The biosynthetic pathway leading to monolignols in switchgrass is not completely known, and difficulties associated with in vivo measurements of these intermediates pose a challenge for a true understanding of the functioning of the pathway.
Drugs can be designed to modify the functioning of the pathway in the diseased state by inhibiting a key molecule, or to enhance the normal pathway by promoting specific molecules that may have been affected in the diseased state.
Thus, aberrant function of the pathways involved might result in chemoresistance.
As this analysis relies solely on genomic material, the active function of the pathways examined cannot be confirmed without further proteomic or expression data.
Therefore, it is important to decode the context-specific regulatory mechanisms of the pathway, and to dissect the function of the pathway in a spatial and temporal specific manner in vivo.
However, the function of the pathway in plants has been more difficult to demonstrate.
During eye development, disruption of the Hpo pathway results in an overgrowth phenotype [7], [8], [12], [15], [17], reflecting the tumor-suppressor function of the pathway.
These identifiers and references are useful for the implementation of many functions of the pathway browser and for the interoperability of the tool.
Our approach to this is the detailed analysis of the molecular function of the pathway driving genes.
Withdrawal of trastuzumab allows return of function of the pathway and reversal of LVEF decline, in contrast to the permanent myocyte dysfunction and loss caused by anthracyclines.
This is an important function of the pathway because the location of a cell determines the local microenvironmental signals it receives [ 3,15].
