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In fact, vascular cellular culture studies have been carried out with the intention to describe the effect of Cbfa1 over osteoblastic differentiation, and they have reported an induced mineralization and OPN expression after inorganic phosphate was added.
Mutations involving the transcription factor CBFA1 cause cleidocranial dysplasia.
Cleidocranial dyplasia (CCD) is a rare skeletal disorder caused by a defect in the CBFA1 gene on chromosome 6p21.
The Cbfa1 and HIF-1 pathways can be modulated to direct bone formation via siGNAS1 and siPHD2, respectively.
Although cell response to micrometer topography and in particular surface microgrooves has been reported, studies have often been limited to using stochastically patterned substrata and covering only a small range of microgroove geometrical values and the influence of this interesting microgeometry on the main osteoblast specific transcription factor Cbfa1 has been ignored.
Mutation involving the transcription factor CBFA1 cause cleidocranial dysplasia.
Mice missing the Cbfa1 gene don't form bones, which leaves them with a skeleton made only of cartilage, like sharks.
Premature osteoporosis was caused by reduced osteoblastic bone formation in both trabecular and cortical bone associated with the down-regulation of osteoblastic gene expression levels of Cbfa1, ALP, type I collagen and osteocalcin in skeletal tissue and immunostaining for PTH/PTHrP receptor (PTHR) was dramatically decreased in bone sections from KI mice.
Cbfa1, a candidate gene for cleidocranial dysplasia syndrome, is essential for osteoblast differentiation and bone development.
The osteoblast-specific transcription factor Cbfa1 contributes to the expression of osteoprotegerin, a potent inhibitor of osteoclast differentiation and function.
7) Cbfa1 activation results in activation of osteocalcin gene, col I and alkaline phosphatase genes which form the matrix and favour mineralization.
Regulation of Cbfa1 expression by total flavonoids of Herba epimedii.
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