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

(1) CCN2缺失导致CCN3在CCN2缺失小鼠中表达上调，从而导致所观察到的表型，如最终分化的延迟。PTHrP-Ihh环也参与了CCN3表达的调控。（Kawaki et al., JBMR 2008）(2)研究CCN家族成员的表达及其成骨分化功能。结果表明，CCN成员是差异表达的，因此可以参与成骨细胞谱系的进展。（手稿正在准备中。）(3)我们发现人类ccn4mrna的稳定性受其3' utr区调控。（手稿正在准备中。）

(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.)