Rohit V. Pappu

The paper designs synthetic scaffold proteins that form cell-cell interfaces with switch-like condensation behaviors, enabling selective and specific intercellular interactions.

The paper shows that alpha-synuclein phase separation can form Lewy body-like structures without pre-existing seeds, suggesting a new mechanism for neurodegeneration.

This study shows that electrostatic interactions between intrinsically disordered regions drive G3BP1 condensate ageing, with RNA modulating these interactions and delaying dynamic arrest.

The paper discovers that intrinsically disordered proteins form condensates with catalytic activity through sequence-dependent electrochemical microenvironments, enabling hydrolysis reactions and gene circuit activation in cells.

ASAP-ID reduces steric disruption in proximity labelling by using small tags and antibodies, identifying new lamin interactors and showing mutant-specific aggregation patterns.

This paper maps the critical regime of an intrinsically disordered protein using simulations and finite-size scaling, identifying three distinct phase behavior regimes.

The paper shows that MALAT1 long noncoding RNA forms condensates with splicing factors to regulate hypoxia-induced alternative splicing near nuclear speckles.

This study shows that ASXL1 mutations promote cancer by unleashing phase separation, which enhances gene activation and leukemogenesis.

This study identifies mast cell extracellular granules as bioactive condensates formed by heparin and polyamines, enhancing enzymatic activity and cytokine bioactivity.

The paper shows that SRSF1 and TDP-43 form microphases through protein interactions, and MALAT1 enhances this process by binding to SRSF1 microphases.

This study shows nuclear-import receptors suppress RNA-binding protein phase transitions by remodeling the dilute phase, preventing disease-linked aggregation.

This paper develops computational rheometry models to study viscoelastic properties of biomolecular condensates using graph-based network simulations.

The paper shows that separable interactions in A1-LCD allow tunable metastability of condensates, which can suppress amyloid fibril formation even with ALS mutations.

The paper investigates anisotropies in RNA-based biomolecular condensate interfaces, finding that purine-rich RNAs drive phase separation while pyrimidine-rich RNAs accumulate at interfaces, with distinct motion patterns observed using single-molecule imaging.

The paper shows how peptide backbones enhance pairwise interactions in dilute phases but weaken them in dense phases, enabling percolation in peptide-based mimics of protein condensates.

The paper introduces GIN, a resource that decodes molecular grammars of human intrinsically disordered regions (IDRs) and identifies their functional roles in biological processes and disease.

This study identifies sequence-encoded molecular grammars in synapsin-1 IDRs that drive condensation and generate pH gradients relevant for synaptic function.

The paper shows that biomolecular condensates generate interphase electric potentials due to ion asymmetry, suggesting they function as mesoscale capacitors.

The paper computes viscoelastic moduli of biomolecular condensates using generalized Rouse models and Monte Carlo simulations, showing that a mixture of single-chain and collective models provides the most accurate results.

The paper identifies three design principles of acidic transcriptional activation domains through experimental analysis and develops a predictor to identify these domains in the human proteome.

The paper identifies inert and seed-competent tau monomers, showing structural differences that influence aggregation potential.

The paper investigates how the charge patterning and sequence complexity of the FtsZ C-terminal tail influence Z-ring formation and bacterial cell division.

This study uses a deep mutational scan to analyze the sequence features of an acidic activation domain, finding that acidic residues help expose hydrophobic motifs and that activity increases under amino acid starvation.