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EMBO reports, ISSN 1469-3178, 2009, Volume 10, Issue 2, pp. 173 - 179
Ubiquilins (UBQLNs) are adaptor proteins thought to deliver ubiquitinated substrates to proteasomes... 
ubiquitin‐like | PLIC | autophagy | ubiquilin | autophagosomes | APOPTOSIS | ubiquitin-like | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL AUTOPHAGY | MITOPHAGY | DEATH | MATURATION | HUNTINGTIN | INCLUSION-BODY FORMATION | CELL BIOLOGY | PROTEASOME | DEGRADATION | PROMOTES | Ubiquitin-Activating Enzymes - physiology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Ubiquitins - genetics | Humans | Adaptor Proteins, Vesicular Transport - genetics | Recombinant Fusion Proteins - physiology | Autophagy - physiology | Autophagy - drug effects | Microscopy, Immunoelectron | Cell Cycle Proteins - antagonists & inhibitors | Recombinant Fusion Proteins - antagonists & inhibitors | RNA Interference | Cell Cycle Proteins - genetics | Carrier Proteins - physiology | Protein Structure, Tertiary | Ubiquitin-Activating Enzymes - genetics | Adaptor Proteins, Vesicular Transport - physiology | Adaptor Proteins, Vesicular Transport - antagonists & inhibitors | Phagosomes - metabolism | Carrier Proteins - antagonists & inhibitors | RNA, Small Interfering - physiology | Microtubule-Associated Proteins - antagonists & inhibitors | Ubiquitins - physiology | HeLa Cells - drug effects | Microtubule-Associated Proteins - physiology | Protein Interaction Mapping | Carrier Proteins - genetics | Autophagy-Related Protein 7 | Animals | Autophagy-Related Protein 5 | Ubiquitin-Activating Enzymes - antagonists & inhibitors | Culture Media - pharmacology | Mice | HeLa Cells - cytology | Cell Cycle Proteins - physiology | Ubiquitins - antagonists & inhibitors | Proteins | Genetics | Nutrients | Molecular biology | Substrates | Scientific Report
Journal Article
Journal Article
Nature medicine, ISSN 1546-170X, 2012, Volume 18, Issue 8, pp. 1239 - 1247
... (encoding tumor protein 53) is a common step in human cancer. However, in melanoma-A highly chemotherapy-resistant disease-TP53 mutations are rare, raising... 
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
The New England journal of medicine, ISSN 1533-4406, 2007, Volume 356, Issue 15, pp. 1517 - 1526
The expression of interleukin-1–receptor antagonist is reduced in pancreatic islets in type 2 diabetes, and high glucose concentrations induce interleukin-1β... 
INSULIN | MEDICINE, GENERAL & INTERNAL | OBESITY | ISLETS | GLUCOSE | BETA-CELL APOPTOSIS | MUSCLE | EXPRESSION | RECEPTOR ANTAGONIST | Recombinant Proteins - therapeutic use | Insulin-Secreting Cells - secretion | Glucose Transporter Type 4 - metabolism | Glycated Hemoglobin A - metabolism | Humans | Middle Aged | Male | Diabetes Mellitus, Type 2 - metabolism | RNA, Messenger - metabolism | Heat-Shock Proteins - genetics | Insulin Resistance - physiology | Interleukin-6 - blood | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Female | Interleukin 1 Receptor Antagonist Protein - pharmacology | Body Mass Index | Glucose Tolerance Test | Double-Blind Method | Glucose Transporter Type 4 - genetics | Heat-Shock Proteins - metabolism | C-Reactive Protein - secretion | Recombinant Proteins - pharmacology | Transcription Factors - genetics | Gene Expression Regulation - drug effects | Transcription Factors - metabolism | Interleukin 1 Receptor Antagonist Protein - therapeutic use | Insulin-Secreting Cells - drug effects | Interleukin 1 Receptor Antagonist Protein - adverse effects | Blood Glucose - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Receptors, Interleukin-1 - antagonists & inhibitors | Type 2 diabetes | Interleukin-1 | Research | Drug therapy | Pancreas | Diabetes | Apoptosis | Clinical Medicine | Endokrinologi och diabetes | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap | Endocrinology and Diabetes
Journal Article
Journal Article
Cancer Research, ISSN 0008-5472, 08/2011, Volume 71, Issue 15, pp. 5067 - 5074
...) or N-RAS which results in resistance or sensitivity to mitogen-activated protein (MAP)/extracellular signal-regulated... 
