Exact(50)
In cells overexpressing any of the antagonists, the propensity for FGF-induced cell elongation was significantly reduced, indicative of a block to lens fiber differentiation.
While much is known about muscle spindle structure, innervation and function, relatively few factors have been identified that regulate intrafusal fiber differentiation and spindle development.
Of these antagonists, Spry1 and Spred2 appeared to be the most potent among their respective family members, demonstrating the greatest block in FGF-induced fiber differentiation based on the percentage of cells that failed to elongate.
Whilst it is now known that the epithelial to fiber differentiation process is driven by FGF, little is known about factors that coordinate the precise assembly of fibers into a functional lens.
In addition, and looking to the future, this review also looks at possibilities for supplanting EMT with normal fiber differentiation and thereby promoting lens regenerative processes after cataract surgery.
Taken together, Spry and Spred proteins that are predominantly expressed in the lens epithelium in situ, appear to have overlapping effects on negatively regulating ERK1/2-signaling associated with FGF-induced lens epithelial cell elongation leading to fiber differentiation.
Similar(10)
The proportions of slow twitch and fast twitch were recorded as the reference parameters after the fibers differentiation.
Results from this work have confirmed that the rate of lens cell proliferation and new fiber cell differentiation progressively slows as the lens differentiates and grows.
The results of present studies are applicable not only for lens fiber cell differentiation but also for understanding how FGF signaling could regulate cellular differentiation in other systems.
Differentiation of rat lens epithelial explants by FGF2 mimics key features of lens fiber cell differentiation (McAvoy and Chamberlain 1989; Zelenka et al. 2009; West-Mays et al. 2010).
Lens fiber cell differentiation represents an advantageous model system to study how extracellular signals induce cell-cycle exit-coupled terminal differentiation (Lovicu and McAvoy 2005; Griep 2006).
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