Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy - Wikidata - wikimedia - TriplyDB

Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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The GNAS complex locus and human diseases associated with loss-of-function mutations or epimutations within this imprinted gene A mouse model for osseous heteroplasia Progressive osseous heteroplasia: diagnosis, treatment, and prognosis Paternally inherited gsα mutation impairs adipogenesis and potentiates a lean phenotype in vivo.An update on the clinical and molecular characteristics of pseudohypoparathyroidism.Somitic disruption of GNAS in chick embryos mimics progressive osseous heteroplasia.Activation of Hedgehog signaling by loss of GNAS causes heterotopic ossification.Gsα Controls Cortical Bone Quality by Regulating Osteoclast Differentiation via cAMP/PKA and β-Catenin Pathways.GNAS mutations in Pseudohypoparathyroidism type 1a and related disorders.Ossifications in Albright Hereditary Osteodystrophy: Role of Genotype, Inheritance, Sex, Age, Hormonal Status, and BMI.Current Nomenclature of Pseudohypoparathyroidism: Inactivating Parathyroid Hormone/Parathyroid Hormone-Related Protein Signaling Disorder.Overexpression of GαS in Murine Osteoblasts In Vivo Leads to Increased Bone Mass and Decreased Bone Quality.GNAS mutations and heterotopic ossification.Progressive osseous heteroplasia, as an isolated entity or overlapping with Albright hereditary osteodystrophy.

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

http://www.wikidata.org/entity/Q33957963

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2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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JOURNAL.PONE.0021755

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Heterotopic ossifications in a mouse model of albright hereditary osteodystrophy

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David L Huso

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Emily L Germain-Lee

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Harald Jüppner

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Sarah Edie

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William Schwindinger

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Yingli Wang

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Scratching the surface of skin development

Diagnostic and mutational spectrum of progressive osseous heteroplasia (POH) and other forms of GNAS-based heterotopic ossification

Progressive osseous heteroplasia: a model for the imprinting effects of GNAS inactivating mutations in humans

Imprinting of the G(s)alpha gene GNAS1 in the pathogenesis of acromegaly

Targeted disruption of Gnas in embryonic stem cells

Deficiency of the G-protein alpha-subunit G(s)alpha in osteoblasts leads to differential effects on trabecular and cortical bone

Activation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2(+P253R) mice.

Imprinting in Albright's hereditary osteodystrophy

Alternative Gnas gene products have opposite effects on glucose and lipid metabolism.

Deficient guanine nucleotide regulatory unit activity in cultured fibroblast membranes from patients with pseudohypoparathyroidism type I. a cause of impaired synthesis of 3',5'-cyclic AMP by intact and broken cells.

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10.1371/JOURNAL.PONE.0021755

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Michael A. Levine

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2011-06-29T00:00:00Z

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51484531

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