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The sera from patients with human Duchenne (X-linked) progressive muscular dystrophy contain elevated adenylate kinase (ATP: AMP phosphotransferase, EC 2.7.4.3) activities, in addition to their characteristically high creatine kinase (ATP; creatine N-phosphotransferase, EC 2.7.3.2) activities. By agarose gel electrophoresis of human Duchenne dystrophic serum, the presence of an apparently normal human serum adenylate kinase together with a variant species of adenylate kinase was detected. The latter enzyme species appeared, in its mobility, to be similar to that of the normal human liver-type adenylate kinase. The presence of this aberrant liver-type adenylate kinase could also be demonstrated by characteristic (for the liver type) inhibition patterns with P1,P5-di-(adenosine-5')pentaphosphate, 5,5'-dithiobis(2-nitrobenzoate) and phosphoenolpyruvate. On the other hand, by inhibition titrations with an anti-muscle-type adenylate kinase, hemolysates from the erythrocytes of several Duchenne and Becker's dystrophics were found to contain approx. 96% muscle-type adenylate kinase and their serum approx. 97% muscle-type adenylate kinase. These same patients contained approx. 89% M-M type creatine kinase in their serum (by inhibition against anti-human muscle-type creatine kinase) indicative of the presence also of M-B plus B-B type active isoenzymes. All of these data can best be explained by the presence of a variant or mutant adenylate kinase isoenzyme in the dystrophic serum. This isoenzyme appears to resemble the liver type in its inhibition patterns with P1,P5-di(adenosine-5')pentaphosphate, 5,5'-dithiobis(2-nitrobenzoate) and phosphoenolpyruvate, and in its heat stability (compare also the agarose gel electrophoresis pattern); but structurally, it is a muscle type, or derived from a muscle type, as shown immunologically by inhibition reactions with anti-muscle-type adenylate kinase. Whether this is a fetal-type isoenzyme of adenylate kinase will require further investigation.
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
October 1986,
Biochimica et biophysica acta,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
November 1978,
Clinical genetics,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
September 1978,
Clinica chimica acta; international journal of clinical chemistry,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
March 1977,
Klinische Wochenschrift,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
March 1977,
Clinica chimica acta; international journal of clinical chemistry,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
January 1981,
Muscle & nerve,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
February 1979,
Biomedicine / [publiee pour l'A.A.I.C.I.G.],
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
May 1977,
Journal of the neurological sciences,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
February 2008,
Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics,
M Hamada, and
H Okuda, and
K Oka, and
T Watanabe, and
K Ueda, and
M Nojima, and
S A Kuby, and
M Manship, and
F H Tyler, and
F A Ziter
January 1979,
Muscle & nerve,
