SP1
- Research ArticleTumor Necrosis Factor Alpha Regulates Skeletal Myogenesis by Inhibiting SP1 Interaction with cis-Acting Regulatory Elements within the Fbxl2 Gene Promoter
Skeletal muscle regeneration and repair involve the recruitment and proliferation of resident satellite cells that exit the cell cycle during the process of myogenic differentiation to form myofibers. We demonstrate that the ubiquitin E3 ligase subunit FBXL2 is essential for skeletal myogenesis through its important effects on cell cycle progression and cell proliferative signaling. Further, we characterize a new mechanism whereby...
- Research ArticleTranscriptional Suppression of CPI-17 Gene Expression in Vascular Smooth Muscle Cells by Tumor Necrosis Factor, Krüppel-Like Factor 4, and Sp1 Is Associated with Lipopolysaccharide-Induced Vascular Hypocontractility, Hypotension, and Mortality
Vasodilatory shock in sepsis is caused by the failure of the vasculature to respond to vasopressors, which results in hypotension, multiorgan failure, and ultimately patient death. Recently, it was reported that CPI-17, a key player in the regulation of smooth muscle contraction, was downregulated by lipopolysaccharide (LPS) in mesenteric arteries concordant with vascular hypocontractilty.
- Research ArticleRegulation of Transcription Factor SP1 by the β-Catenin Destruction Complex Modulates Wnt Response
The ubiquitous transcription factor specificity protein 1 (SP1) is heavily modified posttranslationally. These modifications are critical for switching its functions and modulation of its transcriptional activity and DNA binding and stability.