Figure 4

Possible mechanism for kinase involvement in BMP stimulated type X collagen expression. ERK1/2 is proposed to suppress activated Smad translocation to the nucleus as described by Kretschmer et al. [30] and thereby inhibit Col X transcription. ERK-specific Runx2 phosphorylation is required for regulation of typical osteoblastic genes but may not be required for Col X expression. However p38 facilitates Col X transcription, possibly via Runx2 phosphorylation and although was not shown to be involved in short term increases in ALP in our model, has been shown to be involved in long term increases in ALP over 15 days of chondrocyte differentiation in culture (question mark) [29].