A General Mathematical Model of Symport Based on Conformational Transitions
- 1School of Biomedical Engineering, Southern Medical University, Guangzhou, Guangdong Province, P.R. China
Abstract
General mathematical modeling of symport faces two fundamental challenges: (i) a unified kinetic description independent of protein-specific structural details; and (ii) quantitative cross-scale mapping between microscopic conformational transitions and macroscopic physiological observables. Grounded in the fundamental physiological principle of cellular homeostasis, we propose a unifying hypothesis for symporter gating: symporters actively regulate intracellular concentrations of specific solutes within thermodynamically feasible bounds. Based on this hypothesis, we construct a universal mathematical model of symporters, employing a minimal conformational cycle as the topological scaffold and probabilistic transition rates to quantitatively describe conformational interconversion kinetics. Model simulations of experimental data from the SGLT, NaPi-II, NKCC, and NBC transporter families yield consistent fits. The resulting parameters not only reproduce experimentally observed transport behaviors---but also reveal underlying mechanistic principles of symporter function.
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BibTeX
@misc{wang2026general,
title = {{A General Mathematical Model of Symport Based on Conformational Transitions}},
author = {Q. Wang and F. Liang},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.15.759425},
url = {https://www.biorxiv.org/content/10.64898/2026.10.15.759425v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - A General Mathematical Model of Symport Based on Conformational Transitions
AU - Q. Wang
AU - F. Liang
PY - 2026
DA - 2026/10/15
PB - bioRxiv
DO - 10.64898/2026.10.15.759425
UR - https://www.biorxiv.org/content/10.64898/2026.10.15.759425v1
AB - General mathematical modeling of symport faces two fundamental challenges: (i) a unified kinetic description independent of protein-specific structural details; and (ii) quantitative cross-scale mapping between microscopic conformational transitions and macroscopic physiological observables. Grounded in the fundamental physiological principle of cellular homeostasis, we propose a unifying hypothesis for symporter gating: symporters actively regulate intracellular concentrations of specific solutes within thermodynamically feasible bounds. Based on this hypothesis, we construct a universal mathematical model of symporters, employing a minimal conformational cycle as the topological scaffold and probabilistic transition rates to quantitatively describe conformational interconversion kinetics. Model simulations of experimental data from the SGLT, NaPi-II, NKCC, and NBC transporter families yield consistent fits. The resulting parameters not only reproduce experimentally observed transport behaviors---but also reveal underlying mechanistic principles of symporter function.
ER -