Mechanisms of mechanical response in bony tissues derived from CCN2 deficient mice.

(1)CCN 2的缺乏导致CCN 2缺失小鼠中CCN 3的上调，这导致观察到的表型，例如最终分化的延迟。PTHrP-Ihh环参与CCN 3表达的调节。（Kawaki等人，JBMR 2008.）(2)我们研究了CCN家族成员的表达及其在成骨细胞分化中的作用。结果表明，CCN成员的差异表达，因此可以参与成骨细胞谱系的进展。（手稿正在编写中。）(3)我们发现人ccn 4 mRNA的稳定性受其3 'UTR区的调控。（手稿正在编写中。）

(1) The lack of CCN2 caused up-regulation of CCN3 in CCN2-null mice, which resulted in the observed phenotypes, such as the resultant delay of terminal differentiation. The involvement of the PTHrP-Ihh loop in the regulation of CCN3 expression is also suggested. (Kawaki et al., JBMR 2008.)(2) We investigated the expression of CCN family members and their functions osteoblast differentiation. Results showed that CCN members were differentially expressed and therefore could participate in osteoblast lineage progression. (manuscript in preparation.)(3) We found that the stability of human ccn4 mRNA was regulated by its 3'UTR region. (manuscript in preparation.)