Pertinent to the G1/S transition, activation of ERK1 and ERK2 is required up to late G1 for expression of cyclin D1 and successful S entry, though the activity of these proteins is not necessary after the R-point.
Similar to ApoE−/− mice, nearly identical data were reproduced in the Ldlr−/− mouse strain, including cold-induced WAT-to-BRITE transition, activation of BAT, adipocyte size changes and UCP1 upregulation, lipolysis, body weight and BMI decreases, cholesterol synthesis alterations of blood lipid profiles, plaque growth, and instability index.
Leung, T., Söll, I., Arnold, S. J., Kemler, R. & Driever, W. Direct binding of Lef1 to sites in the boz promoter may mediate pre-midblastula-transition activation of boz expression.
The glass transition temperature (Tg) and glass transition activation energy of asphalt mastic were obtained by the dynamic mechanics analysis (DMA) method, and the effect of fillers on the distribution of wax in asphalt was studied by the differential scanning calorimetry (DSC).
This pattern is characterized by patchy parenchymal inflammation, epithelial cell injury with reactive hyperplasia, epithelial mesenchymal transition, activation and differentiation of fibroblasts to myofibroblasts, basement membrane and alveolar epithelium injuries.
In light of these facts, usage of Kissinger-type equations for the evaluation of the "glass transition activation energy" was shown to be incorrect.
Cyclin E (cycE), encoded by cyclin E/CCNE1, is an important cell cycle regulator, which promotes G1/S transition by activation of Cdk2 kinase activity [1], [2].
For example, BAG3 regulates epithelial-mesenchymal transition and angiogenesis through ERK phosphorylation [ 57, 107]; induces epithelial-mesenchymal transition through activation of the transcription factor ZEB1 [ 108]; and modulates the activity of the transcription factors FoxM1 and Hif1α, the translation regulator HuR and the cell cycle regulators p21 and survivin [ 109].
Zhang, L. et al. Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor-1α in hepatocellular carcinoma.
In mouse models of leukemia and melanoma, IDH mutants accelerated cell cycle transition by activation of the MAPK/ERK pathway and repression of tumor suppressors CDKN2A and CDKN2B (Chaturvedi et al., 2013; Shibata et al., 2011).
The myofibroblast cell, thought to originate from various sources including transformation of resident or bone marrow-derived fibroblasts, transdifferentiation of epithelial cells to mesenchymal-type cells via EMT (epithelial-mesenchymal transition), and activation of resident stellate (astrocyte) cells, is a mediator of tissue fibrosis [117].
