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EMBO reports, ISSN 1469-221X, 01/2010, Volume 11, Issue 1, pp. 45 - 51
Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy... 
mitophagy | Nix | LC3 | GABARAP | selective autophagy | Selective autophagy | Mitophagy | APOPTOSIS | PROTEIN | RETICULOCYTE MATURATION | UBIQUITIN | BNIP3 | BIOCHEMISTRY & MOLECULAR BIOLOGY | 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
Molecular Cell, ISSN 1097-2765, 2005, Volume 17, Issue 3, pp. 393 - 403
Apoptosis is initiated when Bcl-2 and its prosurvival relatives are engaged by proapoptotic BH3-only proteins via interaction of its BH3 domain with a groove... 
CYTOCHROME-C | COMPLEX | SURVIVAL FACTOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIA | BIM | RELEASE | PEPTIDE | CELL-DEATH | FAMILY | MEMBER | CELL BIOLOGY | Humans | Molecular Sequence Data | Proto-Oncogene Proteins - chemistry | Neoplasm Proteins - metabolism | Genetic Complementation Test | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Carrier Proteins - chemistry | Proto-Oncogene Proteins c-bcl-2 - chemistry | Membrane Proteins - metabolism | Neoplasm Proteins - genetics | Peptide Fragments - genetics | Cell Survival - physiology | Binding, Competitive | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | Amino Acid Sequence | bcl-X Protein | Peptide Fragments - metabolism | Membrane Proteins - genetics | Models, Molecular | Recombinant Proteins - chemistry | Neoplasm Proteins - chemistry | Proto-Oncogene Proteins - genetics | Recombinant Proteins - genetics | Proteins - genetics | Sequence Homology, Amino Acid | Carrier Proteins - genetics | Peptide Fragments - chemistry | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Proteins - metabolism | Membrane Proteins - chemistry | Models, Biological | Myeloid Cell Leukemia Sequence 1 Protein | Biosensing Techniques | Ligands | Mice | Apoptosis - physiology | Proteins - chemistry | In Vitro Techniques | Proto-Oncogene Proteins c-bcl-2 - genetics
Journal Article
Nature Medicine, ISSN 1078-8956, 08/2012, Volume 18, Issue 8, pp. 1239 - 1247
The inactivation of the p53 tumor suppressor pathway, which often occurs through mutations in TP53 (encoding tumor protein 53) is a common step in human... 
MEDICINE, RESEARCH & EXPERIMENTAL | N-RAS | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR ACTIVITY | STAPLED P53 | BRAF | MALIGNANT-MELANOMA | P53 PATHWAY | CELL-DEATH | CELL BIOLOGY | BREAST-CANCER | METASTATIC MELANOMA | IN-VIVO | Up-Regulation | Proto-Oncogene Proteins c-mdm2 - genetics | Tumor Suppressor Protein p53 - antagonists & inhibitors | Apoptosis - drug effects | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Recombinant Fusion Proteins - physiology | Skin Neoplasms - chemistry | Male | Melanocytes - metabolism | Neoplasm Proteins - antagonists & inhibitors | Cell Line, Tumor - transplantation | Proto-Oncogene Proteins - biosynthesis | Tumor Suppressor Protein p53 - physiology | Cell-Penetrating Peptides - pharmacology | Nuclear Proteins - biosynthesis | Female | Antineoplastic Agents - pharmacology | Neoplasm Proteins - genetics | Nuclear Proteins - genetics | Cell Line, Tumor - metabolism | Melanoma - chemistry | Proto-Oncogene Proteins c-mdm2 - biosynthesis | Proto-Oncogene Proteins - antagonists & inhibitors | Tumor Stem Cell Assay | Membrane Proteins - genetics | Neoplasm Proteins - biosynthesis | Melanoma, Experimental - etiology | Mice, Inbred C57BL | Mice, Transgenic | Proto-Oncogene Proteins - genetics | Melanoma - pathology | Melanoma - secondary | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | Melanoma, Experimental - genetics | GTP Phosphohydrolases - genetics | Keratinocytes - metabolism | Mice, Nude | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Signal Transduction - physiology | Mice | Nuclear Proteins - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Care and treatment | Gene mutations | Melanoma | Diagnosis | Research | Gene expression | Identification and classification | Skin cancer | Proteins | Cell growth | Mutation | Cell cycle
Journal Article
Science, ISSN 0036-8075, 12/2010, Volume 330, Issue 6009, pp. 1390 - 1393
Although the proteins BAX and BAK are required for initiation of apoptosis at the mitochondria, how BAX and BAK are activated remains unsettled. We provide in... 
