Exact(1)
Thus, we observed that upon Etoposide treatment significantly more of p53 bound to strong binding sites is phosphorylated at S46 than upon Actinomycin D treatment.
Similar(58)
(d) Define the binding partners for effectors whose binding sites are phosphorylated in other layers in the section #layer connections (e.g. RXp = x-xb).
Thus 14-3-3 14-3-3 14-3-3 dimersl logicanates that integrate more than one input to generate an action, and coincidence detectors when the two bendigitaltes are phosphorylogic by different protein kinases.
The effector can only bind if the binding site is phosphorylated.
However, RXE represents the sum of all microscopic species where E is bound to the receptor, and RXp represents the sum of all microscopic species where the binding site is phosphorylated and not occupied.
This SH2 domain binds to the helical domain when PI3K is inactive, but is released from the helical domain when a competing SH2-binding site becomes available in growth factor-stimulated cells; these competing SH2-binding sites are phosphorylated tyrosines of activated growth factor tyrosine kinase receptors (Miled et al, 2007).
The authors develop a model that posits that serine sites are phosphorylated rapidly, but these events are ineffective in promoting rapid arrestin binding; threonine sites are phosphorylated more slowly, but promote rapid arrestin binding.
Our results here provide a clearer biophysical picture for how such coordination could occur: serine sites are phosphorylated rapidly and begin to reduce rhodopsin's catalytic activity, but phosphorylation of serines is ineffective in promoting rapid arrestin-1 binding; threonine sites are phosphorylated more slowly, but promote rapid arrestin-1 binding.
Namely, native serine sites are phosphorylated rapidly and begin to lower rhodopsin's catalytic activity (Ohguro et al., 1993, 1994, 1995; Gibson et al., 2000; Mendez et al., 2000; Kennedy et al., 2001), but serine phosphorylation only weakly promotes arrestin binding; native threonine sites are phosphorylated more slowly but are essential to promote rapid arrestin binding.
There is currently no evidence that this site is phosphorylated naturally, though experiments with Ce-FAR-7 indicate that modification of this site does alter ligand binding.
If the active site is phosphorylated, MPF is inactive.
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