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Journal of Clinical Investigation, ISSN 0021-9738, 01/2017, Volume 127, Issue 1, pp. 293 - 305
Prader-Willi syndrome (PWS) is caused by a loss of paternally expressed genes in an imprinted region of chromosome 15q. Among the canonical PWS phenotypes are... 
MEDICINE, RESEARCH & EXPERIMENTAL | PLASMA GHRELIN | BODY-WEIGHT | HORMONE-RELEASING-HORMONE | HYPERPHAGIA | FOOD-INTAKE | PROPROTEIN CONVERTASE-1 | ONSET OBESITY | KNOCKOUT MICE | CIRCULATING GHRELIN LEVELS | CHILDREN | Diabetes Mellitus - pathology | Neurons - pathology | Proinsulin - metabolism | Diabetes Mellitus - genetics | Humans | Male | Obesity - genetics | RNA, Small Nucleolar - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Hypogonadism - metabolism | Prader-Willi Syndrome - genetics | Female | Neurons - metabolism | Induced Pluripotent Stem Cells - metabolism | Hypogonadism - pathology | Induced Pluripotent Stem Cells - pathology | Basic Helix-Loop-Helix Transcription Factors - genetics | Protein Precursors - genetics | Diabetes Mellitus - metabolism | Proinsulin - genetics | Prader-Willi Syndrome - metabolism | Growth Hormone-Releasing Hormone - genetics | Hyperphagia - metabolism | Proprotein Convertase 1 - deficiency | RNA, Small Nucleolar - genetics | Mice, Knockout | Obesity - metabolism | Obesity - pathology | Protein Precursors - metabolism | Hyperphagia - genetics | Hyperphagia - pathology | Hypogonadism - genetics | Growth Hormone-Releasing Hormone - metabolism | Animals | Prader-Willi Syndrome - pathology | Prader-Willi syndrome | Gene expression | Neurons | Analysis | Risk factors | Proteins | Enzymes | Plasma | Obesity | Rodents | Fibroblasts | Patients | Binding sites
Journal Article
Journal of Immunology, ISSN 0022-1767, 12/2017, Volume 199, Issue 12, pp. 4066 - 4077
Regnase-1 and Roquin are RNA binding proteins that are essential for degradation of inflammatory mRNAs and maintenance of immune homeostasis. Although... 
EFFECTOR | ELEMENT | INTERFERON-GAMMA | RECOGNITION | REPRESSION | IMMUNE-RESPONSES | PROPROTEIN CONVERTASE FURIN | MECHANISMS | MESSENGER-RNA DECAY | IMMUNOLOGY | HELPER T-CELLS | Th1 Cells - pathology | Ribonucleases - genetics | Spleen - immunology | Ribonucleases - deficiency | Humans | Lymphopoiesis - genetics | Homeostasis | Th1 Cells - immunology | Ubiquitin-Protein Ligases - physiology | Recombinant Fusion Proteins - metabolism | RNA, Messenger - biosynthesis | Interleukin-4 - biosynthesis | Furin - genetics | Mice, Mutant Strains | Receptors, Interleukin-12 - genetics | Interferon-gamma - genetics | Interleukin-4 - genetics | 3' Untranslated Regions | Myocarditis - immunology | Myocarditis - genetics | Furin - biosynthesis | Specific Pathogen-Free Organisms | Gene Expression Regulation - immunology | Jurkat Cells | Lymphocyte Activation | Mice, Inbred C57BL | Interleukin-17 - genetics | Myocardium - pathology | Spleen - cytology | Interleukin-17 - biosynthesis | Receptors, Interleukin-12 - biosynthesis | Mice, Knockout | Animals | Fibrosis | Ubiquitin-Protein Ligases - deficiency | Ribonucleases - physiology | Mice | HeLa Cells | Ubiquitin-Protein Ligases - genetics | Interferon-gamma - biosynthesis | Heart | Polarization | Repressing | Helper cells | Activation | Lymphocytes T | Inflammation | T cell receptors | Lethality | mRNA | Proteins | Interleukin 4 | Cell activation | RNA-binding protein | Ribonucleic acids | Lymphocytes | Interleukin 1 | Furin | Mutation | Differentiation | Heart diseases
Journal Article
Journal Article
Journal Article
Analytical Chemistry, ISSN 0003-2700, 06/2015, Volume 87, Issue 12, pp. 6180 - 6185
Journal Article
Journal Article