| pubmed-article:15341516 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0332437 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0228174 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0010287 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0870883 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0024485 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C0392762 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:15341516 | lifeskim:mentions | umls-concept:C1553628 | lld:lifeskim |
| pubmed-article:15341516 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:15341516 | pubmed:dateCreated | 2004-9-2 | lld:pubmed |
| pubmed-article:15341516 | pubmed:abstractText | Creatine kinase (CK)-catalysed ATP-phosphocreatine (PCr) exchange is considered to play a key role in energy homeostasis of the brain. This study assessed the metabolic and anatomical consequences of partial or complete depletion of this system in transgenic mice without cytosolic B-CK (B-CK-/-), mitochondrial ubiquitous CK (UbCKmit-/-), or both isoenzymes (CK -/-), using non-invasive quantitative magnetic resonance (MR) imaging and spectroscopy. MR imaging revealed an increase in ventricle size in a subset of B-CK-/- mice, but not in animals with UbCKmit or compound CK mutations. Mice lacking single CK isoenzymes had normal levels of high-energy metabolites and tissue pH. In the brains of CK double knockouts pH and ATP and Pi levels were also normal, even though PCr had become completely undetectable. Moreover, a 20-30% decrease was observed in the level of total creatine and a similar increase in the level of neuronal N-acetyl-aspartate compounds. Although CKs themselves are not evenly distributed throughout the CNS, these alterations were uniform and concordant across different brain regions. Changes in myo-inositol and glutamate peaks did appear to be mutation type and brain area specific. Our results challenge current models for the biological significance of the PCr-CK energy system and suggest a multifaceted role for creatine in the brain. | lld:pubmed |
| pubmed-article:15341516 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15341516 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15341516 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15341516 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15341516 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:WieringaBB | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:OerlemansFF | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:HeerschapAA | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:JostCC | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:in 't... | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:RenemaW K JWK | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:KlompD W JDW | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:Van der... | lld:pubmed |
| pubmed-article:15341516 | pubmed:author | pubmed-author:StreijgerFF | lld:pubmed |
| pubmed-article:15341516 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15341516 | pubmed:volume | 90 | lld:pubmed |
| pubmed-article:15341516 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15341516 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15341516 | pubmed:pagination | 1321-30 | lld:pubmed |
| pubmed-article:15341516 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15341516 | pubmed:meshHeading | pubmed-meshheading:15341516... | lld:pubmed |
| pubmed-article:15341516 | pubmed:meshHeading | pubmed-meshheading:15341516... | lld:pubmed |
| pubmed-article:15341516 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15341516 | pubmed:articleTitle | Cerebral creatine kinase deficiency influences metabolite levels and morphology in the mouse brain: a quantitative in vivo 1H and 31P magnetic resonance study. | lld:pubmed |
| pubmed-article:15341516 | pubmed:affiliation | Department of Radiology, Nijmegen Centre for Molecular Life Science, University Medical Centre Nijmegen, University of Nijmegen, Nijmegen, The Netherlands. | lld:pubmed |
| pubmed-article:15341516 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15341516 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15341516 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| entrez-gene:12716 | entrezgene:pubmed | pubmed-article:15341516 | lld:entrezgene |
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