STUDIES ON CREATINE

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Studies on the Metabolism of Creatine and Creatinine Iii. Formation of Creatine by Isolated Rat Tissues*

The precursors, mechanism, and site of creatine formation are still uncertain, even though they have received the attention of investigators for many years. An examination of the results on creatine formation summarized in Hunter’s monograph (1928) shows the many contradictions in this field. In the 10 years which have elapsed since the publication of this work, few experiments in vivo have bee...

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Magnetic resonance studies on inactivated forms of creatine kinase.

Magnetic resonance and relative enzymatic velocity studies with the use of the paramagnetic manganese ion were carried out on creatine kinase inactivated by the specific -SH reagents iodoacetic acid and dinitrofluorobenzene and by the nonspecific reagents urea and decyl sulfate. Modification of creatine kinase at the two essential --SH groups by iodoacetic acid or dinitrofluorobenzene affected ...

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Monoclonal-antibody studies of creatine kinase

Proteinase K cleaves a small peptide from native muscle-specific creatine kinase. We present evidence, from the binding of two monoclonal antibodies to formic acidcleavage fragments and proteinase K-digest fragments of chick muscle creatine kinase, that the proteinase K-cleavage site is in the C-terminal region of the molecule. This specificity of proteinase K, which is not normally a highly sp...

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31P NMR studies of creatine kinase flux in M-creatine kinase-deficient mouse heart.

Hearts of wild-type and cytosolic muscle creatine kinase (M-CK)-knockout mice were perfused with Krebs-Henseleit buffer containing 10 mM glucose and 5 mM pyruvate and studied during pacing at 400 and 600 beats/min and during K+ arrest. Phosphocreatine (PCr) and ATP concentrations in M-CK-deficient hearts were not significantly different from those in wild-type hearts. With the use of31P NMR sat...

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Creatine transporter deficiency: Novel mutations and functional studies

X-linked cerebral creatine deficiency (MIM 300036) is caused by deficiency of the creatine transporter encoded by the SLC6A8 gene. Here we report three patients with this condition from Israel. These unrelated patients were evaluated for global developmental delays and language apraxia. Borderline microcephaly was noted in one of them. Diagnosis was prompted by brain magnetic resonance imaging ...

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ژورنال

عنوان ژورنال: Journal of Biological Chemistry

سال: 1929

ISSN: 0021-9258

DOI: 10.1016/s0021-9258(18)77151-2