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Although they can serve as focal points for association of signaling molecules and downstream pathways that regulate tumorigenesis, little is known about how the tumor microenvironment affects the expression and activity of scaffold proteins.
A possible consequence might have been a general effect on process outgrowth via disruption of interactions between gMSD-associated signaling molecules and downstream effectors that mediate changes in cytoskeletal organization or attachment to cytoskeletal elements.
The gene expression signature of EGFR TKI sensitivity displays significant biological relevance in lung cancer biology in that pertinent signalling molecules and downstream effector molecules are present in the signature.
Certain Wnt molecules and downstream signaling events are known to regulate the balance between these factors, and thus are described as gatekeepers for the bifurcation of MSCs to various cell fates (Ross et al. 2000).
The regulator effects algorithm connects upstream regulators, dataset molecules and downstream functions or diseases affected in the dataset to generate a hypothesis that can explain how the upstream regulators affect the downstream target molecule expression and the impact of the molecular expression on functions and diseases.
These transcriptional data have been recently corroborated by genome-wide copy number analysis in BLBC cell lines: although focal amplification of MET was not detected, specific enrichment of the HGF/Met pathway was reflected in frequent copy number gains and overexpression of key adapter molecules and downstream signal transducers [ 54].
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Scaffold proteins are critical hubs within cells that have the ability to modulate upstream signaling molecules and their downstream effectors to fine-tune biological responses.
Bioenergetics consists of a multitude of different cellular pathways and processes that include mitochondrial respiration and the metabolism of various fuel molecules and their downstream products to produce and utilize energy.
In other words, the initial high temperature stress signals must be transmitted by some signaling molecules and trigger downstream signaling processes and transcription controls, which in-turn activate stress-responsive mechanisms to reestablish homeostasis and protect and repair damaged proteins and membranes.
Alterations in adhesion molecules and the downstream signaling consequences may account for the stimulated invasion of tumor cells from their site of origin.
Hence balanced ROS generation in resistant plants act as signaling molecules and communicate downstream defense signals.
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