The structures of protein kinase A in complex with CFTR: Mechanisms of phosphorylation and noncatalytic activation
Protein kinase A (PKA) is a key regulator of cellular functions by selectively phosphorylating numerous substrates, including ion channels, enzymes, and transcription factors. It has long served as a model system for understanding the eukaryotic kinases. Using cryoelectron microscopy, we present complex structures of the PKA catalytic subunit (PKA-C) bound to a full-length protein substrate, the cystic fibrosis transmembrane conductance regulator (CFTR)-an ion channel vital to human health. CFTR gating requires phosphorylation of its regulatory (R) domain. Unphosphorylated CFTR engages PKA-C at two locations, establishing two "catalytic stations" near to, but not directly involving, the R domain. This configuration, coupled with the conformational flexibility of the R domain, permits transient interactions of the eleven spatially separated phosphorylation sites. Furthermore, we determined two structures of the open-pore CFTR stabilized by PKA-C, providing a molecular basis to understand how PKA-C stimulates CFTR currents even in the absence of phosphorylation.
Authors
- Csaba Mihályi (ORCID: https://orcid.org/0000-0001-7536-3066)
- I Iordanov (ORCID: https://orcid.org/0000-0001-8251-5857)
- András Szöllősi (ORCID: https://orcid.org/0000-0002-5570-4609)
- Karol Fiedorczuk (ORCID: https://orcid.org/0000-0001-7439-0222)
- László Csanády (ORCID: https://orcid.org/0000-0002-6547-5889)
- Jue Chen (ORCID: https://orcid.org/0000-0003-2075-4283)
Institutions
- Semmelweis University (HU)
- Rockefeller University (US)
Publication Details
- Journal
- Proceedings of the National Academy of Sciences
- Published
- 2024-11-04
- DOI
- https://doi.org/10.1073/pnas.2409049121
- Citations
- 16
- Primary Topic
- Cystic Fibrosis Research Advances
- Type
- article
- Field-Weighted Citation Impact
- 6.70
Funders
- Howard Hughes Medical Institute
- Cystic Fibrosis Foundation
- National Research, Development and Innovation Office
- National Cancer Institute