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Volumn 64, Issue 2, 2009, Pages 161-163

Can we develop genetically tractable models to assess healthspan (rather than life span) in animal models?

Author keywords

C. elegans; Drosophila; Functional senescence; Healthspan

Indexed keywords

IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; POLYPEPTIDE ANTIBIOTIC AGENT; DROSOPHILA PROTEIN;

EID: 64949168686     PISSN: 10795006     EISSN: None     Source Type: Journal    
DOI: 10.1093/gerona/gln067     Document Type: Conference Paper
Times cited : (46)

References (12)
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    • KCNQ potassium channel mutations cause cardiac arrhythmias in Drosophila that mimic the effects of aging
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    • Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans
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    • Aging of the innate immune response in Drosophila melanogaster
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    • Increased internal and external bacterial load during Drosophila aging without life-span trade-off
    • Ren C, Webster P, Finkel SE, Tower J. Increased internal and external bacterial load during Drosophila aging without life-span trade-off. Cell Metab. 2007;6:144-152.
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    • Functional analysis of the Drosophila immune response during aging
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    • Trade-offs between longevity and pathogen resistance in Drosophila melanogaster are mediated by NFkappaB signaling
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.