The mouse benign keratinocyte cell line 308 was previously shown to have less AP-1 DNA binding and transactivation ability than its malignant variant 10Gy5. Because elevated AP-1 activity in 10Gy5 appears to be critical for its malignant phenotype, we were interested in examining the molecular mecha
Integrin-mediated signaling regulates AP-1 transcription factors and proliferation in osteoblasts
β Scribed by Cowles, Elizabeth A. ;Brailey, Lisa L. ;Gronowicz, Gloria A.
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 772 KB
- Volume
- 52
- Category
- Article
- ISSN
- 0021-9304
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
## Abstract Transforming growth factor (TGFβΞ²1) is a potent inducer of chondrogenesis and stimulant of cartilage extracellular matrix (ECM) synthesis. Tissue inhibitor of metalloproteinasesβ3 (TIMPβ3) is located in ECM and is the major inhibitor of matrix metalloproteinases (MMPs) and aggrecanase,
## Abstract Perβ1 is one of the clock genes and is known to regulate various biological events including bone mass determination. Parathyroid hormone is anabolic to bone while the mechanism of its action is not fully understood. Here, we examined the role of PTH on Perβ1 gene expression under osteo
## Abstract Basic fibroblast growth factor (bFGF) and transforming growth factorβΞ²1 (TGFβΞ²1) play an important role in proliferation, differentiation, and survival of malignant gliomas and in normal glial cell biology. Because of these critical roles, potential interactions between these key growth
## Abstract Although estrogen replacement has been the main therapy to prevent and treat osteoporosis, there are concerns about its safety. Phytoestrogens have attracted attention to their potential impacts in osteoporosis prevention and treatment. Among phytoestrogens, the isoflavone daidzein (Dz)
## Abstract Receptor activator of nuclear factor kappa B ligand (RANKL), a potent regulator of osteoclast formation and function, is expressed by osteoblasts and bone marrow stromal cells. However, the molecular mechanism underlying RANKL expression in osteoblast/stromal cells remains largely uncle