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Point mutation in AML1 disrupts subnuclear targeting, prevents myeloid differentiation, and effects a transformation-like phenotype.
Secreted frizzled related protein 1 regulates Wnt signaling for BMP2 induced chondrocyte differentiation.
Mitotic control of RUNX2 phosphorylation by both CDK1/cyclin B kinase and PP1/PP2A phosphatase in osteoblastic cells.
Mitotic retention of gene expression patterns by the cell fate-determining transcription factor Runx2.
Cell cycle related modulations in Runx2 protein levels are independent of lymphocyte enhancer-binding factor 1 (Lef1) in proliferating osteoblasts.
Expression of Runx2 transcription factor in non-skeletal tissues, sperm and brain.
The osteogenic transcription factor Runx2 regulates components of the fibroblast growth factor/proteoglycan signaling axis in osteoblasts.
Biological functions of miR-29b contribute to positive regulation of osteoblast differentiation.
Expression of the osteoblast differentiation factor RUNX2 (Cbfa1/AML3/Pebp2alpha A) is inhibited by tumor necrosis factor-alpha.
Ribonucleoprotein immunoprecipitation (RNP-IP): a direct in vivo analysis of microRNA-targets.
The Runx2 osteogenic transcription factor regulates matrix metalloproteinase 9 in bone metastatic cancer cells and controls cell invasion.
The histone gene activator HINFP is a nonredundant cyclin E/CDK2 effector during early embryonic cell cycles.
Altered Runx1 subnuclear targeting enhances myeloid cell proliferation and blocks differentiation by activating a miR-24/MKP-7/MAPK network.
A program of microRNAs controls osteogenic lineage progression by targeting transcription factor Runx2.
Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition.