Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5. - Wikidata - awgldk - TriplyDB

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5.

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5.

http://www.wikidata.org/entity/Q34457990

about

Endocrine parameters and phenotypes of the growth hormone receptor gene disrupted (GHR-/-) mouse Doubly truncated FosB isoform (Delta2DeltaFosB) induces osteosclerosis in transgenic mice and modulates expression and phosphorylation of Smads in osteoblasts independent of intrinsic AP-1 activity Nuclear receptors in bone physiology and diseases Angiogenesis and intramembranous osteogenesis The DNA helicase recql4 is required for normal osteoblast expansion and osteosarcoma formation Ciliary neurotrophic factor inhibits bone formation and plays a sex-specific role in bone growth and remodeling Wnt inhibitory factor 1 is epigenetically silenced in human osteosarcoma, and targeted disruption accelerates osteosarcomagenesis in mice Dissociation of bone resorption and bone formation in adult mice with a non-functional V-ATPase in osteoclasts leads to increased bone strength Proportionate Dwarfism in Mice Lacking Heterochromatin Protein 1 Binding Protein 3 (HP1BP3) Is Associated With Alterations in the Endocrine IGF-1 Pathway.Unreplaced sex steroid deficiency, corticotropin deficiency, and lower IGF-I are associated with lower bone mineral density in adults with growth hormone deficiency: a KIMS database analysis Minireview: osteoprotective action of estrogens is mediated by osteoclastic estrogen receptor-alpha Matrix metalloproteinases are not essential for aggrecan turnover during normal skeletal growth and development.Deletion of IGF-I receptor (IGF-IR) in primary osteoblasts reduces GH-induced STAT5 signaling.Update in new anabolic therapies for osteoporosis Minireview: mechanisms of growth hormone-mediated gene regulation.Insulin-like growth factor 1 (IGF-1): a growth hormone Effect of GH/IGF-1 on Bone Metabolism and Osteoporsosis.Evidence that sensitivity to growth hormone (GH) is growth period and tissue type dependent: studies in GH-deficient lit/lit mice.Insulin-like growth factor regulates peak bone mineral density in mice by both growth hormone-dependent and -independent mechanisms.Lrp5-independent activation of Wnt signaling by lithium chloride increases bone formation and bone mass in mice A functional androgen receptor is not sufficient to allow estradiol to protect bone after gonadectomy in estradiol receptor-deficient mice Direct stimulation of bone mass by increased GH signalling in the osteoblasts of Socs2-/- mice Strain-dependent differences in bone development, myeloid hyperplasia, morbidity and mortality in ptpn2-deficient mice.The different functions of Stat5 and chromatin alteration through Stat5 proteins The loss of Cbl-phosphatidylinositol 3-kinase interaction perturbs RANKL-mediated signaling, inhibiting bone resorption and promoting osteoclast survival.Growth factor control of bone mass.Bone protection by estrens occurs through non-tissue-selective activation of the androgen receptor.Gene regulation by growth hormone.SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent inflammatory arthritis.Interactions between GH, IGF-I, glucocorticoids, and thyroid hormones during skeletal growth.Knockout of nuclear high molecular weight FGF2 isoforms in mice modulates bone and phosphate homeostasis.Prostacyclin regulates bone growth via the Epac/Rap1 pathway.Generation and analysis of Siah2 mutant mice.Elevated serum levels of IGF-1 are sufficient to establish normal body size and skeletal properties even in the absence of tissue IGF-1.IGF-1 and bone: New discoveries from mouse models Abrogation of Cbl-PI3K interaction increases bone formation and osteoblast proliferation.Invited Review: Pathogenesis of osteoporosis.Glycoprotein 130 regulates bone turnover and bone size by distinct downstream signaling pathways.An ethyl-nitrosourea-induced point mutation in phex causes exon skipping, x-linked hypophosphatemia, and rickets.Dwarfism in mice lacking collagen-binding integrins α2β1 and α11β1 is caused by severely diminished IGF-1 levels.

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P2860

Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5.

http://www.wikidata.org/entity/Q34457990

description

2000 nî lūn-bûn

@nan

2000 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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name

Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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Journal of Clinical Investigation

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Bone homeostasis in growth hor ...... GF-I but independent of Stat5.

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F Da Ponte

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J Kopchick

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K Coschigano

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M Gaillard-Kelly

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P2860

Null mutation of the prolactin receptor gene produces multiple reproductive defects in the mouse

A mammalian model for Laron syndrome produced by targeted disruption of the mouse growth hormone receptor/binding protein gene (the Laron mouse)

Genetic pituitary dwarfism with high serum concentration of growth hormone--a new inborn error of metabolism?

Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses

Bone histomorphometry: standardization of nomenclature, symbols, and units. Report of the ASBMR Histomorphometry Nomenclature Committee

Disproportional skeletal growth and markedly decreased bone mineral content in growth hormone receptor -/- mice.

Recombinant human insulin-like growth factor I stimulates growth and has distinct effects on organ size in hypophysectomized rats.

Liver-derived insulin-like growth factor I (IGF-I) is the principal source of IGF-I in blood but is not required for postnatal body growth in mice

Normal growth and development in the absence of hepatic insulin-like growth factor I

Age-related alterations of the growth hormone/insulin-like-growth-factor I axis.

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1095-1103

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10.1172/JCI10753

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106

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301420

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