{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T15:39:57Z","timestamp":1787499597351,"version":"build-2736575974"},"reference-count":17,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2002,7,8]],"date-time":"2002-07-08T00:00:00Z","timestamp":1026086400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2002,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Adenine nucleotide translocator\u20101 (ANT\u20101), encoded by chromosome 4 (4q34\u201035 locus), is a component of the mitochondrial permeability transition pores that are involved in apoptotic mechanisms. We studied muscle biopsies from seven individuals with autosomal dominant progressive external ophthalmoplegia caused by ANT\u20101 mutations. We found no instance of terminal deoxynucleotidyltransferase\u2010mediated dUTP nick end labeling (TUNEL) positivity nor significant expression of apoptosis\u2010related proteins. Furthermore, there was no morphological evidence of apoptosis at the ultrastructural level. Thus, degeneration of muscle in this disorder is nonapoptotic. \u00a9 2002 Wiley Periodicals, Inc. 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