α2-HS Glycoprotein/Fetuin, a Transforming Growth Factor-β/Bone Morphogenetic Protein Antagonist, Regulates Postnatal Bone Growth and Remodeling (Q56999751)

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scientific article published in Journal of Biological Chemistry

Language	Label	Description	Also known as
English	α2-HS Glycoprotein/Fetuin, a Transforming Growth Factor-β/Bone Morphogenetic Protein Antagonist, Regulates Postnatal Bone Growth and Remodeling	scientific article published in Journal of Biological Chemistry

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scholarly article

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α2-HS Glycoprotein/Fetuin, a Transforming Growth Factor-β/Bone Morphogenetic Protein Antagonist, Regulates Postnatal Bone Growth and Remodeling (English)

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based on heuristic

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Willi Jahnen-Dechent

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Willi Jahnen-Dechent

7

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author name string

Melanie Szweras

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Danmei Liu

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Emily A. Partridge

3

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Judy Pawling

4

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Balram Sukhu

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Cameron Clokie

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Howard C. Tenenbaum

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Carol J. Swallow

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Marc D. Grynpas

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James W. Dennis

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language of work or name

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publication date

18 March 2002

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Journal of Biological Chemistry

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277

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22

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19991-19997

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Localisation of plasma α2HS glycoprotein in mineralising human bone

1 reference

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Genetic polymorphism of desialyzed alpha 2 HS-glycoprotein by ultrathin isoelectric focusing

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Genetic variation in alpha 2HS-glycoprotein is related to calcaneal broadband ultrasound attenuation in older women

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Serum concentration of human alpha 2 HS glycoprotein during the inflammatory process: evidence that alpha 2 HS glycoprotein is a negative acute-phase reactant

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The serum protein alpha2-HS glycoprotein/fetuin inhibits apatite formation in vitro and in mineralizing calvaria cells. A possible role in mineralization and calcium homeostasis

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Fetuin/alpha2-HS glycoprotein is a transforming growth factor-beta type II receptor mimic and cytokine antagonist

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Characterization of unique binding kinetics of follistatin and activin or inhibin in serum

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Regulation of osteogenesis by fetuin.

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Morphogens and pattern formation

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Bone morphogenetic proteins: multifunctional regulators of vertebrate development

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Establishment of a BMP-4 morphogen gradient by long-range inhibition.

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Noggin, cartilage morphogenesis, and joint formation in the mammalian skeleton

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Betaglycan can act as a dual modulator of TGF-beta access to signaling receptors: mapping of ligand binding and GAG attachment sites

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Negative regulation of transforming growth factor-beta by the proteoglycan decorin

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Interaction of the small interstitial proteoglycans biglycan, decorin and fibromodulin with transforming growth factor beta

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Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice

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Cloning and targeted deletion of the mouse fetuin gene

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Immunohistochemical localization of TGF beta 1, TGF beta 2, and TGF beta 3 in the mouse embryo: expression patterns suggest multiple roles during embryonic development

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Transforming growth factor-beta and the initiation of chondrogenesis and osteogenesis in the rat femur

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Bone matrix proteins in osteogenesis and remodelling in the neonatal rat mandible as studied by immunolocalization of osteopontin, bone sialoprotein, alpha 2HS-glycoprotein and alkaline phosphatase

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Effects of mechanical forces on maintenance and adaptation of form in trabecular bone

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Indian hedgehog signaling regulates proliferation and differentiation of chondrocytes and is essential for bone formation

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Lethal skeletal dysplasia from targeted disruption of the parathyroid hormone-related peptide gene

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Patterns of gene expression associated with BMP-2-induced osteoblast and adipocyte differentiation of mesenchymal progenitor cell 3T3-F442A.

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Domain-specific mutations of a transforming growth factor (TGF)-beta 1 latency-associated peptide cause Camurati-Engelmann disease because of the formation of a constitutively active form of TGF-beta 1.

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Decreased bone mass and bone elasticity in mice lacking the transforming growth factor-beta1 gene

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Increased expression of TGF-beta 2 in osteoblasts results in an osteoporosis-like phenotype

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Osteoblastic responses to TGF-beta during bone remodeling

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Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease

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Murine alpha-macroglobulins demonstrate divergent activities as neutralizers of transforming growth factor-beta and as inducers of nitric oxide synthesis. A possible mechanism for the endotoxin insensitivity of the alpha2-macroglobulin gene knock-ou

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Mitotic misregulation and human aging

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Transforming growth factor-beta in disease: the dark side of tissue repair

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TGFbeta1 inhibits the formation of benign skin tumors, but enhances progression to invasive spindle carcinomas in transgenic mice

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Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

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Fetuin, a New Globulin Isolated from Serum

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Identifiers

10.1074/JBC.M112234200

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