T lymphocytes | Mitochondria | Cytokines | Thymocytes | Neurons | Cell death | REPORTS | Cytochromes | Mice | Potassium | Apoptosis | NEURONAL APOPTOSIS | CYTOCHROME-C | MITOCHONDRIAL APOPTOSIS | MECHANISM | MULTIDISCIPLINARY SCIENCES | BH3 DOMAINS | RELEASE | JNK PATHWAY | PROTEINS | BCL-2 FAMILY-MEMBERS | MEMBRANE PERMEABILIZATION | BH3 Interacting Domain Death Agonist Protein - deficiency | T-Lymphocytes - physiology | bcl-2-Associated X Protein - chemistry | Protein Multimerization | Stress, Physiological | bcl-2 Homologous Antagonist-Killer Protein - genetics | BH3 Interacting Domain Death Agonist Protein - genetics | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Membrane Proteins - deficiency | Caspases - metabolism | Bcl-2-Like Protein 11 | Apoptosis Regulatory Proteins - deficiency | Tumor Suppressor Proteins - deficiency | Tumor Suppressor Proteins - genetics | Neurons - physiology | Apoptosis Regulatory Proteins - genetics | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | bcl-2-Associated X Protein - genetics | Proto-Oncogene Proteins - metabolism | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Cytochromes c - metabolism | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Mitochondria - metabolism | Permeability | Proto-Oncogene Proteins - deficiency | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Models, Biological | Cerebellum - cytology | Intracellular Membranes - metabolism | bcl-2 Homologous Antagonist-Killer Protein - chemistry | Protein research | Genetic aspects | Mitochondrial DNA | Biochemical genetics | Research | Properties | Methods
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 04/2008, Volume 28, Issue 7, pp. 2426 - 2436
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
INACTIVATION | APOPTOSIS | PROTEIN | SIGNALING PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSCRIPTION | YAP | SIZE-CONTROL | DIFFERENTIATION | DROSOPHILA | TUMOR-SUPPRESSOR PATHWAY | CELL BIOLOGY | 14-3-3 Proteins - physiology | Phosphorylation | Transferases (Other Substituted Phosphate Groups) - genetics | Humans | Receptor Protein-Tyrosine Kinases - physiology | Recombinant Fusion Proteins - physiology | Transferases (Other Substituted Phosphate Groups) - physiology | Mesoderm - cytology | Drosophila Proteins - physiology | Cell Transdifferentiation - physiology | Membrane Proteins - physiology | Cell Division | c-Mer Tyrosine Kinase | Cell Cycle Proteins - genetics | Conserved Sequence | Transcription, Genetic | Epithelial Cells - cytology | Proteins - physiology | Nerve Tissue Proteins - physiology | Transcription Factors - physiology | Membrane Proteins - genetics | Protein-Serine-Threonine Kinases - physiology | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Protein Processing, Post-Translational - physiology | Amino Acid Motifs | Proteins - genetics | Receptor Protein-Tyrosine Kinases - genetics | Cell Transformation, Neoplastic | Proto-Oncogene Proteins - physiology | Cell Line, Tumor | Nuclear Proteins - physiology | Drosophila Proteins - genetics | Cell Cycle Proteins - physiology | Cell Movement
Journal Article
Nature Immunology, ISSN 1529-2908, 12/2013, Volume 14, Issue 12, pp. 1247 - 1255
The inflammasome adaptor ASC contributes to innate immunity through the activation of caspase-1. Here we found that signaling pathways dependent on the kinases... 
