Characterization of the osteoblast-specific transmembrane protein IFITM5 and analysis of IFITM5-deficient mice
Interferon-inducible transmembrane protein 5 (IFITM5) is an osteoblast-specific membrane protein whose expression peaks around the early mineralization stage during the osteoblast maturation process. To investigate IFITM5 function, we first sought to identify which proteins interact with IFITM5. Liq...
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Published in | Journal of bone and mineral metabolism Vol. 29; no. 3; pp. 279 - 290 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Japan
Springer Japan
01.05.2011
Springer Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Interferon-inducible transmembrane protein 5 (IFITM5) is an osteoblast-specific membrane protein whose expression peaks around the early mineralization stage during the osteoblast maturation process. To investigate IFITM5 function, we first sought to identify which proteins interact with IFITM5. Liquid chromatography mass spectrometry revealed that FK506-binding protein 11 (FKBP11) co-immunoprecipitated with IFITM5. FKBP11 is the only protein it was found to interact with in osteoblasts, while IFITM5 interacts with several proteins in fibroblasts. FKBPs are involved in protein folding and immunosuppressant binding, but we could not be sure that IFITM5 participated in these activities when bound to FKBP11. Thus, we generated
Ifitm5
-deficient mice and analyzed their skeletal phenotypes. The skeletons, especially the long bones, of homozygous mutants (
Ifitm5
−/−
) were smaller than those of heterozygous mutants (
Ifitm5
+/−
), although we did not observe any significant differences in bone morphometric parameters. The effect of
Ifitm5
deficiency on bone formation was more significant in newborns than in young and adult mice, suggesting that
Ifitm5
deficiency might have a greater effect on prenatal bone development. Overall, the effect of
Ifitm5
deficiency on bone formation was less than we expected. We hypothesize that this may have resulted from a compensatory mechanism in
Ifitm5
-deficient mice. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0914-8779 1435-5604 |
DOI: | 10.1007/s00774-010-0221-0 |