Structural Model of the Human BTG2–PABPC1 Complex by Combining Mutagenesis, NMR Chemical Shift Perturbation Data and Molecular Docking

•BTG2, which is frequently mutated in non-Hodgkin lymphoma, can stimulate deadenylation of poly(A)-PABPC1 by the Caf1/CNOT7 subunit of the Ccr4-Not complex.•To understand the interaction between BTG2 and PABPC1 in detail, interfacing residues of PABPC1 and BTG2 were mapped using a mutagenesis approach.•PABPC1 variant R49E has reduced BTG2 binding, but can interact with poly(A).•A structural model of PABPC1-BTG2 was generated using NMR-guided molecular docking followed by validation using mutagenesis data.•A model of the quaternary poly(A)-PABPC1-BTG2-Caf1/CNOT7 complex provides structural insight into enhanced deadenylation by Caf1/CNOT7 of poly(A)-PABPC1 in the presence of BTG2.