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45 Here we suggest that these regimens targeting Nogo-A in addition to gene knockdown might be utilized to treat bone-erosive diseases such as rheumatoid arthritis and osteoporosis. To summarize, the present study showed previously unappreciated extraneural role of Nogo-A in osteoclastogenesis that modulates MAPK activity and Ca2+ oscillation, leading to the enhanced NFATc1 activity and induction. An unambiguous understanding of the mechanism underlying the Nogo-A enhancement of osteoclast differentiation will not only benefit the selection of effective target molecules to treat skeletal diseases but also expand our knowledge on the function of Nogo-A in various biological processes in addition to the its well-characterized role in the nervous system. All authors state that they have no conflicts of interest. This work was supported by the 21C Frontier Functional Proteomics Project http://www.selleckchem.com/products/ly2157299.html (FPR08B1-170 to H-HK), Science Research Center (2010-0001744 to H-HK), and National Research Foundation of Korea grants funded by the http://www.selleckchem.com/products/z-vad-fmk.html Korean Government, Ministry of Education, Science, and Technology (NRF-2010-359-E00016 to YL and NRF-2010-860-20100096 to HJK). Authors' roles: YL designed and performed the experiments, analyzed the data, and wrote the paper. HJK provided crucial reagents and analyzed the data. CKP and W-SK performed in vivo resorption experiments. ZHL analyzed the data. H-HK designed the experiments, analyzed the data, and wrote the paper. Additional Supporting Information http://www.selleck.cn/products/BIBW2992.html may be found in the online version of this article. ""Parent-of-origin�Cdependent (epi)genetic factors are important determinants of prenatal development that program adult phenotype. However, data on magnitude and specificity of maternal and paternal genome effects on fetal bone are lacking. We used an outbred bovine model to dissect and quantify effects of parental genomes, fetal sex, and nongenetic maternal effects on the fetal skeleton and analyzed phenotypic and molecular relationships between fetal muscle and bone. Analysis of 51 bone morphometric and weight parameters from 72 fetuses recovered at day 153 gestation (54% term) identified six principal components (PC1�C6) that explained 80% of the variation in skeletal parameters. Parental genomes accounted for most of the variation in bone wet weight (PC1, 72.1%), limb ossification (PC2, 99.8%), flat bone size (PC4, 99.7%), and axial skeletal growth (PC5, 96.9%). Limb length showed lesser effects of parental genomes (PC3, 40.8%) and a significant nongenetic maternal effect (gestational weight gain, 29%). Fetal sex affected bone wet weight (PC1, p?