Log in

Muscle LIM protein promotes expression of the acetylcholine receptor γ-subunit gene cooperatively with the myogenin-E12 complex

  • Research Article
  • Published:
Cellular and Molecular Life Sciences CMLS Aims and scope Submit manuscript

Abstract

Muscle LIM protein (MLP, also referred to as CRP3) is a muscle-specific LIM-only protein, which consists of two LIM motifs. MLP functions as a positive regulator during myogenesis. Here we report that MLP serves as a cofactor regulating the expression of the nicotinic acetylcholine receptor (AChR) γ-subunit gene in skeletal muscle cells. We found that MLP promoted the expression of the AChR γ-subunit gene in C2C12 myotubes, but not in C2C12 myoblasts or NIH3T3 fibroblasts. Furthermore, we showed that MLP interacted with myogenin in vivo and enhanced the binding ability of the myogenin-E12 heterodimer to the E boxes in the AChR γ-subunit gene promoter. Together, these results suggest that MLP promotes the specific expression of the AChR γ-subunit gene cooperatively with the myogenin-E12 complex during myogenesis.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Subscribe and save

Springer+ Basic
EUR 32.99 /Month
  • Get 10 units per month
  • Download Article/Chapter or Ebook
  • 1 Unit = 1 Article or 1 Chapter
  • Cancel anytime
Subscribe now

Buy Now

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to J. H. Ni.

Additional information

Received 17 May 2004; received after revision 22 July 2004; accepted 26 July 2004

Rights and permissions

Reprints and permissions

About this article

Cite this article

Lu, P.Y., Taylor, M., Jia, H.T. et al. Muscle LIM protein promotes expression of the acetylcholine receptor γ-subunit gene cooperatively with the myogenin-E12 complex. CMLS, Cell. Mol. Life Sci. 61, 2386–2392 (2004). https://doi.org/10.1007/s00018-004-4213-x

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00018-004-4213-x

Navigation