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Examinations of the genetic basis for this response in the yeast Saccharomyces cerevisiae indicate that the RAD9 gene product is essential for arrest of cell division induced by DNA damage.
Examining changes in global gene expression to determine a genetic basis for this response, we demonstrate a vascular endothelial growth factor (VEGF -induced upregulation of genes associated with VEGF -inducedsion and remodeling when cell adhesion was limited, whereas cells on highly adhesive supregulationgulated genes assofiated with proliferation.
However, the molecular basis for this response remains largely unexplored.
Some NLPs induce a hypersensitive-like response in dicot plants though the basis for this response remains unclear.
Both the basis for this response and the contribution of rods, cones and melanopsin-based photosensitive retinal ganglion cells (pRGCs) remains unknown.
The basis for this response is unknown, although it might be related to a primary central nervous system effect of this cell-wall dose.
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We were interested in a better understanding of the basis for this differential response to various anti-VEGF therapies that may help to identify a predictive marker(s) of response, and would greatly aid in the identification of a suitable patient population for treatment.
While the basis for this remarkable response is not clearly understood, focusing on such approaches may provide better direction for future drug development.
The basis for this differential response is not known but may be related to both tissues originating from different types of precursor cells, having different differentiation potential [26], [27].
The fundamental basis for this reduced response was linked to the lower production of ET-1 by gingival fibroblasts; addition of ET-1 rescued the ability of gingival fibroblasts to respond to TGFβ.
The basis for this shared response is not yet clear.
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