BMPs was first discovered and described by Marshall Urist. BMP2 gene, located on chromosome 20p12, encompasses 2 exons with a coding region of 1191 nucleotides, produces a protein molecule of 396 amino acids that belongs to the TGF-b superfamily and induces cartilage and bone formation. In the present study, immunohistochemical localization of BMP2 was GPR120-IN-1 examined using ligament tissues from the OPLL and non-OPLL patients, the results were consistent with the previous studies that BMP2 were present at the ossifying matrix and chondrocytes of ossifying ligaments, and also localized at mesenchymal cells adjacent to these areas. At the same time, we demonstrated the BMP2 was expressed significantly higher in the OPLL patients through Western blotting which was consistent with the immunohisto chemisty observations. Functional impacts of the BMP2 variants on the OPLL phenotype are currently obscure due to the lack of biochemical evidences. Genetic variations must fulfill two criteria to be considered candidate modifiers of OPLL: the corresponding gene encodes a protein involved in ectopic ossification of OPLL, and the nucleotide change affects gene expression and/or function. In hundreds of cases, a single DNA sequence polymorphism affecting a protein coding sequence has been linked to a clear simple Mendelian phenotype and, for a much smaller but increasing number of cases, to more complex phenotypes. These findings ONO-4059 hydrochloride highlight the importance of better understanding the mechanisms leading to inter-individual differences in gene expression in humans. Our study has numerous limitations. First, although the C3H10T1/2 cell has been utilized as a surrogate stem cell model for the human embryonic fibroblast to study molecular mechanisms of stem cell commitment and differentiation to osteoblast, adipocyte and chondrocyte, there exhibits a similar but not completely identical phenotype which may lead to deviation phenomenon. Second, we didn��t detect the expression of other osteogenic genes, such as ALP, RUNX2, COLA1, OPL and OCN, so that it is difficult to understand other susceptible genes and their pathogenetic relevance.