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Titolo:
Changes in glycolytic network and mitochondrial design in creatine kinase-deficient muscles
Autore:
de Groof, AJC; Oerlemans, FTJJ; Jost, CR; Wieringa, B;
Indirizzi:
Univ Nijmegen, Univ Med Ctr, Nijmegen Ctr Mol Life Sci, Dept Cell Biol, NL-6500 HB Nijmegen, Netherlands Univ Nijmegen Nijmegen Netherlands NL-6500HB 0 HB Nijmegen, Netherlands
Titolo Testata:
MUSCLE & NERVE
fascicolo: 9, volume: 24, anno: 2001,
pagine: 1188 - 1196
SICI:
0148-639X(200109)24:9<1188:CIGNAM>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
SKELETAL-MUSCLE; ENERGY-METABOLISM; COMPARTMENTATION; MICE; RAT; RESPIRATION; ENZYMES; PHOSPHOFRUCTOKINASE; IDENTIFICATION; HOMEOSTASIS;
Keywords:
adenosine triphosphate (ATP) production; creatine kinase; glycolytic enzymes; metabolic signaling; mitochondrial enzymes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Wieringa, B Univ Nijmegen, Univ Med Ctr, Nijmegen Ctr Mol Life Sci, Dept Cell Biol, POB 9101, NL-6500 HB Nijmegen, Netherlands Univ Nijmegen POB 9101Nijmegen Netherlands NL-6500 HB rlands
Citazione:
A.J.C. de Groof et al., "Changes in glycolytic network and mitochondrial design in creatine kinase-deficient muscles", MUSCLE NERV, 24(9), 2001, pp. 1188-1196

Abstract

Skeletal muscles respond with high plasticity to pathobiological conditions or changes in physiological demand by remodeling cytoarchitectural and metabolic characteristics of individual myocytes. We have previously shown that muscles of mice without mitochondrial and/or cytosolic creatine kinases (ScCKmit(-/-) and/or M-CK-/-) partly compensate for the defect(s) by redirecting metabolic pathways and ultrastructural characteristics. Here, we showby semiquantitative Western blot analysis that the compensatory changes involve mutation- and fiber-type-specific coordinated regulation of divergentbut functionally coupled groups of proteins. Fast-twitch gastrocnemius muscle of CK-/- mice display a two- to fourfold upregulation of mitochondrial cytochrome c oxidase, inorganic phosphate carrier, adenine nucleotide translocator, and voltage-dependent anion channel proteins. In parallel, cytosolic myoglobin is upregulated. Slow-twitch soleus muscle responds with changes in the glycolytic enzyme pattern, including a shift in lactate dehydrogenase isoenzyme composition. Adaptations in the network for oxidative adenosine triphosphate (ATP) production are already apparent at 17 days of age. (C) 2001 John Wiley & Sons, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:47:45