Leboy Phoebe S
Department of Biochemistry, School of Dental Medicine, University of Pennsylvania, 240 South 40th Street, Philadelphia, PA 19104-6030, USA.
Ann N Y Acad Sci. 2006 Apr;1068:14-8. doi: 10.1196/annals.1346.003.
There are many gene products reported to promote osteoblast differentiation and thus increase bone formation, but only the transcription factor Runx2 and members of the bone morphogenetic protein (BMP) family of growth/differentiation factors have been shown to be absolute requirements for osteogenesis. Mice lacking the transcription factor Runx2 (also known as cbfa1) develop no bone. Similarly, osteoblast differentiation and bone formation is blocked when BMP signaling is suppressed by overexpression of noggin, a selective BMP antagonist. It is therefore not unexpected that several different mechanisms have evolved to regulate the effects of BMP-induced signaling. In this session we focus on the multiple ways in which cells can modulate BMP-induced osteogenesis and mechanisms by which BMP signaling can lead to transcriptional control of gene expression.
据报道，有许多基因产物可促进成骨细胞分化，从而增加骨形成，但只有转录因子Runx2和骨形态发生蛋白（BMP）家族的生长/分化因子成员已被证明是骨生成的绝对必要条件。缺乏转录因子Runx2（也称为cbfa1）的小鼠不会形成骨骼。同样，当noggin（一种选择性BMP拮抗剂）过度表达抑制BMP信号传导时，成骨细胞分化和骨形成也会受阻。因此，进化出几种不同机制来调节BMP诱导信号的作用也就不足为奇了。在本环节中，我们将重点关注细胞调节BMP诱导的骨生成的多种方式以及BMP信号传导导致基因表达转录控制的机制。
