rdf:type |
|
lifeskim:mentions |
umls-concept:C0026809,
umls-concept:C0086418,
umls-concept:C0162638,
umls-concept:C0205217,
umls-concept:C0205234,
umls-concept:C0205307,
umls-concept:C0205374,
umls-concept:C0221198,
umls-concept:C0291573,
umls-concept:C0871261,
umls-concept:C0917798,
umls-concept:C1704243,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
|
pubmed:issue |
10
|
pubmed:dateCreated |
2004-9-17
|
pubmed:abstractText |
Caspase 3 activation has been implicated in cell death following a number of neurodegenerative insults. To determine whether caspase genes can affect the susceptibility of cells to neurodegeneration, a transgenic mouse line was created, expressing human caspase 3 under control of its own promoter. The human gene was regulated by the murine homeostatic machinery and human procaspase 3 was expressed in the same tissues as mouse caspase 3. These novel transgenic mice appeared phenotypically and developmentally normal and survived in excess of 2 years. Behavioural assessment using the 5-choice serial reaction time task found no differences from wild-type littermates. Caspase activity was found to be tightly regulated under physiological conditions, however, significantly larger lesions were obtained when transgenic mice were subjected to focal cerebral ischaemia/reperfusion injury compared to wild-type littermates. These data demonstrate that mice overexpressing human caspase 3 are essentially normal, however, they have increased susceptibility to degenerative insults.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
1350-9047
|
pubmed:author |
pubmed-author:AllsoppT ETE,
pubmed-author:AmetL E ALE,
pubmed-author:AsadaTT,
pubmed-author:CarlsonGG,
pubmed-author:HarmarA JAJ,
pubmed-author:KellyJ SJS,
pubmed-author:KirkP LPL,
pubmed-author:LoganNN,
pubmed-author:McGregorA LAL,
pubmed-author:SharkeyJJ,
pubmed-author:ShenSS,
pubmed-author:SprattCC
|
pubmed:issnType |
Print
|
pubmed:volume |
11
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1102-11
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15153940-Animals,
pubmed-meshheading:15153940-Apoptosis,
pubmed-meshheading:15153940-Behavior, Animal,
pubmed-meshheading:15153940-Caspase 3,
pubmed-meshheading:15153940-Caspases,
pubmed-meshheading:15153940-Cell Size,
pubmed-meshheading:15153940-Cells, Cultured,
pubmed-meshheading:15153940-Enzyme Activation,
pubmed-meshheading:15153940-Gene Expression Regulation,
pubmed-meshheading:15153940-Humans,
pubmed-meshheading:15153940-Immunohistochemistry,
pubmed-meshheading:15153940-Ischemic Attack, Transient,
pubmed-meshheading:15153940-Mice,
pubmed-meshheading:15153940-Mice, Transgenic,
pubmed-meshheading:15153940-Phenotype,
pubmed-meshheading:15153940-Time Factors,
pubmed-meshheading:15153940-Transgenes
|
pubmed:year |
2004
|
pubmed:articleTitle |
Mice overexpressing human caspase 3 appear phenotypically normal but exhibit increased apoptosis and larger lesion volumes in response to transient focal cerebral ischaemia.
|
pubmed:affiliation |
Fujisawa Institute of Neuroscience in Edinburgh, University of Edinburgh, Edinburgh EH8 9JZ, UK. Lorraine.Kerr@ed.ac.uk
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pubmed:publicationType |
Journal Article
|