Interestingly, KRAS mutations at G12C and G12V have a worse clinical outcome possibly due to their ability to engage in multiple downstream effectors including the RAL pathway [14].
This is further delineated using known metabolic effectors including the mitochondrial modulators, oligomycin, antimycin A and FCCP and the CPT-1 inhibitor Etomoxir.
Signals of the active (GTP-bound) Ras from the inner plasma membrane (PM) and from endomembranes activate a multitude of effectors including the Raf/MEK/ERK cascade, phosphatidylinositol-3-OH kinases, and Ral-guanine nucleotide exchange factors [5].
Overall the results are consistent with a model where erlotinib sensitivity is associated with particularly strong signaling from activated EGFR to known core downstream effectors, including the MAPK (Grb2 and ShcA), PI3K/Akt (p85B), and PLCγ (PLCg1) pathways.
Rho1GTP has several effectors including the yeast protein kinase C homolog, Pkc1.
Rho family GTPases modulate actin cytoskeleton dynamics by signaling through multiple effectors, including the p21-activated kinases (PAKs).
For example, the hypertension pathophysiology involves a complex interaction of multiple vascular effectors including the sympathetic nervous and renin-angiotensin-aldosterone systems and the inflammatory mediator activations.
This process is, in turn, controlled by signaling cascades regulated through multiple effectors, including the protein-tyrosine kinase Syk, but the mechanisms involved are poorly understood.
This activates the TβRI kinase, which phosphorylates cytoplasmic effectors, including the canonical nuclear-translocating Smad proteins, but others as well.
