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Whereas due to their cellular retention and/or low cellular concentrations, CoA and Fe–S clusters are not likely to consume substantial amounts of Cys, taurine and likely also H 2 S and sulfate can be abundantly excreted, and therefore might drive substantial consumption of cellular Cys (38, 130)
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These findings and others led to the development of a ‘classical' model for the agonist-induced desensitization of GPCRs (Krupnick and Benovic, 1998
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