D. Thirumalai

This paper develops an evolutionary model explaining intratumor heterogeneity through unequal allocation of paracrine growth factors, showing it persists only under specific exogenous resource conditions.

The paper resolves the SAXS-FRET controversy by showing that unfolded protein states are universally compact, with β-sheet-rich proteins being more collapsible, and suggests collapsibility constrains protein evolution.

The paper uses molecular simulations to study how ions affect RNA folding thermodynamics, showing a linear relationship between folding free energy and ion preferential coefficient.

The paper investigates frictional effects on RNA folding rates using simulations, finding a maximum folding rate at moderate viscosity and a speed limit of 1-4 seconds at water viscosity.

This study derives analytic expressions for helicase velocity and processivity, showing processivity increases with force and reveals T7 is a weakly active helicase with high back-stepping probability.

This study identifies interface residues that drive allosteric transitions and control tetramer assembly in L-lactate dehydrogenase using computational simulations and structural perturbation methods.

The paper investigates charge fluctuation effects on flexible polyampholytes, showing non-monotonic size dependence and implications for intrinsically disordered proteins.

This study uses simulations to show how ATP binding and linker domain dynamics drive allosteric transitions in dynein, enabling its motility.

The paper models human interphase chromosomes as a self-avoiding polymer to study their glassy dynamics and shows agreement between simulations and experimental data.

This study investigates the structure of APP-C99 in model membranes, revealing how extra-membrane domains influence Aβ oligomerization and γ-secretase processing.

The paper studies collective cell migration in tumor evolution, finding that growth rate influences the transition from glassy to super-diffusive behavior and reveals super-diffusion's universality in non-equilibrium systems.

The paper develops a TIS model for DNA that accurately reproduces experimental data on melting temperatures, ssDNA size, and persistence lengths without parameter tuning.

The paper uses simulations to study how denaturants affect the folding pathways of the PDZ3 domain, revealing concentration-dependent flux changes through intermediates.

The paper uses a heteropolymer model with Hi-C data to study chromatin dynamics, finding that chromosome architecture determines spatiotemporal behavior and cell-to-cell variability.

The paper uses simulations to study the rupture mechanics of cell-adhesion complexes, revealing an abrupt switch between two brittle states under different loading conditions.

The paper introduces a method to analyze allostery in GroEL-GroES and shows that salt-bridge dynamics drive its allosteric transitions and function.

This study investigates how monovalent ions affect the folding pathways of an RNA pseudoknot, showing that salt concentration modulates the flux between parallel folding pathways.

This study uses molecular simulations to quantify how neck-linker docking and trailing head diffusion contribute to kinesin's 16 nm step on microtubules, showing diffusion accounts for most of the movement.

The paper develops a stochastic model to explain how molecular chaperones maximize native state production rates by driving substrates out of equilibrium, reconciling conflicting experimental results on ribozyme and protein folding.

The paper develops a field-theoretic approach to calculate signal transmission error in enzymatic networks and validates it against simulations.

The paper develops a polymer physics-based theory to assess protein collapsibility using contact maps, showing that beta-sheet proteins are more collapsible than alpha-helical ones and explaining the origin of multi-domain proteins.

This paper develops a stochastic model to study how driver, mini-driver, and deleterious passenger mutations influence cancer progression and shows its predictions align with clinical data.

This study uses molecular simulations to show that ubiquitin folding is preceded by collapse, resolving discrepancies between experimental methods.