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Previous studies indicated that neuronal plasticity results in a cascade of modifications in structures following modification of neural input [ 6– 8].
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In mitosis, it is believed that this cascade of histone modifications is acting independently of condensin to compact chromosomes [ 45].
The cytosolic protein KRAS requires a cascade of posttranslational modifications initiated by a CAAX motif, catalyzed by farnesyltransferase (FTase) in order to localize to the cell surface for normal function.
In bacteria, the linkage of input signals to output responses entails a cascade of protein modifications, basically of two modes: One-component and two-component systems (denominated as 1CST and 2CST, respectively).
Together, this cascade of histone modifications was proposed to drive chromatin hypercondensation during mitosis, independently from condensin [ 45].
Signal transduction by TGFb involves a cascade of molecules resulting in modification of gene transcription to elicit the cellular response [reviewed in (8)].
Hence, a comprehensive pathway map with detailed descriptions of different types of chemical modifications in the reaction cascades is required.
Information transmission in cells occurs through complex networks of proteins and genes and is relayed through cascades of biochemical modifications, which are typically studied through ordinary differential equations.
The regime unleashed a cascade of abuse in response.
This results in the arrest of the C-24 hydroxylation initiated cascade of side chain modifications at the C-24 oxo stage, thus producing the stable C-24 oxo metabolites which are as active as their parent analogs.
We chose the NFκB signal transduction cascade as a model system to validate this approach because specific target proteins in this signaling pathway undergo a multitude of posttranslational modifications in response to pathway stimulation.
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