Factors

We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o

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  • symbol name observation species
    ENSRNOG00000044070 is transcriptional upregulated in the cerebral cortex at the age 28 months under different longevity conditions such as under dietary restriction (DR) as well as in feeding switch regimens that result in extended lifespan, like early age switch to DR as well as the reverse switch under the influence of the DR-mimetic α-lipoic acid (i.e. DR switched to ad libitum+ lipoic acid) [Shona et al. 2013]. Norway rat
    Mir98 microRNA mir-98 miR-98-3p is the only miRNA significantly differentially expressed (upregulated) under DR and LA (lipoic acid; a DR-mimetic) treatment. Across mouse, rat and human predicted targets of miR-98-3p include the glutamate receptors, calcium transporters, histones and histone acetyltransferase/deacetylases. miR-89-3p is expressed at a low level and is highly conserved in rat, mouse, human and anplis lizard. Mir-98 precursor is located on the X-chromosome. In the rat, mouse and human genome it overlaps an E3 ubiquitin ligase HUWE which is involved in regulation of apoptosis, regulation of neural differentiation and proliferation, DNA damage repair [Shona et al. 2013]. miR-98 expression is significantly decreased in the adventitia and endomembrane ath different degrees in Goto-Kakizaki rat, a model of type 2 diabetes. miR-98 targets TRB2 which is increased in expression in this model of type 2 diabetes. TRB2 phosphorylates Akt [22012613]. The mouse ortholog of Mir98 may by associated with the germline [16766679]. Norway rat
    • 2 factors
    Factors are an extension of GenAge and GenDR.

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