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DOI: http://dx.doi.org/10.7554/eLife.01857.012 To determine whether asymmetric BMP signaling plays an instructive role in the regulation of ISC self-renewal, we ectopically activated the pathway in precursor cells by expressing a constitutively active form of Tkv (TkvQ235D) (Nellen et al., 1996).
As previously described, the related oxysterol, 7β-hydroxysterol, neither induced Smo translocation nor activated the pathway (Fig. 1C, Fig. 2B) [15].
When activated, the pathway also contributes to G2/M cell cycle arrest.
IGF-1 stimulation that activated the pathway was used as a positive control.
To determine further TGF-β1 signalling in oral cancer cell lines, we activated the pathway by TGF-β1 stimulation and suppressed it with an anti-TGF-β1 antibody.
To obtain direct evidence that the Wnt/β-catenin signaling pathway can trigger extracellular matrix degradation and hypertrophic chondrocyte differentiation in osteoarthritis, we activated the pathway in vitro by using LiCl in normal and osteoarthritic chondrocytes and evaluated the expression levels of basic catabolic (MMP-7, 9, 13, 14, ADAMTS-5, and 4) and hypertrophic markers (collagen X).
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This amount increased but activity decreased insulin failed to activate the pathway.
To activate the pathway in neurons, we expressed the constitutively active HEP (hepCA) with the elavGal4 driver.
Overexpression of Rheb activates the pathway independent of Tsc gene function [11] [13].
Mutations in these genes also result in accumulation of Notch protein, but do not activate the pathway [8].
Increased signalling via the epidermal growth factor family (ERBB) receptors also activates the pathway.
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