Apoptosis - drug effects | Humans | Multiprotein Complexes | Neoplasm Proteins - physiology | Recombinant Fusion Proteins - physiology | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Receptor, Platelet-Derived Growth Factor beta - genetics | Quinolines - pharmacology | Mechanistic Target of Rapamycin Complex 1 | Receptor, Platelet-Derived Growth Factor beta - antagonists & inhibitors | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Spheroids, Cellular - drug effects | MAP Kinase Kinase Kinases - antagonists & inhibitors | Proteins - physiology | Transcription Factors - physiology | Receptor, Platelet-Derived Growth Factor beta - physiology | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Imidazoles - pharmacology | Proto-Oncogene Proteins c-akt - physiology | Melanoma - pathology | Sulfonamides - pharmacology | Drug Synergism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Point Mutation | Vemurafenib | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Phosphatidylinositol 3-Kinases - physiology | Signal Transduction - physiology | TOR Serine-Threonine Kinases | Drug Resistance, Neoplasm - physiology | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Drug Screening Assays, Antitumor | vemurafenib | targeted therapy | melanoma | AKT | B-RAF | acquired resistance
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2017, Volume 292, Issue 39, pp. 16199 - 16210
Tumor cell invasion involves targeted localization of proteins required for interactions with the extracellular matrix and for proteolysis... 
MEMBRANE-FUSION | MIGRATION | GLUT4 TRANSLOCATION | SM PROTEIN | METALLOPROTEINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | TRAFFICKING | PLASMA-MEMBRANE | SNARE | VAMP3 | Qb-SNARE Proteins - chemistry | Adenocarcinoma - pathology | Humans | Protein Multimerization | Qb-SNARE Proteins - metabolism | Extracellular Matrix - metabolism | Munc18 Proteins - metabolism | Neoplasm Proteins - antagonists & inhibitors | Green Fluorescent Proteins - genetics | Fibrosarcoma - metabolism | Neoplasm Proteins - metabolism | Vesicle-Associated Membrane Protein 2 - antagonists & inhibitors | Recombinant Fusion Proteins - metabolism | Podosomes - metabolism | Qa-SNARE Proteins - chemistry | Receptor, Epidermal Growth Factor - metabolism | Adenocarcinoma - metabolism | Fibrosarcoma - pathology | Qc-SNARE Proteins - metabolism | RNA Interference | Vesicle-Associated Membrane Protein 2 - chemistry | Munc18 Proteins - chemistry | Qa-SNARE Proteins - genetics | Protein Interaction Domains and Motifs | Neoplasm Proteins - genetics | Peptide Fragments - genetics | Binding, Competitive | Green Fluorescent Proteins - metabolism | Peptide Fragments - metabolism | Munc18 Proteins - genetics | Neoplasm Invasiveness | Neoplasm Proteins - chemistry | Recombinant Fusion Proteins - chemistry | Matrix Metalloproteinase 14 - metabolism | Munc18 Proteins - antagonists & inhibitors | Protein Transport | Podosomes - pathology | Peptide Fragments - chemistry | Qc-SNARE Proteins - chemistry | Qa-SNARE Proteins - metabolism | Cell Line, Tumor | Qc-SNARE Proteins - antagonists & inhibitors | Qb-SNARE Proteins - antagonists & inhibitors | Vesicle-Associated Membrane Protein 2 - metabolism | Extracellular Matrix - pathology | invadopodia | epidermal growth factor receptor (EGFR) | matrix metalloproteinase (MMP) | syntaxin4 | cell invasion | trafficking | Munc18c | Cell Biology
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2016, Volume 291, Issue 9, pp. 4323 - 4333
...) undergo rapid remodeling into dynamic extracellular matrix-degrading rosettes by distinct G protein-coupled receptor agonists, notably lysophosphatidic acid (LPA... 
Receptors, Lysophosphatidic Acid - metabolism | Lysophospholipids - metabolism | Receptors, G-Protein-Coupled - metabolism | Humans | Extracellular Matrix - metabolism | Melanoma - enzymology | Podosomes - enzymology | Neoplasm Proteins - antagonists & inhibitors | Receptors, Lysophosphatidic Acid - agonists | Receptors, Lysophosphatidic Acid - genetics | cdc42 GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - genetics | Endothelins - metabolism | Neoplasm Proteins - metabolism | Time-Lapse Imaging | Podosomes - metabolism | RNA Interference | cdc42 GTP-Binding Protein - antagonists & inhibitors | Fluorescence Resonance Energy Transfer | Receptors, Lysophosphatidic Acid - antagonists & inhibitors | Neoplasm Proteins - genetics | Biomarkers - metabolism | Melanoma - metabolism | Recombinant Proteins - metabolism | rac1 GTP-Binding Protein - agonists | rhoA GTP-Binding Protein - antagonists & inhibitors | Recombinant Proteins - genetics | Melanoma - pathology | cdc42 GTP-Binding Protein - agonists | Hydrolysis | Podosomes - pathology | Microscopy, Confocal | Neoplasm Proteins - agonists | cdc42 GTP-Binding Protein - genetics | Receptors, G-Protein-Coupled - antagonists & inhibitors | rac1 GTP-Binding Protein - antagonists & inhibitors | Cell Line, Tumor | Luminescent Proteins - genetics | Receptors, G-Protein-Coupled - genetics | Extracellular Matrix - pathology | Microscopy, Fluorescence | rac1 GTP-Binding Protein - metabolism | Luminescent Proteins - metabolism | rac1 GTP-Binding Protein - genetics | CDC42 | invadopodia | biosensor | fluorescence resonance energy transfer (FRET) | calcium intracellular release | G protein-coupled receptor (GPCR) | Rho (Rho GTPase) | phosphatidylinositide 3-kinase (PI 3-kinase) | imaging | Rac (Rac GTPase) | Cell Biology
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 03/2017, Volume 24, Issue 3, pp. 481 - 491
Peptido-mimetic inhibitor of apoptosis protein (IAP) antagonists (Smac mimetics (SMs)) can kill tumour cells by depleting endogenous IAPs and thereby inducing tumour necrosis factor... 
