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While further investigations are required to fully elucidate why the phospho-null mutant GLP-1R is unable to sustain GLP-1-induced cAMP signalling in -cells, alterations in the recruitment of specific PDEs, which can potentially be cell-type specific and therefore not always replicated in non--cell systems, are likely to play an important role, as shown here by the capacity of the PDE4-specific inhibitor rolipram to restore cAMP responses from the triple AA phospho-null mutant receptor

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