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Life Sciences

Gene expression

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Age And Sex-Specific Effect Of Caloric Restriction On Circadian Clock And Longevity-Associated Gene Expression, Arten Andreyevich Astafev Jan 2017

Age And Sex-Specific Effect Of Caloric Restriction On Circadian Clock And Longevity-Associated Gene Expression, Arten Andreyevich Astafev

ETD Archive

The rhythms in the expression of circadian clock genes are affected by calorie restriction (CR), a dietary paradigm known to increase lifespan. In our current study, we show that circadian rhythms are influenced by sex and the effects of CR are different between males and females. In particular, we found a group of clock genes which showed a sex-dependent difference in expression, as well as in response to CR (Rev-Erb α, Ror γ and both Cryptochromes: Cry1 and Cry2 genes). Two clock genes showed no difference in expression but their response to CR showed sexual dimorphism (Ror α and Rev-Erb …


Calorie Restriction Effect On Circadian Clock Gene Expression, Sonal Arvind Patel Jan 2016

Calorie Restriction Effect On Circadian Clock Gene Expression, Sonal Arvind Patel

ETD Archive

Calorie Restriction (CR) is a powerful paradigm known to delay aging and thus increase longevity in several organisms, from yeast to non-human primates. Many molecular pathways have been proposed to mediate the beneficial effects of CR, however, the mechanism is still unknown. Circadian clock which is an internal time keeping system is regulated by feeding. Thus our aim was to study the effect of CR on the circadian clock. Here we show that CR significantly affects the expression of circadian clock genes in mice at the mRNA and protein levels, suggesting that CR reprograms the clocks at the transcriptional and …


Genetics And Genomics Of Complex Diseases;Mouse Atherosclerosis Modifier Genes And Human Gene Expression After Bariatric Surgery, Stela Z. Berisha Jan 2010

Genetics And Genomics Of Complex Diseases;Mouse Atherosclerosis Modifier Genes And Human Gene Expression After Bariatric Surgery, Stela Z. Berisha

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The overall goal of our research was to study and identify genes involved in the development of complex diseases in mice and humans through integrative genetic/genomic approaches. Two complex diseases were the focus of research, atherosclerosis and type 2 diabetes. Mouse models of atherosclerosis, in which the genetic background and the environment can be controlled for, were used to identify and validate atherosclerosis modifier genes. We studied an atherosclerosis quantitative trait locus (QTL) on the distal end of chromosome 5, called Ath24, and generated interval-specific congenic mice on the atherosclerosis resistant AKR and susceptible DBA/2 apoE-deficient strains. To date we …