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Cationic peptides, for example, are often attracted to negatively charged lipid headgroups, leading to surface adsorption or partial insertion into the bilayer

Activation of these kinase domains results in the activation of multiple signaling pathways including the PI3K/Akt pathway and the Raf/MEK/ERK cascade that ultimately prevent apoptosis and promote cellular growth and survival [1]

Since LCA5 signal at the bulge is also lost in deglutamylase mutants, a possible explanation is that hyperglutamylation leads to the loss of the bulge region, thus causing IFT components to diffuse to the distal cilium and preventing their recycling

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