bioRxiv Science⌕ Search

Biology subjects

Hou, T.

Publications and source records attributed to Hou, T..

38 records · Page 3Linked to original sources

A physics-based energy function allows the computational redesign of a PDZ domain

A powerful approach to understand protein structure and evolution is to perform computer simulations that mimic aspects of evolution. In particular, structure-based computational protein design (CPD) can address the inverse folding problem, exploring a large space of amino acid sequences and selecting ones predicted to adopt a given fold. Previously, CPD has been used to entirely redesign several proteins: all or most of the protein sequence was allowed to mutate freely; among sampled sequences, those with low computed folding energy were selected, and a few percent of them did indeed adopt the correct fold. Those studies used an energy function that was partly or largely knowledge-based, with several empirical terms. Here, we show that a PDZ domain can be entirely redesigned using a \"physics-based\" energy function that combines standard molecular mechanics and a recent, continuum electrostatic solvent model. Many thousands of sequences were generated by Monte Carlo simulation. Among the lowest-energy sequences, three were chosen for experimental testing. All three could be overexpressed and had native-like circular dichroism and 1D-NMR spectra. Two exhibited an increase in their thermal denaturation curves when a peptide ligand was present, indicating binding and suggesting correctly folded proteins. Evidently, the physical principles that govern molecular mechanics and continuum electrostatics are sufficient to perform whole-protein redesign. This is encouraging, since these methods provide physical insights, can be systematically improved, and are transferable to other biopolymers and ligands of medical or technological interest.\n\n\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=73 SRC=\"FIGDIR/small/790667v3_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (26K):\norg.highwire.dtl.DTLVardef@145ea28org.highwire.dtl.DTLVardef@10ffa2forg.highwire.dtl.DTLVardef@1f2460eorg.highwire.dtl.DTLVardef@d5691c_HPS_FORMAT_FIGEXP M_FIG Table of Contents Graphic\n\nC_FIG

biophysics↗

NDUFAB1 Protects Heart by Coordinating Mitochondrial Respiratory Complex and Supercomplex Assembly

The impairment of mitochondrial bioenergetics, often coupled with exaggerated reactive oxygen species (ROS) production, is emerging as a common mechanism in diseases of organs with a high demand for energy, such as the heart. Building a more robust cellular powerhouse holds promise for protecting these organs in stressful conditions. Here, we demonstrate that NDUFAB1 (NADH:ubiquinone oxidoreductase subunit AB1), acts as a powerful cardio-protector by enhancing mitochondrial energy biogenesis. In particular, NDUFAB1 coordinates the assembly of respiratory complexes I, II, and III and supercomplexes, conferring greater capacity and efficiency of mitochondrial energy metabolism. Cardiac-specific deletion of Ndufab1 in mice caused progressive dilated cardiomyopathy associated with defective bioenergetics and elevated ROS levels, leading to heart failure and sudden death. In contrast, transgenic overexpression of Ndufab1 effectively enhanced mitochondrial bioenergetics and protected the heart against ischemia-reperfusion injury. Our findings identify NDUFAB1 as a central endogenous regulator of mitochondrial energy and ROS metabolism and thus provide a potential therapeutic target for the treatment of heart failure and other mitochondrial bioenergetics-centered diseases.

cell biology↗