubiquitin-Protein Ligases - genetics | Microscopy, Fluorescence | Promyelocytic Leukemia Protein | Physiological aspects | Tumor suppressor genes | Research | Tumor proteins | Ligases | Proteins | Enzymes | Biochemistry | Cellular biology | Gene expression
Journal Article
PloS one, ISSN 1932-6203, 05/2009, Volume 4, Issue 5, pp. e5622 - e5622
Background: The INK4/ARF locus encodes three tumor suppressor genes (p15(Ink4b), Arf and p16(Ink4a)) and is frequently inactivated in a large number of human... 
INACTIVATION | MAMMALIAN TRITHORAX | DELAYED REPLICATION | METHYLATION | DOMAIN | GROUP GENE | MULTIDISCIPLINARY SCIENCES | METHYLTRANSFERASE ACTIVITY | MLL | CELLULAR SENESCENCE | HISTONE | NIH 3T3 Cells | Myeloid-Lymphoid Leukemia Protein - metabolism | Cellular Senescence | Repressor Proteins - metabolism | Fibroblasts - metabolism | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Cycle Proteins - metabolism | Gene Silencing | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Nuclear Proteins - metabolism | Polycomb-Group Proteins | Enhancer of Zeste Homolog 2 Protein | Polycomb Repressive Complex 2 | Animals | Cyclin-Dependent Kinase Inhibitor p16 - chemistry | Polycomb Repressive Complex 1 | Histone-Lysine N-Methyltransferase - metabolism | Embryo, Mammalian - cytology | Models, Biological | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Protein Binding | DNA Replication Timing | Fibroblasts - cytology | Mice | Histones - metabolism | Methylation | Proteins | Epigenetic inheritance | DNA replication | Senescence | Chromatin | Genes | INK4a protein | Genomes | Recruitment | Cell growth | Transcription activation | Cell cycle | Fibroblasts | Cyclin-dependent kinase inhibitors | Dissociation | Deoxyribonucleic acid--DNA | p16 Protein | INK4 protein | Embryo fibroblasts | Gene expression | Embryos | Loci | DNA biosynthesis | Polycomb group proteins | Replication origins | Pilot projects | Insects | Stem cells | Epigenetics | Tumor suppressor genes | Replication | Embryo, Mammalian | Histone-Lysine N-Methyltransferase | Repressor Proteins | Cell Aging | Nuclear Proteins | Cyclin-Dependent Kinase Inhibitor p16 | Life Sciences | Immunology | Histones | Myeloid-Lymphoid Leukemia Protein | Proto-Oncogene Proteins | Cell Cycle Proteins | Deoxyribonucleic acid | DNA
Journal Article
Oncogene, ISSN 0950-9232, 11/2003, Volume 22, Issue 50, pp. 8102 - 8116
Journal Article
Molecular cell, ISSN 1097-2765, 2009, Volume 36, Issue 3, pp. 487 - 499
.... BAK, an integral mitochondrial membrane protein, has bypassed the first activation step, explaining why its killing kinetics are faster than those of... 
CELLCYCLE | CYTOCHROME-C | PROAPOPTOTIC BAX | OLIGOMERIZES BAK | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOPLASMIC-RETICULUM | SUBCELLULAR LOCATION | PROTEINS | BCL-2 FAMILY-MEMBERS | BH3 DOMAIN | CELL-DEATH | MEMBRANE PERMEABILIZATION | CELL BIOLOGY | bcl-2-Associated X Protein - chemistry | Immunoprecipitation | Apoptosis - drug effects | Protein Multimerization | bcl-2 Homologous Antagonist-Killer Protein - genetics | Immunoblotting | BH3 Interacting Domain Death Agonist Protein - genetics | Green Fluorescent Proteins - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Bcl-2-Like Protein 11 | Protein Binding - drug effects | Tumor Suppressor Proteins - genetics | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Fibroblasts - metabolism | Proto-Oncogene Proteins - metabolism | Green Fluorescent Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Etoposide - pharmacology | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Tunicamycin - pharmacology | Fibroblasts - drug effects | Thapsigargin - pharmacology | Fibroblasts - cytology | Mice | Mutation | Microscopy, Fluorescence | Staurosporine - pharmacology | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Monomers | Apoptosis | Oligomers
Journal Article
Cell death & disease, ISSN 2041-4889, 04/2016, Volume 7, Issue 4, pp. e2195 - e2195
Inactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously... 
CISPLATIN | DNA-DAMAGE RESPONSE | P53 ACTIVATION | KINASE | GAMMA-H2AX | HISTONE H2AX | ATM | TP53 MUTATIONS | WIP1 | H2AX PHOSPHORYLATION | CELL BIOLOGY | Apoptosis - drug effects | Protein Phosphatase 2C - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Caspase 3 - metabolism | Antineoplastic Agents - therapeutic use | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Colorectal Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Colorectal Neoplasms - mortality | DNA Damage - drug effects | Carrier Proteins - antagonists & inhibitors | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Mice, Transgenic | Nuclear Proteins - metabolism | Survival Rate | Mitochondria - metabolism | Cisplatin - pharmacology | Tumor Suppressor Protein p53 - deficiency | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Cisplatin - therapeutic use | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Histones - metabolism | Protein Phosphatase 2C - genetics | Colorectal Neoplasms - pathology | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Phosphorylation | Cancer therapies | Apoptosis | Tumors | Protein-Serine-Threonine Kinases | Cellular Biology | Life Sciences | Mitochondria | Histones | Caspase 3 | Colorectal Neoplasms | Carrier Proteins | Protein Phosphatase 2C | Antineoplastic Agents | G2 Phase Cell Cycle Checkpoints | Cisplatin | Nuclear Proteins | Tumor Suppressor Protein p53 | DNA Damage | Protein-Tyrosine Kinases | Cell Cycle Proteins | Original
Journal Article
EMBO reports, ISSN 1469-3178, 2009, Volume 11, Issue 1, pp. 45 - 51
.... Recent evidence indicates that autophagy mediates selective removal of protein aggregates, organelles and microbes in cells... 
mitophagy | Nix | LC3 | GABARAP | selective autophagy | Selective autophagy | Mitophagy | APOPTOSIS | PROTEIN | RETICULOCYTE MATURATION | UBIQUITIN | BNIP3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | E3 | CELL-DEATH | CELL BIOLOGY | STRUCTURAL BASIS | DEGRADATION | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Humans | Cercopithecus aethiops | Molecular Sequence Data | Substrate Specificity | Autophagy - physiology | Mitochondrial Proteins - genetics | Proto-Oncogene Proteins - chemistry | Mitochondrial Proteins - metabolism | Tumor Suppressor Proteins - chemistry | Tumor Suppressor Proteins - genetics | Membrane Proteins - metabolism | Binding Sites | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cells, Cultured | Ubiquitin-Protein Ligases - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Saccharomyces cerevisiae Proteins - genetics | Blotting, Western | Amino Acid Motifs | Autophagy-Related Protein 8 Family | Animals | Membrane Proteins - chemistry | Reticulocytes - cytology | Mitochondrial Proteins - chemistry | Saccharomyces cerevisiae Proteins - metabolism | Protein Binding | Mice | Receptors, GABA-A - metabolism | COS Cells | Proteins | Mitochondria | Cellular biology | Cytoplasm | Scientific Report
Journal Article