Cheryl O. Quinn

TL;DR: It is proposed that the glucocorticoid promote changes in gene expression involved in cell‐cell and cell‐extracellular matrix signaling mechanism that support the growth and differentiation of cells capable of osteoblast phenotype development and bone tissue‐like organization, while inhibiting the growth of cells that cannot progress to the mature osteoblow phenotype in fetal rat calvarial cultures.

TL;DR: PTH is a potent regulator of osteoblast gene expression, yet the nuclear events that mediate PTH action are poorly understood, and nuclear run-on assays demonstrated an increased rate of c-fos and c-jun transcription after PTH exposure.

TL;DR: The PTH-mediated induction of collagenase transcriptional activity was completely abolished by cycloheximide, while transcription of the beta-actin gene was unaffected by the translation inhibitor, suggesting that a protein factor(s) is required for P TH-mediated transcriptional induction ofcollagenase.

TL;DR: It is proposed that Nmp4/CIZ is a component of a multiprotein assemblage or enhanceosome within the MMP-13 PTH response region and that, within this context, Nmp-13 basal transcription and PTH responsiveness in osteoblasts promotes both basal expression and hormonal synergy.

TL;DR: It is proposed that deficiencies of these BMPs seen in chronic kidney disease (CKD) result in decreased bone remodeling and a compensatory secondary hyperparathyroidism (high turnover state), and their implications for vascular calcification are proposed.