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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

Lifelong accumulation of bone in mice lacking Pten in osteoblasts

http://www.wikidata.org/entity/Q35844528

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Mice lacking pten in osteoblasts have improved intramembranous and late endochondral fracture healing Akt promotes BMP2-mediated osteoblast differentiation and bone development Cross-Talk Between VEGF and BMP-6 Pathways Accelerates Osteogenic Differentiation of Human Adipose-Derived Stem Cells.Akt1 in osteoblasts and osteoclasts controls bone remodeling.Accumulating progenitor cells in the luminal epithelial cell layer are candidate tumor initiating cells in a Pten knockout mouse prostate cancer model Tsc2 is a molecular checkpoint controlling osteoblast development and glucose homeostasis Selective signaling by Akt2 promotes bone morphogenetic protein 2-mediated osteoblast differentiation.Increased skeletal VEGF enhances beta-catenin activity and results in excessively ossified bones.Intermittent parathyroid hormone administration counteracts the adverse effects of glucocorticoids on osteoblast and osteocyte viability, bone formation, and strength in mice.Akt activation is required for TGF-β1-induced osteoblast differentiation of MC3T3-E1 pre-osteoblasts.Conditional ablation of Pten in osteoprogenitors stimulates FGF signaling The heparin-binding domain of IGFBP-2 has insulin-like growth factor binding-independent biologic activity in the growing skeleton Fracture healing in mice lacking Pten in osteoblasts: a micro-computed tomography image-based analysis of the mechanical properties of the femur.Distinct actions of akt1 on skeletal architecture and function Insulin-like growth factor 2 (IGF-2) potentiates BMP-9-induced osteogenic differentiation and bone formation.Selective signaling by Akt1 controls osteoblast differentiation and osteoblast-mediated osteoclast development.mTORC1 Prevents Preosteoblast Differentiation through the Notch Signaling Pathway.Rb1 and Pten Co-Deletion in Osteoblast Precursor Cells Causes Rapid Lipoma Formation in Mice.Role of Cbl-PI3K Interaction during Skeletal Remodeling in a Murine Model of Bone Repair.Genetic mouse models for bone studies--strengths and limitations Protein kinase G and focal adhesion kinase converge on Src/Akt/β-catenin signaling module in osteoblast mechanotransduction A specific role for phosphoinositide 3-kinase and AKT in osteoblasts?Telomerase activity promotes osteoblast differentiation by modulating IGF-signaling pathway Loss of Cbl-PI3K interaction modulates the periosteal response to fracture by enhancing osteogenic commitment and differentiation.Microarray gene expression profiling of osteoarthritic bone suggests altered bone remodelling, WNT and transforming growth factor-beta/bone morphogenic protein signalling.Gender-specific changes in bone turnover and skeletal architecture in igfbp-2-null mice.The insulin-like growth factor system in bone: basic and clinical implications.Insulin-like growth factor-binding protein-5 inhibits osteoblast differentiation and skeletal growth by blocking insulin-like growth factor actions.Contributions of the Insulin/Insulin-Like Growth Factor-1 Axis to Diabetic Osteopathy.In vivo targeted deletion of calpain small subunit, Capn4, in cells of the osteoblast lineage impairs cell proliferation, differentiation, and bone formation Portrait of PTEN: messages from mutant mice.Liver-specific deletion of the growth hormone receptor reveals essential role of growth hormone signaling in hepatic lipid metabolism.Asperosaponin VI promotes bone marrow stromal cell osteogenic differentiation through the PI3K/AKT signaling pathway in an osteoporosis model.The skeleton: a multi-functional complex organ: new insights into osteoblasts and their role in bone formation: the central role of PI3Kinase.Signaling pathways affecting skeletal health.Inpp4b is a novel negative modulator of osteoclast differentiation and a prognostic locus for human osteoporosis.Possible roles of insulin signaling in osteoblasts.Conditional disruption of calcineurin B1 in osteoblasts increases bone formation and reduces bone resorption.PlexinA2 mediates osteoblast differentiation via regulation of Runx2.Role of apoptosis in pathogenesis and treatment of bone-related diseases.

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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2007 nî lūn-bûn

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Proceedings of the National Academy of Sciences of the United States of America

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Lifelong accumulation of bone in mice lacking Pten in osteoblasts

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Cassandra R Zylstra

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Jiarong Liu

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Katia J Bruxvoort

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Marie-Claude Faugere

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Mary L Bouxsein

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Rachel Cichowski

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Thomas L Clemens

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Ximeng Liu

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P2860

TEP1, encoded by a candidate tumor suppressor locus, is a novel protein tyrosine phosphatase regulated by transforming growth factor beta

Will the real Cowden syndrome please stand up (again)? Expanding mutational and clinical spectra of the PTEN hamartoma tumour syndrome

The phosphoinositide 3-kinase pathway

PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer

PTEN: life as a tumor suppressor

Identification of a candidate tumour suppressor gene, MMAC1, at chromosome 10q23.3 that is mutated in multiple advanced cancers

Pten is essential for embryonic development and tumour suppression

Negative regulation of PKB/Akt-dependent cell survival by the tumor suppressor PTEN

Mutation of Pten/Mmac1 in mice causes neoplasia in multiple organ systems

PTEN modulates cell cycle progression and cell survival by regulating phosphatidylinositol 3,4,5,-trisphosphate and Akt/protein kinase B signaling pathway

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