Morphogenesis of multicellular organisms is driven by changes in cell behavior, which happen at precise locations and defined developmental stages.
The exact mechanism of Tsc2 mediated tumor suppression is not known, however, there is evidence that it is most likely mediated by changes in cell cycle regulation via the PI3K/Akt pathway.
As activity-stimulated protein synthesis can be triggered by changes in cell Ca2+, cAMP, and ATP levels, their relative contributions to synthesis of competent new insulin granules is receiving intense scrutiny.
Degradation and recovery of electrode performance during the operation of polymer electrolyte fuel cells (PEFCs) with sulfonated polyimide (SPI-8) and Nafion® membranes were evaluated by changes in cell voltage (Ecell), mass activity (MA), Tafel slope (TS), and electrochemical surface area (ECA) of the Pt catalyst.
Altered adhesion/motility of those cells was accompanied by changes in cell morphology, density of adhesion-associated proteins, and actin staining.
This activation of Rac was accompanied by changes in cell morphology and proliferation, Rac localization, fibronectin deposition, and the organization of actin filament-based networks [10].
However, combined treatment with these subeffective doses of γ-tocotrienol and SU11274 results in reversal of EMT, as demonstrated by changes in cell marker expression including augmentation of epithelial protein markers E-cadherin, β-catenin, cytokeratin-8, and cytokeratin-18, and corresponding reduction in mesenchymal protein marker (vimentin) expression [25].
The effect of RA and FGF4 was also evident by changes in cell morphology.
Such reductions can be explained by changes in cell numbers as a result of apoptosis or reductions in neurogenesis.
Impaired β1-integrin recycling affected cell motility, as reflected by changes in cell spreading and wound healing.
The differentiation of these cells is mirrored by changes in cell morphology apparent in high resolution TPEF images and by the detection of collagen production via SHG imaging.
