Thus, B-Myb induction, IRF1 decrease, and IRF8 protein degradation are recognized as TNF-specific induced osteoclastogenic mechanisms, which form an inflammatory osteoclastogenic program. Targeting the mechanisms in this specific program has therapeutic implications in the selective treatment of ...
To determine the significance between two groups, comparisons were made using two-tailed Mann–Whitney non-parametric test by using wilcox.text() function form Stats R package. For correlation, the non-parametric Spearman coefficient was calculated and significance was calculated using Fisher exact ...
A: EL4 tumor cells were infected with either empty retroviral vector (pRS), with retroviruses expressing short-hairpin RNAs against TGF-β1 (shTGF-β1), or encoding a soluble form of TβR-II. Northern analysis was performed for TβR-II and Tgf-β1. Soluble TβR-II expression was dete...
TGF-β is synthesized in a latent form that must be activated to allow for engagement of a tetrameric receptor complex composed of TGF-β receptors I and II (TGF-βRI, TGF-βRII). Activated TGF-β complexes, with additional factors, form a serine/threonine kinase complex that binds to ...
[103,104,105]. TGF-β is synthesized in a precursor form in the cell, which needs furin activity for maturation [106]. Pre-pro-TGF-β contains a signal peptide (pre-region), latency-associated peptide (LAP, which is also called the pro-region), and TGF-β region. This complex, ...
Studies with transgenic mice overexpressing a constitutively activated form of TGF-β 1 [6], as well as functionablating mutant TGF-β signaling receptors, were confirmatory. The ectopic expression of...
The activity of TGF-β1 is regulated primarily extracellularly where the secreted latent form must be modified to expose the active molecule. Here we show ... SE Crawford,V Stellmach,JE Murphy-Ullrich,... - 《Cell》 被引量: 2536发表: 1998年 ...
is required for the targeting to the cell surface. In the endoplasmic reticulum, in its immature form (i.e. with a prosegment and lacking full N-glycosylation), interacts with CNIH. In the Golgi apparatus, may form a complex with CNIH and GORASP2. Interacts (via cytoplasmic C-terminal ...
After phosphorylation, R-Smads can form a ternary complex with a common partner Smad4 and then translocate to the nucleus, where they regulate the transcription of target genes (Shi and Massagué, 2003). TGF-β family members, which include TGF-βs, activins, and BMPs, play key roles in...
Interestingly, our studies reveal that macrophages lacking TβRII have defects in expression of a set of genes that form the hallmark of the M2 polarizing program, suggesting that TGFβ signaling is needed for the alternative activation of macrophages....