TUMOR-NECROSIS-FACTOR | INTERFERON-GAMMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | ALPHA-DEPENDENT APOPTOSIS | RECEPTOR | FAS-MEDIATED APOPTOSIS | TNF-ALPHA | NF-KAPPA-B | SIGNALING COMPLEXES | EXPRESSION | CELL BIOLOGY | Protein Kinases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Caspase Inhibitors - pharmacology | Apoptosis - drug effects | Humans | Caspase 8 - metabolism | Caspase 8 - chemistry | Cytokine TWEAK - pharmacology | Interferon-gamma - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Recombinant Proteins - biosynthesis | Caspase 8 - genetics | Recombinant Proteins - isolation & purification | Receptors, Tumor Necrosis Factor, Type I - deficiency | Inhibitor of Apoptosis Proteins - antagonists & inhibitors | Pentanoic Acids - pharmacology | Inhibitor of Apoptosis Proteins - metabolism | Protein Kinases - deficiency | Interferon-gamma - genetics | Cell Line | Caspase 10 - metabolism | Recombinant Proteins - pharmacology | Receptors, Tumor Necrosis Factor, Type I - genetics | CRISPR-Cas Systems - genetics | Mice, Knockout | Drug Synergism | HT29 Cells | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Caspase 10 - genetics | Caspase 10 - chemistry | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Interferon-gamma - pharmacology | Original Paper
Journal Article
Biochemical journal, ISSN 1470-8728, 2013, Volume 454, Issue 2, pp. 201 - 208
.... However, only NAC, and not catalase or another ROS scavenger Trolox, was able to prevent effects linked to proteasome inhibition, such as protein stabilization, apoptosis and accumulation of ubiquitin conjugates... 
Catalase | N-acetyl-L-cysteine (NAC) | Proteasome inhibitor | Reactive oxygen species (ROS) | Forkhead box protein M1 (FOXM1) | CANCER-CELLS | TARGET | APOPTOSIS | OXIDATIVE STRESS | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | reactive oxygen species (ROS) | ENDOPLASMIC-RETICULUM STRESS | BORTEZOMIB | FOXM1 | INACTIVATION | proteasome inhibitor | LACTACYSTIN | catalase | Free Radical Scavengers - pharmacology | Oxidants - pharmacology | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Acetylcysteine - metabolism | Proteasome Inhibitors - chemistry | Proteasome Inhibitors - metabolism | Viral Proteins - metabolism | Antineoplastic Agents, Phytogenic - antagonists & inhibitors | Chromans - metabolism | Proteasome Endopeptidase Complex - drug effects | Chromans - pharmacology | Dioxolanes - pharmacology | Forkhead Transcription Factors - metabolism | Forkhead Transcription Factors - antagonists & inhibitors | Ubiquitinated Proteins - metabolism | Recombinant Proteins - metabolism | Recombinant Proteins - antagonists & inhibitors | Free Radical Scavengers - metabolism | Proteasome Inhibitors - pharmacology | Catalase - genetics | Chromans - antagonists & inhibitors | Hydrogen Peroxide - pharmacology | Viral Proteins - genetics | Oxidants - antagonists & inhibitors | Dioxolanes - antagonists & inhibitors | Forkhead Transcription Factors - genetics | Catalase - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Protein Stability - drug effects | Acetylcysteine - pharmacology | Cell Line, Tumor | Cytomegalovirus - enzymology | Proteasome Endopeptidase Complex - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Forkhead Box Protein M1 | Hydrogen Peroxide - antagonists & inhibitors | N-acetyl-l-cysteine (NAC)
Journal Article