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PLoS Biology, ISSN 1544-9173, 2014, Volume 12, Issue 9, p. e1001952
Characterization of the genetic defects causing gonadotropic deficiency has made a major contribution to elucidation of the fundamental role of Kisspeptins and... 
V-ATPASE | CATALYTIC SUBUNIT | GDP/GTP EXCHANGE PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | HYPOMYELINATING LEUKODYSTROPHY | POL III | MUTATIONS | GTPASE-ACTIVATING PROTEIN | HYPOGONADOTROPIC HYPOGONADISM | NEUROKININ B | PUBERTY | Hypothyroidism - pathology | Hypothyroidism - metabolism | Testis - metabolism | Humans | Nerve Tissue Proteins - deficiency | Diabetes Mellitus, Type 1 - metabolism | Male | Luteinizing Hormone - metabolism | Polyneuropathies - metabolism | Intellectual Disability - metabolism | Young Adult | Infertility, Male - genetics | Base Sequence | Neurons - metabolism | Hypoglycemia - genetics | Gonadotropin-Releasing Hormone - genetics | Diabetes Mellitus, Type 1 - pathology | Intellectual Disability - pathology | Hypothalamus - pathology | Hypoglycemia - metabolism | Infertility, Male - pathology | Testis - growth & development | Mice, Knockout | Hypothalamus - metabolism | Testis - pathology | Adaptor Proteins, Signal Transducing - deficiency | Adolescent | Gonadotropin-Releasing Hormone - metabolism | Polyneuropathies - genetics | Mice | Neurons - pathology | Sequence Deletion | Hypothalamus - growth & development | Pituitary Gland - metabolism | Molecular Sequence Data | Hypoglycemia - pathology | Intellectual Disability - genetics | Hypothyroidism - genetics | Follicle Stimulating Hormone - genetics | Sexual Maturation | Follicle Stimulating Hormone - metabolism | Luteinizing Hormone - genetics | Pituitary Gland - pathology | Diabetes Mellitus, Type 1 - genetics | Pituitary Gland - growth & development | Nerve Tissue Proteins - genetics | Syndrome | Haploinsufficiency | Homozygote | Animals | Polyneuropathies - pathology | Adaptor Proteins, Signal Transducing - genetics | Infertility, Male - metabolism | Life Sciences | Human health and pathology | Neurons and Cognition | Neurobiology | Pituitary gland | Neurons | Infertility | Rodents
Journal Article
Journal Article
American Journal of Hematology, ISSN 0361-8609, 12/2014, Volume 89, Issue 12, pp. 1102 - 1106
Iron overload in β‐thalassemia major (TM) typically results in iron‐induced cardiomyopathy, liver disease, and endocrine complications. We examined the... 
IMPACT | TRANSFUSIONAL IRON OVERLOAD | MRI | MASS | REPLACEMENT THERAPY | IMPROVEMENT | COMPLICATIONS | PREVALENCE | HEMATOLOGY | HYPOGONADISM | NORTH-AMERICA | Diabetes Mellitus - pathology | Hypothyroidism - pathology | Hypothyroidism - metabolism | Benzoates - therapeutic use | Humans | Middle Aged | Child, Preschool | Male | Puberty, Delayed - metabolism | Iron Overload - etiology | Osteoporosis - metabolism | Hypogonadism - metabolism | Bone and Bones - metabolism | Diphosphonates - therapeutic use | Child | Triazoles - therapeutic use | Iron Chelating Agents - therapeutic use | Hypoparathyroidism - metabolism | beta-Thalassemia - drug therapy | Puberty, Delayed - pathology | Diabetes Mellitus - prevention & control | Osteoporosis - pathology | Adolescent | beta-Thalassemia - metabolism | Hypogonadism - etiology | beta-Thalassemia - pathology | Bone and Bones - pathology | Iron Overload - drug therapy | Calcium - administration & dosage | Chelation Therapy | beta-Thalassemia - complications | Hypoparathyroidism - pathology | Hypoparathyroidism - prevention & control | Iron Overload - pathology | Osteoporosis - etiology | Bone and Bones - drug effects | Hypogonadism - prevention & control | Iron Overload - metabolism | Puberty, Delayed - etiology | Adult | Diabetes Mellitus - etiology | Female | Vitamin D - administration & dosage | Retrospective Studies | Hypothyroidism - prevention & control | Hypogonadism - pathology | Bone Density | Osteoporosis - prevention & control | Diabetes Mellitus - metabolism | Hypothyroidism - etiology | Puberty, Delayed - prevention & control | Hypoparathyroidism - etiology
Journal Article
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
Neurobiology of Disease, ISSN 0969-9961, 12/2016, Volume 96, pp. 227 - 235
Journal Article