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Transgenic mouse models in studies of skeletal disorders.
J Rheumatol Suppl. 1995 Feb; 43:39-41.JR

Abstract

Studies of mutations in mice and humans are identifying molecular defects in a number of osteochondrodysplasias. Disruption of collagen IX function in mice using 3 transgenic approaches causes a degenerative joint disease resembling osteoarthritis (OA). Mapping of a multiple epiphyseal dysplasia locus to the chromosomal region of COL9A2 suggests that certain heritable forms of OA in humans are also associated with collagen IX mutations. Colocalization of a murine chondrodysplasia, cho, with the Col11a1 locus, as well as mapping of the Stickler syndrome locus to COL11A2, implicate collagen XI genes as other candidates in heritable chondrodysplasias. The murine models permit exploration of pathogenetic mechanisms and testing of novel therapies.

Authors+Show Affiliations

Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

7752133

Citation

Jacenko, O, and B R. Olsen. "Transgenic Mouse Models in Studies of Skeletal Disorders." The Journal of Rheumatology. Supplement, vol. 43, 1995, pp. 39-41.
Jacenko O, Olsen BR. Transgenic mouse models in studies of skeletal disorders. J Rheumatol Suppl. 1995;43:39-41.
Jacenko, O., & Olsen, B. R. (1995). Transgenic mouse models in studies of skeletal disorders. The Journal of Rheumatology. Supplement, 43, 39-41.
Jacenko O, Olsen BR. Transgenic Mouse Models in Studies of Skeletal Disorders. J Rheumatol Suppl. 1995;43:39-41. PubMed PMID: 7752133.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transgenic mouse models in studies of skeletal disorders. AU - Jacenko,O, AU - Olsen,B R, PY - 1995/2/1/pubmed PY - 1995/2/1/medline PY - 1995/2/1/entrez SP - 39 EP - 41 JF - The Journal of rheumatology. Supplement JO - J Rheumatol Suppl VL - 43 N2 - Studies of mutations in mice and humans are identifying molecular defects in a number of osteochondrodysplasias. Disruption of collagen IX function in mice using 3 transgenic approaches causes a degenerative joint disease resembling osteoarthritis (OA). Mapping of a multiple epiphyseal dysplasia locus to the chromosomal region of COL9A2 suggests that certain heritable forms of OA in humans are also associated with collagen IX mutations. Colocalization of a murine chondrodysplasia, cho, with the Col11a1 locus, as well as mapping of the Stickler syndrome locus to COL11A2, implicate collagen XI genes as other candidates in heritable chondrodysplasias. The murine models permit exploration of pathogenetic mechanisms and testing of novel therapies. SN - 0380-0903 UR - https://www.unboundmedicine.com/medline/citation/7752133/Transgenic_mouse_models_in_studies_of_skeletal_disorders_ L2 - https://medlineplus.gov/osteoarthritis.html DB - PRIME DP - Unbound Medicine ER -