# The role of BEX1 in translational control of muscle regeneration and reparative growth

> **NIH NIH F31** · OHIO STATE UNIVERSITY · 2021 · $11,763

## Abstract

Project Summary/Abstract
Muscular Dystrophy (MD) is a group of incurable, genetic, muscle disorders that result in progressive declines
in muscle strength, mass, and function among affected patients. Current treatments for MD are ineffective at
preventing muscle degeneration and merely postpone dysfunction and death. For dystrophic muscles to resist
degeneration, they must be able to continuously synthesize specific proteins required for muscle repair,
contraction, and function at rates greater than their degradation. While many therapies have unsuccessfully
focused on treating the underlying genetic defects of these diseases, the preserved functionality of patients in
their early stages highlights the need for new therapeutics that focus on prolonging the regenerative capacity
and functionality of dystrophic muscles. This need can be met by identifying mechanisms regulating
translational control of protein synthesis. Indeed, targeting impairments in protein translation represents a
critical strategy to preserve dystrophic muscle functionally by improving its repair capabilities using novel
therapeutics that enhance the translation of repair specific proteins. In this proposal, we will examine the role of
BEX1 as a novel regulator of translation efficiency in repairing skeletal muscles. We have identified that the
poorly characterized protein BEX1 is induced in response to muscle damage or membrane overload and that
in these repair-inducing conditions, it interacts with molecules required for protein translation. We hypothesize
that BEX1 enhances the translation of proteins required for muscle regeneration and reparative growth by
functioning with the multi-tRNA synthetase complex to mediate translational efficiency. We will test our
hypothesis by carrying out the following aims: (1) To characterize the role of BEX1 in muscle injury and
regeneration in vivo. (2) To determine the role of BEX1 in regulating translational control of protein synthesis.
(3) To test the therapeutic potential of restoring BEX1 levels in muscular dystrophy. This work will be carried
out in the laboratory of Dr. Federica Accornero, an expert on the post-transcriptional regulation of muscle
hypertrophy, under the co-supervision of Dr. Denis Guttridge, a world-renowned skeletal muscle expert in the
areas of myogenesis and muscle atrophy. With the successful completion of this work, we will have the
positive impact of elucidating novel BEX1-dependent mechanisms that regulate translational efficacy during
muscle repair and determining the therapeutic potential of targeting BEX1 to improve muscle regeneration and
function for patients with MD.

## Key facts

- **NIH application ID:** 10405149
- **Project number:** 3F31AR073638-03S1
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Jennifer Morgan Petrosino
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $11,763
- **Award type:** 3
- **Project period:** 2018-08-16 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10405149

## Citation

> US National Institutes of Health, RePORTER application 10405149, The role of BEX1 in translational control of muscle regeneration and reparative growth (3F31AR073638-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10405149. Licensed CC0.

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