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Scientific Reports, ISSN 2045-2322, 09/2016, Volume 6, Issue 1, p. 33504
BCL-2-associated athanogene-1 (BAG-1) is expressed by osteoblast-lineage cells; early embryonic lethality in Bag-1 null mice, however, has limited the investigation of BAG-1 function in osteoblast development... 
HIP FRACTURE | LATER LIFE | IN-VITRO | STROMAL CELL-LINES | MULTIDISCIPLINARY SCIENCES | RECEPTOR | GROWTH-FACTOR | DIFFERENTIATION | MOUSE BONE-MARROW | EXPRESSION | HEAT-SHOCK-PROTEIN | Bone Morphogenetic Protein 2 - pharmacology | Thiazoles - metabolism | Receptors, Estrogen - metabolism | Estrogens - pharmacology | Transcription Factors - chemistry | Apoptosis - drug effects | HSC70 Heat-Shock Proteins - metabolism | DNA-Binding Proteins - metabolism | Bone Marrow Cells - drug effects | Female | Haploinsufficiency - drug effects | Osteoblasts - cytology | Cell Survival - drug effects | Bone Marrow Cells - cytology | Osteoblasts - drug effects | Osteogenesis - drug effects | Cells, Cultured | DNA - metabolism | DNA-Binding Proteins - chemistry | Peptides - pharmacology | Gene Expression Regulation - drug effects | Transcription Factors - metabolism | Animals | Cell Differentiation - drug effects | Heterozygote | Cell Proliferation - drug effects | Mice | Osteoblasts - metabolism | Bone Marrow Cells - metabolism | Bone morphogenetic protein 2 | Bcl-2 protein | Heat shock proteins | Estrogen receptors | 17β-Estradiol | Hsp70 protein | Lethality | Proteins | Bone growth | Osteoblastogenesis | Mineralization | Rodents | Stromal cells | Bcl protein | Bone marrow | Hsc70 protein | Bone matrix | Protein interaction | Adenosine triphosphatase
Journal Article
Developmental biology, ISSN 0012-1606, 2012, Volume 369, Issue 1, pp. 101 - 114
Embryonic development is controlled by a small set of signal transduction pathways, with vastly different phenotypic outcomes depending on the time and place of their recruitment... 
Development | Calvarial mesenchyme | Mouse model | Ror2 | Hair follicles | Wnt5a | PLANAR CELL POLARITY | CONVERGENT EXTENSION | DEVELOPMENTAL BIOLOGY | BETA | XENOPUS | PATHWAY | GENE-EXPRESSION | BONE | PROTEINS | RECEPTOR TYROSINE KINASE | Embryo, Mammalian - drug effects | Meninges - embryology | Skin - metabolism | Wnt-5a Protein | Wnt Proteins - metabolism | Embryo, Mammalian - metabolism | Bone and Bones - drug effects | Intercellular Signaling Peptides and Proteins - metabolism | Wnt Proteins - genetics | Female | Models, Animal | Hair Follicle - embryology | Repressor Proteins - metabolism | Skin - embryology | Calcification, Physiologic - genetics | Calcification, Physiologic - drug effects | Receptor Tyrosine Kinase-like Orphan Receptors - metabolism | Osteogenesis - drug effects | Tetracycline - pharmacology | Embryonic Development - genetics | Gene Expression Regulation, Developmental - drug effects | Mice, Transgenic | Meninges - drug effects | beta Catenin - metabolism | Hair Follicle - drug effects | Pregnancy | Hair Follicle - cytology | Phenotype | Animals | Wnt Signaling Pathway - drug effects | Wnt Signaling Pathway - genetics | Receptor Tyrosine Kinase-like Orphan Receptors - genetics | Mice | Bone and Bones - abnormalities | Bone and Bones - embryology | Embryonic Development - drug effects | Skin - drug effects | development | hair follicles | calvarial mesenchyme | mouse model
Journal Article
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 488, Issue 7413, pp. 621 - 626
Journal Article
Journal of Cell Science, ISSN 0021-9533, 05/2008, Volume 121, Issue 9, pp. 1455 - 1465
The Wnt/beta-catenin signaling pathway is essential for normal skeletal development because conditional gain or loss of function of beta-catenin in cartilage results in embryonic or early postnatal death... 
