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Endocrinology, ISSN 0013-7227, 05/2014, Volume 155, Issue 5, pp. 1970 - 1981
FSH is an essential regulator of mammalian reproduction. Its synthesis by pituitary gonadotrope cells is regulated by multiple endocrine and paracrine factors,... 
PATHWAYS | GROWTH-FACTOR-BETA | ACTIVATION | ACTIVIN-A INDUCTION | TGF-BETA | L45 LOOP | II RECEPTOR | TRANSCRIPTION | KINASE | ENDOCRINOLOGY & METABOLISM | HORMONE BETA-SUBUNIT | Phosphorylation | Humans | Activins - antagonists & inhibitors | Activins - metabolism | Gonadotrophs - metabolism | Smad3 Protein - metabolism | Smad2 Protein - antagonists & inhibitors | Smad3 Protein - genetics | Bone Morphogenetic Protein 2 - metabolism | Smad2 Protein - genetics | Follicle Stimulating Hormone, beta Subunit - metabolism | Bone Morphogenetic Protein Receptors, Type I - agonists | Transcription, Genetic | Follicle Stimulating Hormone, beta Subunit - biosynthesis | Genes, Reporter | Bone Morphogenetic Protein Receptors, Type I - antagonists & inhibitors | Recombinant Proteins - metabolism | Bone Morphogenetic Protein 2 - agonists | Bone Morphogenetic Protein 2 - genetics | Cell Line | Signal Transduction | Bone Morphogenetic Protein 2 - antagonists & inhibitors | Gene Silencing | Smad2 Protein - metabolism | Bone Morphogenetic Protein Receptors, Type I - genetics | Recombinant Proteins - chemistry | Bone Morphogenetic Protein Receptors, Type I - metabolism | Smad3 Protein - antagonists & inhibitors | Animals | Follicle Stimulating Hormone, beta Subunit - genetics | Mice | Protein Processing, Post-Translational | RNA, Small Interfering
Journal Article
Haematologica, ISSN 0390-6078, 2016, Volume 101, Issue 3, pp. 297 - 308
Iron overload results in significant morbidity and mortality in beta-thalassemic patients. Insufficient hepcidin is implicated in parenchymal iron overload in... 
CROSS-TALK | IRON-METABOLISM | TGF-BETA | BONE MORPHOGENETIC PROTEIN-2 | INEFFECTIVE ERYTHROPOIESIS | IN-VIVO | DOWN-REGULATION | MOUSE-LIVER | BETA-THALASSEMIA | HEMATOLOGY | ERYTHROID REGULATOR | Hepcidins - metabolism | beta-Thalassemia - pathology | Nitriles - pharmacology | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | beta-Thalassemia - genetics | Apoproteins - pharmacology | Hepatocytes - metabolism | RNA, Messenger - metabolism | Bone Morphogenetic Protein 6 - genetics | Liver - drug effects | Bone Morphogenetic Protein 2 - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | RNA, Messenger - antagonists & inhibitors | Muscle Proteins - metabolism | Hepcidins - agonists | Phosphorylation - drug effects | Cytokines - genetics | Hepcidins - antagonists & inhibitors | Hepatocytes - drug effects | Disease Models, Animal | Bone Morphogenetic Protein 2 - agonists | Bone Morphogenetic Protein 2 - genetics | Butadienes - pharmacology | Cytokines - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Liver - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | RNA, Messenger - genetics | Bone Morphogenetic Protein 2 - antagonists & inhibitors | Gene Expression Regulation | Antibodies, Neutralizing - pharmacology | Mice, Transgenic | Smad Proteins - genetics | Muscle Proteins - genetics | Animals | Bone Morphogenetic Protein 6 - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Hepcidins - genetics | Mice | beta-Thalassemia - metabolism | Smad Proteins - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Transferrin - pharmacology
Journal Article
Toxicology and Applied Pharmacology, ISSN 0041-008X, 02/2017, Volume 316, pp. 63 - 73
Journal Article
Endocrine Journal, ISSN 0918-8959, 2013, Volume 60, Issue 12, pp. 1309 - 1319
Fibrodysplasia ossificans progressiva (FOP) is a skeletal disorder with progressive heterotopic ossification in skeletal muscle. A mutation causing... 
