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Biology subjects

Cardani, L. P.

Publications and source records attributed to Cardani, L. P..

2 recordsLinked to original sources

Quantitative machine learning of protein interactions reveals the multiscale organization and molecular syntax of signaling networks

Cells employ dense networks of transient protein-protein interactions mediated by modular peptide-binding domains and unstructured peptidic motifs for high-fidelity information processing. How these networks physically execute computations through protein interactions governed by complex intra- and intermolecular mechanisms remains indiscernible from current, sparse and non-quantitative, maps of the human interactome. Here, we introduce a quantitative statistical mechanical modeling (QSM) approach for machine learning domain-peptide affinities with experimental-level accuracy. Leveraging a new, principled algorithm for data harmonization and a biophysically informed neural network architecture, QSM learns to predict dissociation constants directly from amino acid sequences with calibrated confidence. We use QSM to construct the first quantitative drafts of human signaling networks and study these networks across three physical scales--recognition mechanisms of modular binding domains, combinatorial logic of multi-dentate proteins, and pathways inferred from de novo inference of protein interaction networks. We find that (i) modular domains, based on their binding preferences, selectivities, and strengths, fall into a limited number of biophysical equivalence groups, (ii) those domains, along with peptidic motifs, are "syntactically" combined within proteins to yield multivalent recognition mechanisms, and (iii) the organization of cellular function can be traced back to algorithmically detectable modules induced by domain-mediated interactions. In aggregate, these analyses instantiate a tractable roadmap towards a comprehensive, mechanistic, and simulatable articulation of the systems biology of signaling.

systems biology↗

Signaling specificity and kinetics of the human metabotropic glutamate receptors.

Metabotropic glutamate receptors (mGluRs) are obligate dimer G protein coupled receptors that can all function as homodimers. Here, each mGluR homodimer was examined for its G protein coupling profile using a BRET based assay that detects the interaction between a split YFP-tagged G{beta}1{gamma}2 and a Nanoluc tagged free G{beta}{gamma} sensor, MAS-GRK3-ct-NLuc with 14 specific G proteins heterologously expressed, representing each family. Canonically, the group II and III mGluRs (2&3, and 4, 6, 7&8, respectively) are thought to couple to Gi/o exclusively. In addition, the group I mGluRs (1&5) are known to couple to the Gq/11 family, and generally thought to also couple to the PTX-sensitive Gi/o family; some reports have suggested Gs coupling is possible as cAMP elevations have been noted. In this study, coupling was observed with all 8 mGluRs through the Gi/o proteins, and only mGluR1&5 through Gq/11, and perhaps surprisingly, not G14. None activated any Gs protein. Interestingly, coupling was seen with the group I and II, but not the group III mGluRs to G16. Slow but significant coupling to Gz was also seen with the group II receptors.

pharmacology and toxicology↗