LISTERIA-MONOCYTOGENES | AIM2 INFLAMMASOME | PROTEIN | INNATE IMMUNE-RESPONSES | MACROPHAGES | KINASE | HOST-DEFENSE | NLRP3 INFLAMMASOME | IMMUNOLOGY | CASPASE-1 ACTIVATION | VIRAL-INFECTION | Interleukin-18 - immunology | Inflammasomes - metabolism | Cytoskeletal Proteins - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Protein-Tyrosine Kinases - metabolism | Dendritic Cells - immunology | Humans | JNK Mitogen-Activated Protein Kinases - immunology | Caspase 1 - metabolism | Immunoblotting | Intracellular Signaling Peptides and Proteins - metabolism | RNA Interference | Bone Marrow Cells - immunology | Phosphorylation - immunology | JNK Mitogen-Activated Protein Kinases - genetics | Intracellular Signaling Peptides and Proteins - genetics | Syk Kinase | Carrier Proteins - immunology | DNA-Binding Proteins | Tyrosine - immunology | Mice, Knockout | Macrophages - metabolism | Tyrosine - metabolism | Lipopolysaccharides - pharmacology | Mice | Interleukin-18 - metabolism | Intracellular Signaling Peptides and Proteins - immunology | JNK Mitogen-Activated Protein Kinases - metabolism | Caspase 1 - immunology | Protein-Tyrosine Kinases - immunology | Protein-Tyrosine Kinases - genetics | HEK293 Cells | Cytoskeletal Proteins - metabolism | Female | Nuclear Proteins - genetics | Dendritic Cells - metabolism | Macrophages - immunology | Mice, Inbred C57BL | Cells, Cultured | Nuclear Proteins - metabolism | Nuclear Proteins - immunology | Inflammasomes - genetics | Carrier Proteins - genetics | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Cytoskeletal Proteins - immunology | CARD Signaling Adaptor Proteins | Inflammasomes - immunology | Macrophages - drug effects | Nigericin - pharmacology | Bone Marrow Cells - metabolism | Tyrosine - genetics | Cellular signal transduction | Inflammation | Genetic aspects | Research | Properties | Phosphotransferases
Journal Article
Molecular Cell, ISSN 1097-2765, 11/2009, Volume 36, Issue 3, pp. 487 - 499
While activation of BAX/BAK by BH3-only molecules (BH3s) is essential for mitochondrial apoptosis, the underlying mechanisms remain unsettled. Here we... 
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
Science, ISSN 0036-8075, 2/2007, Volume 315, Issue 5813, pp. 856 - 859
A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential... 
Research fellowships | Protein isoforms | Medical research | Myeloid cells | Antibodies | Cytochromes | Ligands | Reports | Grants | Viability | Apoptosis | RESPONSES | FAMILY-MEMBERS | X-L | MULTIDISCIPLINARY SCIENCES | BIM | HELIX | MITOCHONDRIAL-MEMBRANE | PUMA | DOMAINS | BH3-ONLY PROTEINS | CELL-DEATH | bcl-2-Associated X Protein - chemistry | Humans | BH3 Interacting Domain Death Agonist Protein - genetics | Proto-Oncogene Proteins - chemistry | Neoplasm Proteins - metabolism | bcl-2 Homologous Antagonist-Killer Protein - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Bcl-2-Like Protein 11 | Tumor Suppressor Proteins - genetics | BH3 Interacting Domain Death Agonist Protein - chemistry | Apoptosis Regulatory Proteins - genetics | bcl-Associated Death Protein - metabolism | Membrane Proteins - metabolism | BH3 Interacting Domain Death Agonist Protein - metabolism | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | Membrane Proteins - genetics | Apoptosis Regulatory Proteins - chemistry | Cells, Cultured | bcl-2-Associated X Protein - metabolism | Proto-Oncogene Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Animals | Proteins - metabolism | Membrane Proteins - chemistry | Models, Biological | Myeloid Cell Leukemia Sequence 1 Protein | Mice | Mutation | bcl-X Protein - metabolism | Research | Peptides | Analysis
Journal Article
EMBO reports, ISSN 1469-221X, 06/2017, Volume 18, Issue 6, pp. 947 - 961
Journal Article