FXIIIA and TGF-β over-expression produces normal musculo-skeletal phenotype in TG2-/- mice
Copyright policy )FXIIIA and TGF-β over-expression produces normal musculo-skeletal phenotype in TG2-/- mice
Transglutaminase (TGs) enzymes and proteins crosslinking have for long time been implicated in the formation of hard tissue development, matrix maturation and mineralization. Among the TGs family members, in the context of connective tissue formation, TG2 and Factor XIII are expressed in cartilage by hypertrophic chondrocytes. Here, we analyse the morphological consequences of TG2 deficiency, during the development of skeletal elements. When TG2 is absent, there are not gross abnormalities in the development of the skeletal system, probably from compensatory mechanisms resulting in increased expression of FXIIIA and TGF-beta 1. In vivo other TGs may be involved in promoting chondrocytes and osteoblast differentiation and matrix mineralisation.
- University of Rome Tor Vergata Italy
- Sapienza University of Rome Italy
- Keele University United Kingdom
- Università degli studi di Salerno Italy
Mice, Knockout, Transglutaminases, Endochondral ossification; Transglutaminase, Settore MED/33 - MALATTIE APPARATO LOCOMOTORE, Transforming Growth Factor beta1, Mice, Phenotype, GTP-Binding Proteins, Animals, Protein Glutamine gamma Glutamyltransferase 2, Factor XIIIa, Muscle, Skeletal
Mice, Knockout, Transglutaminases, Endochondral ossification; Transglutaminase, Settore MED/33 - MALATTIE APPARATO LOCOMOTORE, Transforming Growth Factor beta1, Mice, Phenotype, GTP-Binding Proteins, Animals, Protein Glutamine gamma Glutamyltransferase 2, Factor XIIIa, Muscle, Skeletal
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