β-catenin | Endochondral bone formation | Chondrocyte | Inhibitor of β-catenin and TCF (ICAT) | Vascular endothelial growth factor (VEGF) | beta-catenin | OSTEOBLAST DIFFERENTIATION | II COLLAGEN GENE | BINDING-PROTEIN | inhibitor of beta-catenin and TCF (ICAT) | vascular endothelial growth factor (VEGF) | CELL-FATE | endochondral bone formation | CHONDROCYTE DIFFERENTIATION | NEGATIVE REGULATOR | CELL BIOLOGY | COLON-CANCER | chondrocyte | WNT/BETA-CATENIN | BONE-FORMATION | GROWTH-PLATE | Embryo, Mammalian - drug effects | Growth Plate - pathology | Neovascularization, Physiologic - drug effects | Transcription, Genetic - drug effects | Chondrogenesis - drug effects | Cartilage - pathology | Repressor Proteins | Cartilage - drug effects | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Wnt Proteins - metabolism | Promoter Regions, Genetic - genetics | Embryo, Mammalian - metabolism | Chondrocytes - drug effects | Growth Plate - drug effects | Transgenes | Bone Morphogenetic Proteins - pharmacology | Chondrocytes - metabolism | Animals, Newborn | Cartilage - growth & development | Chondrocytes - pathology | Bone Development - drug effects | Bone Morphogenetic Protein 2 | Cell Cycle Proteins - metabolism | Gene Expression Regulation, Developmental - drug effects | Mice, Transgenic | beta Catenin - metabolism | Embryo, Mammalian - abnormalities | Transcription Factors - metabolism | Cartilage - abnormalities | Transforming Growth Factor beta - pharmacology | Animals | Signal Transduction - drug effects | Cell Differentiation - drug effects | Cell Proliferation - drug effects | Mice
Journal Article
Journal of bone and mineral research, ISSN 0884-0431, 2017, Volume 32, Issue 10, pp. 2128 - 2141
ABSTRACT Autophagy is activated during nutritionally depleted or hypoxic conditions to facilitate cell survival. Because growth plate is an avascular and... 
ENDOCHONDRAL OSSIFICATION | AUTOPHAGY | GROWTH PLATE CHONDROCYTES | ATG7 | ER STRESS | MATRIX | CHONDROCYTES | ENDOPLASMIC-RETICULUM STRESS | CELL-DEATH | UNFOLDED PROTEIN RESPONSE | PATHWAY | ENDOCRINOLOGY & METABOLISM | GROWTH-PLATE | BONE | DIFFERENTIATION | Chondrogenesis - drug effects | Apoptosis - drug effects | eIF-2 Kinase - metabolism | Autophagy-Related Protein 7 - metabolism | Growth Plate - embryology | Cartilage - drug effects | Autophagy - drug effects | Chondrocytes - drug effects | Gene Deletion | Phenylbutyrates - pharmacology | Tibia - growth & development | Growth Plate - ultrastructure | Chondrocytes - metabolism | Femur - growth & development | Endoplasmic Reticulum Stress - drug effects | Osteogenesis - drug effects | Cells, Cultured | Femur - drug effects | Cartilage - metabolism | Growth Plate - metabolism | Organ Specificity | Tibia - drug effects | Autophagy-Related Protein 7 - genetics | Mice, Knockout | Animals | Activating Transcription Factor 4 - metabolism | Cell Differentiation - drug effects | Chondrocytes - ultrastructure | Cell Proliferation - drug effects | Embryonic Development - drug effects | Transcription Factor CHOP - metabolism | Autophagy-Related Protein 7 - deficiency | Analysis | Stress (Physiology) | Cell proliferation | Cell survival | Growth rate | Homeostasis | Collagenase 3 | Autophagy | Ossification | Cartilage | Growth plate | Bone growth | Rodents | Chondrocytes | Hypoxia | Chondrogenesis | Stress response | Endoplasmic reticulum | Bone (endochondral) | Phenylbutyric acid | Phagocytosis | Apoptosis
Journal Article
Journal of biomedical materials research. Part A, ISSN 1549-3296, 2014, Volume 102, Issue 10, pp. 3379 - 3392
Journal Article
Leukemia, ISSN 0887-6924, 07/2011, Volume 25, Issue 7, pp. 1064 - 1079
It has become apparent that regulation of protein translation is an important determinant in controlling cell growth and leukemic transformation. The... 
mTOR | translation | sensitivity | PI3K | therapy | resistance | TUMOR-SUPPRESSOR CANDIDATE | PROTEIN-KINASE | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | GROWTH-FACTOR RECEPTOR | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | AKT/PROTEIN-KINASE-B | ACUTE LYMPHOBLASTIC-LEUKEMIA | HEMATOPOIETIC STEM-CELLS | CHRONIC LYMPHOCYTIC-LEUKEMIA | HEMATOLOGY | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Neoplasm Proteins - physiology | PTEN Phosphohydrolase - physiology | Apoptosis - genetics | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Gene Expression Regulation, Leukemic - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | Transcription Factors - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | PTEN Phosphohydrolase - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | TOR Serine-Threonine Kinases - physiology | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Leukemia - genetics | Multiprotein Complexes - drug effects | PTEN Phosphohydrolase - genetics | Proteins - physiology | Transcription Factors - physiology | RNA, Messenger - genetics | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Transcription Factors - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - physiology | Multiprotein Complexes - physiology | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | Pseudogenes | Signal Transduction - drug effects | Phosphatidylinositol 3-Kinases - physiology | Proteins - drug effects | RNA, Neoplasm - genetics | Protein Biosynthesis - drug effects | MicroRNAs - genetics | Proteins - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Genes | Leukemia | Physiological aspects | Development and progression | Genetic aspects | Research | Antineoplastic agents | Drug therapy | Health aspects
Journal Article