Fibrodysplasia ossificans progressiva | Osteoblast | Matrix metalloproteinase-10 | Bone morphogenetic protein | Muscle ossification | CHONDROCYTES | CRUCIAL ROLE | MATRIX-METALLOPROTEINASE-2 | MUTATION | GROWTH | ENDOCRINOLOGY & METABOLISM | HUMAN BONE | TRANSCRIPTION FACTOR | EXPRESSION | SKELETAL DEVELOPMENT | Smad7 Protein - agonists | Humans | Osteocalcin - genetics | Myoblasts - metabolism | Collagen Type I - genetics | RNA Interference | Bone Morphogenetic Protein 2 - metabolism | Myoblasts - cytology | Matrix Metalloproteinase 10 - metabolism | Cell Differentiation | Osteoblasts - cytology | Smad6 Protein - genetics | Smad7 Protein - genetics | Osteocalcin - agonists | Smad7 Protein - metabolism | Recombinant Proteins - metabolism | Bone Morphogenetic Protein 2 - agonists | Bone Morphogenetic Protein 2 - genetics | Cell Line | Matrix Metalloproteinase 10 - genetics | Collagen Type I - metabolism | Osteoblasts - enzymology | Signal Transduction | Osteocalcin - metabolism | Matrix Metalloproteinase 10 - chemistry | Bone Morphogenetic Protein Receptors, Type I - genetics | Recombinant Proteins - chemistry | Activin Receptors, Type I - metabolism | Mutant Proteins - metabolism | Transcription Factors - genetics | Bone Morphogenetic Protein Receptors, Type I - metabolism | Activin Receptors, Type I - genetics | Gene Expression Regulation, Enzymologic | Transcription Factors - metabolism | Animals | Collagen Type I - agonists | Sp7 Transcription Factor | Mice | Smad6 Protein - agonists | Smad6 Protein - metabolism | Transcription Factors - agonists | Osteoblasts - metabolism | Myoblasts - enzymology | Amino Acid Substitution | Mutant Proteins - agonists
Journal Article
Journal Article
Life Sciences, ISSN 0024-3205, 2011, Volume 88, Issue 7, pp. 335 - 342
Journal Article
Journal Article
International journal of molecular medicine, 12/2011, Volume 28, Issue 6, p. 1049
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 01/2016, Volume 291, Issue 3, pp. 1148 - 1161
Background: Mutations in NFATc1 and BMP-2 genes result in bone abnormalities in mice. Results: BMP-2 activates intracellular Ca2+ release, thus activating... 
NF-ATC | RANKL | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CALCIUM | KINASE | RECEPTOR ACTIVATOR | DIFFERENTIATION | EXPRESSION | KAPPA-B LIGAND | OSTEOBLASTIC CELLS | Calcineurin - chemistry | NFATC Transcription Factors - agonists | Promoter Regions, Genetic - drug effects | Protein Processing, Post-Translational - drug effects | Smad5 Protein - metabolism | Bone Morphogenetic Protein 2 - metabolism | Calcium Chelating Agents - pharmacology | Osteoblasts - cytology | Phosphorylation - drug effects | Smad5 Protein - genetics | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Recombinant Proteins - metabolism | Bone Morphogenetic Protein 2 - genetics | Cell Line | NFATC Transcription Factors - metabolism | Osteoblasts - drug effects | Cells, Cultured | Rats | Recombinant Proteins - chemistry | Mice, Knockout | Gene Expression Regulation - drug effects | Animals | Signal Transduction - drug effects | Calcium Signaling - drug effects | Active Transport, Cell Nucleus - drug effects | Mice | Smad5 Protein - agonists | Osteoblasts - metabolism | Calcineurin - metabolism | NFATC Transcription Factors - genetics | phosphatidylinositol 3-kinase (PI 3-kinase) | Smad signaling | SMAD transcription factor | bone morphogenetic protein (BMP) | NFAT transcription factor | calcium-calcineurin signaling | NFATc1 | osteoblast | calcineurin | BMP-2 | Cell Biology
Journal Article
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 08/2017, Volume 292, Issue 33, pp. 13714 - 13726
Bone morphogenetic proteins 9 and 10 (BMP9/BMP10) are circulating cytokines with important roles in endothelial homeostasis. The aim of this study was to... 
ADHESION | LEUKOCYTE RECRUITMENT | INHIBITION | GENE | INFLAMMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CALCIFICATION | TNF-ALPHA | HYPERTENSION | EXPRESSION | ALK1 | Activin Receptors, Type I - antagonists & inhibitors | Endothelium, Vascular - cytology | Tumor Necrosis Factor-alpha - metabolism | Activin Receptors, Type II - metabolism | Monocytes - cytology | Humans | Activin Receptors, Type II - antagonists & inhibitors | Endothelium, Vascular - drug effects | Monocytes - metabolism | Monocytes - immunology | Tumor Necrosis Factor-alpha - agonists | Bone Morphogenetic Proteins - metabolism | Protein Processing, Post-Translational - drug effects | RNA Interference | E-Selectin - genetics | Aorta | Vascular Cell Adhesion Molecule-1 - genetics | Phosphorylation - drug effects | Endothelium, Vascular - immunology | Pyrazoles - pharmacology | Cells, Cultured | Activin Receptors, Type I - metabolism | E-Selectin - metabolism | Pyrimidines - pharmacology | Cell Adhesion - drug effects | Activin Receptors, Type I - genetics | Vascular Cell Adhesion Molecule-1 - chemistry | Monocytes - drug effects | Up-Regulation - drug effects | Growth Differentiation Factors - metabolism | Intercellular Adhesion Molecule-1 - metabolism | Intercellular Adhesion Molecule-1 - chemistry | Signal Transduction - drug effects | Endothelium, Vascular - metabolism | Intercellular Adhesion Molecule-1 - genetics | Activin Receptors, Type II - genetics | E-Selectin - chemistry | Protein Kinase Inhibitors - pharmacology | Kinetics | Vascular Cell Adhesion Molecule-1 - metabolism | atherosclerosis | monocyte | SMAD transcription factor | bone morphogenetic protein (BMP) | endothelial cell | Cell Biology
Journal Article