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

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Standard

Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice. / Xu, T; Bianco, P; Fisher, L W; Longenecker, G; Smith, E; Goldstein, S; Bonadio, J; Boskey, A; Heegaard, Anne-Marie; Sommer, B; Satomura, K; Dominguez, P; Zhao, C; Kulkarni, A B; Robey, P G; Young, M F.

I: Nature Genetics, Bind 20, Nr. 1, 1998, s. 78-82.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Xu, T, Bianco, P, Fisher, LW, Longenecker, G, Smith, E, Goldstein, S, Bonadio, J, Boskey, A, Heegaard, A-M, Sommer, B, Satomura, K, Dominguez, P, Zhao, C, Kulkarni, AB, Robey, PG & Young, MF 1998, 'Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice', Nature Genetics, bind 20, nr. 1, s. 78-82. https://doi.org/10.1038/1746

APA

Xu, T., Bianco, P., Fisher, L. W., Longenecker, G., Smith, E., Goldstein, S., Bonadio, J., Boskey, A., Heegaard, A-M., Sommer, B., Satomura, K., Dominguez, P., Zhao, C., Kulkarni, A. B., Robey, P. G., & Young, M. F. (1998). Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice. Nature Genetics, 20(1), 78-82. https://doi.org/10.1038/1746

Vancouver

Xu T, Bianco P, Fisher LW, Longenecker G, Smith E, Goldstein S o.a. Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice. Nature Genetics. 1998;20(1):78-82. https://doi.org/10.1038/1746

Author

Xu, T ; Bianco, P ; Fisher, L W ; Longenecker, G ; Smith, E ; Goldstein, S ; Bonadio, J ; Boskey, A ; Heegaard, Anne-Marie ; Sommer, B ; Satomura, K ; Dominguez, P ; Zhao, C ; Kulkarni, A B ; Robey, P G ; Young, M F. / Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice. I: Nature Genetics. 1998 ; Bind 20, Nr. 1. s. 78-82.

Bibtex

@article{bb741e5c615b49c29afc8c26518976fc,
title = "Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice",
abstract = "The resilience and strength of bone is due to the orderly mineralization of a specialized extracellular matrix (ECM) composed of type I collagen (90%) and a host of non-collagenous proteins that are, in general, also found in other tissues. Biglycan (encoded by the gene Bgn) is an ECM proteoglycan that is enriched in bone and other non-skeletal connective tissues. In vitro studies indicate that Bgn may function in connective tissue metabolism by binding to collagen fibrils and TGF-beta (refs 5,6), and may promote neuronal survival. To study the role of Bgn in vivo, we generated Bgn-deficient mice. Although apparently normal at birth, these mice display a phenotype characterized by a reduced growth rate and decreased bone mass due to the absence of Bgn. To our knowledge, this is the first report in which deficiency of a non-collagenous ECM protein leads to a skeletal phenotype that is marked by low bone mass that becomes more obvious with age. These mice may serve as an animal model to study the role of ECM proteins in osteoporosis.",
keywords = "Age Factors, Animals, Biglycan, Bone Density, Bone Development, Bone and Bones, Extracellular Matrix Proteins, Female, Femur, Gene Expression Regulation, Developmental, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Osteoporosis, Phenotype, Proteoglycans, Tibia",
author = "T Xu and P Bianco and Fisher, {L W} and G Longenecker and E Smith and S Goldstein and J Bonadio and A Boskey and Anne-Marie Heegaard and B Sommer and K Satomura and P Dominguez and C Zhao and Kulkarni, {A B} and Robey, {P G} and Young, {M F}",
year = "1998",
doi = "10.1038/1746",
language = "English",
volume = "20",
pages = "78--82",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Targeted disruption of the biglycan gene leads to an osteoporosis-like phenotype in mice

AU - Xu, T

AU - Bianco, P

AU - Fisher, L W

AU - Longenecker, G

AU - Smith, E

AU - Goldstein, S

AU - Bonadio, J

AU - Boskey, A

AU - Heegaard, Anne-Marie

AU - Sommer, B

AU - Satomura, K

AU - Dominguez, P

AU - Zhao, C

AU - Kulkarni, A B

AU - Robey, P G

AU - Young, M F

PY - 1998

Y1 - 1998

N2 - The resilience and strength of bone is due to the orderly mineralization of a specialized extracellular matrix (ECM) composed of type I collagen (90%) and a host of non-collagenous proteins that are, in general, also found in other tissues. Biglycan (encoded by the gene Bgn) is an ECM proteoglycan that is enriched in bone and other non-skeletal connective tissues. In vitro studies indicate that Bgn may function in connective tissue metabolism by binding to collagen fibrils and TGF-beta (refs 5,6), and may promote neuronal survival. To study the role of Bgn in vivo, we generated Bgn-deficient mice. Although apparently normal at birth, these mice display a phenotype characterized by a reduced growth rate and decreased bone mass due to the absence of Bgn. To our knowledge, this is the first report in which deficiency of a non-collagenous ECM protein leads to a skeletal phenotype that is marked by low bone mass that becomes more obvious with age. These mice may serve as an animal model to study the role of ECM proteins in osteoporosis.

AB - The resilience and strength of bone is due to the orderly mineralization of a specialized extracellular matrix (ECM) composed of type I collagen (90%) and a host of non-collagenous proteins that are, in general, also found in other tissues. Biglycan (encoded by the gene Bgn) is an ECM proteoglycan that is enriched in bone and other non-skeletal connective tissues. In vitro studies indicate that Bgn may function in connective tissue metabolism by binding to collagen fibrils and TGF-beta (refs 5,6), and may promote neuronal survival. To study the role of Bgn in vivo, we generated Bgn-deficient mice. Although apparently normal at birth, these mice display a phenotype characterized by a reduced growth rate and decreased bone mass due to the absence of Bgn. To our knowledge, this is the first report in which deficiency of a non-collagenous ECM protein leads to a skeletal phenotype that is marked by low bone mass that becomes more obvious with age. These mice may serve as an animal model to study the role of ECM proteins in osteoporosis.

KW - Age Factors

KW - Animals

KW - Biglycan

KW - Bone Density

KW - Bone Development

KW - Bone and Bones

KW - Extracellular Matrix Proteins

KW - Female

KW - Femur

KW - Gene Expression Regulation, Developmental

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Osteoporosis

KW - Phenotype

KW - Proteoglycans

KW - Tibia

U2 - 10.1038/1746

DO - 10.1038/1746

M3 - Journal article

C2 - 9731537

VL - 20

SP - 78

EP - 82

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

IS - 1

ER -

ID: 38426650