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المؤلفون: Gareth J. Browne, Loredana Zocchi, Martina Malatesta, Aaron Ciechanover, Francesca Bernassola, Angelo Peschiaroli, Ewen Gallagher, Richard A. Knight, Mario Rossi, Rami I. Aqeilan, Flavia Scialpi, Gerry Melino
المصدر: Cell death and differentiation. 15(7)
مصطلحات موضوعية: adaptor protein, cytokine, mutant protein, Notch receptor, protein c jun, protein Itch, regulator protein, transcription factor, transforming growth factor beta, ubiquitin protein ligase E3, apoptosis, autoimmune disease, autoimmunity, binding affinity, carboxy terminal sequence, cell differentiation, cell fate, cell growth, cell proliferation, cell renewal, cell stress, clonal anergy, disease course, DNA damage, enzyme activation, enzyme activity, enzyme analysis, enzyme localization, enzyme specificity, enzyme substrate, epidermis cell, gene expression regulation, gene mutation, growth regulation, human, immune response, immunological tolerance, immunopathogenesis, immunopathology, immunoregulation, inflammation, keratinocyte, lung disease, lymphocyte differentiation, malignant neoplastic disease, malignant transformation, mutational analysis, nonhuman, pathophysiology, priority journal, protein binding, protein degradation, protein expression, protein family, protein phosphorylation, protein processing, protein protein interaction, protein stability, regulatory mechanism, review, signal transduction, skin disease, T lymphocyte activation, transcription regulation, ubiquitination, Animals, Cell Death, Immune System, Keratinocytes, Mice, Mice, Mutant Strains, Neoplasms, Phosphorylation, Protein Transport, Receptor, Epidermal Growth Factor, Receptors, Chemokine, Repressor Proteins, Signal Transduction, Skin, Substrate Specificity, Transforming Growth Factor beta, TRPC Cation Channels, Ubiquitin, Ubiquitin-Protein Ligases, Agouti, Mus, skin and connective tissue diseases, Settore BIO/11, Ubiquitin ligase, ErbB Receptors, Molecular Biology, Epidermal Growth Factor, Immunology, Chemokine, Receptors, biology, Mutant Strains, medicine.symptom, Signal transduction, Receptor, Inflammation, Immune system, Immunity, medicine, Cell Biology, Transforming growth factor beta, biology.protein
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d75d8a9d69263a342ecb749494c14652Test
https://pubmed.ncbi.nlm.nih.gov/18552861Test -
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المؤلفون: Marco Ranalli, Massimo Federici, Alessandro Terrinoni, Gennaro Citro, Ornella Massa, Marco Corazzari, Fabrizio Barbetti, Vincenzo De Laurenzi, Gerry Melino, W.H. Irwin McLean, Francesca Bernassola, Giorgio Sesti, Marta Letizia Hribal
مصطلحات موضوعية: Male, amidation, medicine.medical_treatment, Sequence Homology, animal cell, Biochemistry, Mice, Models, protein cross linking, Insulin, Child, Cells, Cultured, Cultured, integumentary system, Settore BIO/11, disease course, Intracellular Signaling Peptides and Proteins, protein glutamine gamma glutamyltransferase, reaction analysis, Italy, priority journal, Knockout mouse, Type 2, medicine.medical_specialty, pancreas islet beta cell, Cells, Knockout, Molecular Sequence Data, animal tissue, Islets of Langerhans, Genetics, Diabetes Mellitus, Humans, Secretion, human, Amino Acid Sequence, Molecular Biology, mouse, catalysis, animal model, Molecular, Glucose Tolerance Test, transglutaminase 2, Receptor, Insulin, Endocrinology, Diabetes Mellitus, Type 2, Mutation, knockout mouse, Models, Molecular, Blood Glucose, Tissue transglutaminase, glucose tolerance, maturity onset diabetes mellitus, calcium transport, insulin release, gene mutation, glucose, Phosphorylation, Mice, Knockout, Glucose tolerance test, medicine.diagnostic_test, article, unclassified drug, Amino Acid, enzyme active site, enzyme regulation, gene disruption, Biotechnology, Receptor, Insulin Receptor Substrate Proteins, Adolescent, animal experiment, Mutation, Missense, Biology, GTP-Binding Proteins, Internal medicine, medicine, Animals, Animalia, Protein Glutamine gamma Glutamyltransferase 2, controlled study, gene identification, nonhuman, Transglutaminases, Sequence Homology, Amino Acid, disease model, missense mutation, insulin receptor substrate 2, Phosphoproteins, IRS2, Glutamine, Kinetics, hypoglycemia, biology.protein, Missense
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::05790ed133c4df7b6858d7f40c222f33Test
http://hdl.handle.net/11573/1312571Test