| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
American Journal of Pathology, Vol 144, 874-882, Copyright © 1994 by American Society for Investigative Pathology
REGULAR ARTICLES |
J Nalbantoglu, G Karpati and S Carpenter
Department of Neurology-Neurosurgery, McGill University, Montreal, Quebec, Canada.
In muscle biopsies from patients with inclusion body myositis (IBM), multiple sites were found in many muscle fibers that bound single- stranded but not double-stranded DNA without sequence specificity, as exemplified by several different cDNA probes. This activity was attributable to a protein, because it was abolished by proteases but not by RNAse. Most of the sites of binding were myonuclei, whereas some were rimmed vacuoles, which probably result from nuclear breakdown. No comparable binding was seen in 27 control biopsies. A number of human and viral single-stranded DNA binding proteins exist but our data does not identify the protein responsible for DNA binding in IBM. Our findings reinforce the supposition that nuclear damage plays a basic role in the pathogenesis of IBM.
This article has been cited by other articles:
 |
|
 |
|
  S. A. Greenberg Comment on 'Interrelation of inflammation and APP in sIBM: IL-1{beta} induces accumulation of {beta}-amyloid in skeletal muscle' Brain, July 24, 2008; (2008) awn163v1. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Karpati and R. Hohlfeld Biologically stressed muscle fibers in sporadic IBM: A clue for the enigmatic etiology? Neurology, March 14, 2000; 54(5): 1020 - 1021. [Full Text] [PDF]
|
|
|
|
|
|
B. L. Banwell and A. G. Engel {alpha}B-Crystallin immunolocalization yields new insights into inclusion body myositis Neurology, March 14, 2000; 54(5): 1033 - 1041. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
