Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Sep 7;7(2):165–180. doi: 10.1002/jcsm.12057

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2015 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of the Society of Sarcopenia, Cachexia and Wasting Disorders

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

PMC Copyright notice

Double knockout (DKO) mice displayed a protein aggregate myopathy and a shift towards slow myofibres in extensor digitorum longus (EDL) muscle. (A) Electron microscopy of soleus (Sol) and EDL sections displayed accumulation of amorphous material in DKO myofibres. Asterisks indicate accumulating aggregates, arrow points to abnormal Z‐line. Scale bar, 5 µm (α–δ), 2 µm (ε, ζ). (B) ATPase stain of Sol and EDL showed accumulations inside of slow/type I fibres (dark blue, white arrows) and fast/type II fibres (bright blue, black arrows) of DKO mice. Slow/type I fibres occurred in EDL of DKO mice (asterisk). Scale bar, 50 µm. (C) Immunoblotting of proteins from the soluble (supernatant) and particulate (pellet) fractions of EDL revealed accumulation of slow/type I myosin heavy chain protein in DKO muscle. Actin was used as a control.