Evolutionary crossroads of cell signaling: PP1 and PP2A substrate sites in intrinsically disordered regions
Open accessAbstract
Phosphorylation of the hydroxyl group of the amino acids serine and threonine is among the most prevalent post-translational modifications in mammalian cells. Phospho-serine (pSer) and -threonine (pThr) represent a central cornerstone in the cell's toolbox for adaptation to signal input. The true power for the fast modulation of the regulatory pSer/pThr sites arises from the timely attachment, binding and removal of the phosphate. The phosphorylation of serine and threonine by kinases and the binding of pSer/pThr by phosphorylation-dependent scaffold proteins is largely determined by the sequence motif surrounding the phosphorylation site (p-site). The removal of the phosphate is regulated by pSer/pThr-specific phosphatases with the two most prominent ones being PP1 and PP2A. For this family, recent advances brought forward a more complex mechanism for p-site selection. The interaction of regulatory proteins with the substrate protein constitutes a first layer for substrate recognition, but also interactions of the catalytic subunit with the amino acids in close proximity to pSer/pThr contribute to p-site selection. Here, we review the current pieces of evidence for this multi-layered, complex mechanism and hypothesize that, depending on the degree of higher structure surrounding the substrate site, recognition is more strongly influenced by regulatory subunits away from the active site for structured substrate regions, whereas the motif context is of strong relevance with p-sites in disordered regions. The latter makes these amino acid sequences crossroads for signaling and motif strength between kinases, pSer/pThr-binding proteins and phosphatases.
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The 14-3-3 protein binding motif is a firmly established PP2A-B56α target in many signal transduction proteins.
“among the enriched motifs, 14-3-3 protein binding motif is a firmly established PP2A-B56α target in many signal transduction proteins49.”
From Structural mechanism for inhibition of PP2A-B56α and oncogenicity by CIP2A (2023) · cites this paper as [49]
The ‘Enzymes and interactors’ section identifies established 14-3-3-binding motifs in phosphosignaling. But ‘The role of IDRs’ section describes an LxxIxE motif for PP2A:B56 substrate binding and gives PP1—not PP2A-B56α—examples involving 14-3-3 sites. It does not establish 14-3-3-binding motifs as PP2A-B56α targets in many signal-transduction proteins. (LLM, conf=0.85)
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References 79 · Cited by 14
- Authors
- Hoermann, B., & Köhn, M.
- Affiliations
- University of Freiburg (DE)
- Corresponding author
- Hoermann, Bernhard
- Köhn, Maja
- Venue
- Biochemical Society Transactions
- Publisher
- Portland Press Ltd.
- Published
- 2021-06-08
- Volume
- 49
- Issue
- 3
- Pages
- 1065-1074
- ISSN
- 0300-5127 (ISSN-L)
- 1470-8752
- PMC
- PMC8286827
- OpenAlex
- W3168424926
- Cited by
- 14
- References
- 79
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 4 · 2022: 3
- FWCI
- 0.29
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Biochemical Society Transactions (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft ((EXC 294))
- H2020 European Research Council (865119)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Structure and Dynamics
- Keywords
- protein phosphatase 1, protein phosphatase 2A, serine/threonine phosphorylation, intrinsically disordered regions, substrate recognition, post-translational modification, signal transduction
- MeSH terms
- Animals, Binding Sites, Humans, Phosphorylation, Serine, Substrate Specificity, Threonine, Signal Transduction, Evolution, Molecular, Protein Phosphatase 1, Protein Phosphatase 2, Intrinsically Disordered Proteins
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