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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Updated: Sep 13, 2025

Identification of MyoD Interactome Using Tandem Affinity Purification Coupled to Mass Spectrometry
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LMOD2 interaction with ACTC1 regulates myogenic differentiation.

Kaiming Wang1, Caihong Liu1, Lei Yi1

  • 1College of Animal Science and Technology, Hunan Agricultural University, Changsha, 410128, China.

BMC Genomics
|July 31, 2025
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Summary

Leiomodin2 (LMOD2) knockout inhibits myoblast proliferation and alters muscle fiber types, impacting skeletal muscle development. MyoG transcriptionally regulates LMOD2, while miR-335-3p negatively controls its expression, revealing new molecular targets.

Keywords:
ACTC1LMOD2KnockoutMyoblastSkeletal muscle

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Area of Science:

  • Muscle physiology and molecular biology.
  • Gene expression and regulation in skeletal muscle.
  • Cellular mechanisms of muscle development and regeneration.

Background:

  • Skeletal muscle, the largest mammalian tissue, is vital for metabolism and homeostasis.
  • Muscle development and regeneration involve complex gene expression regulation.
  • Leiomodin2 (LMOD2) is expressed in cardiac and skeletal muscle, but its function in skeletal muscle development is unknown.

Purpose of the Study:

  • To investigate the physiological functions and regulatory mechanisms of Leiomodin2 (LMOD2) in skeletal muscle development.
  • To identify upstream regulators and interacting proteins of LMOD2.
  • To explore the role of LMOD2 in myoblast proliferation, differentiation, and muscle fiber type determination.

Main Methods:

  • Examined LMOD2 expression in porcine tissues and C2C12 cells.
  • Performed LMOD2 knockout in C2C12 cells to assess functional impacts.
  • Utilized transcriptome analysis (RNA-seq) and Co-immunoprecipitation (Co-IP) assays.
  • Conducted in vivo studies using lentivirus-mediated LMOD2 knockdown.

Main Results:

  • LMOD2 expression decreased with muscle growth but increased post-injury, and rose with C2C12 cell proliferation/differentiation.
  • LMOD2 knockout altered muscle fiber types (inhibited MyHC-I/2b, promoted MyHC-2a/2x), suppressed cell viability, and reduced PAX7 expression.
  • MyoG was identified as an LMOD2 transcription factor, miR-335-3p as a negative regulator, and ACTC1 as an interacting protein.
  • In vivo LMOD2 knockdown reduced muscle mass and suppressed specific MyHC isoforms.

Conclusions:

  • LMOD2 knockout inhibits myoblast proliferation and alters skeletal muscle fiber type composition.
  • MyoG and miR-335-3p are key regulators of LMOD2 expression.
  • LMOD2 interacts with ACTC1 to modulate myogenic differentiation.
  • LMOD2 represents a potential therapeutic target for skeletal muscle development.