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

prometheus--2.jpg

  • symbol name observation species
    sdhC succinate dehydrogenase, cytochrome b556 subunit Mutants expressing a dominant negative form of sdhC in the nervous system have a 22% reduced mean lifespan and signs of oxidative stress induction [17854771]. Fruit fly
    S6k RPS6-p70-protein kinase Ubiquitous overexpression of a dominant-negative form of S6k (alias dS6K) increases mean lifespan by 22% and overexpression of a constitutively active form of S6k decreases mean lifespan by 34% at 29°C. Overexpression of a dominant-negative form of S6k protects mutants from deleterious effects of rich food, as if mimicking the effect of DR [15186745]. Fruit fly
    lin-14 abnormal cell LINeage 14 A loss-of-function mutation in lin-14 extends lifespan by 31% while a gain-of-function mutation decreases lifespan. The life-extending effects is dependent on daf-16 and hsf-1. Also, lin-14 is a target of lin-4 [16373574]. lin-14(n719) mutation extends mean and maximum lifespan of control animals by 20 and 67%, respectively [23097426]. Knockdown of lin-14 only during adulthood is sufficient to extend lifespan and suppresses the short lifespan phenotype of lin-4 mutants. Nematode
    let-60 LEThal The let-60(n1046gf) activating mutation greatly reduces lifespan of wild-type, weakly suppresses constitutive dauer diapause in daf-2 and age-1 mutants and extends lifespan induced by mutation of daf-2 [16164423]. Nematode
    Gh Growth hormone Overexpression of GH is associated wtih markedly reduced lifespan and various indices of premature aging [8100276]. Transgenic mice overexpressing bovine GH1 are bigger than controls and display signs of premature aging such as a shortened lifespan, glomerulosclerosis and glomerulonephritis, increased astrogliosis, and early onset of age-related changes in cognitive function [14583653]. House mouse
    FBP1 Fructose-1,6-BisPhosphatase 1 Deletion of FBP1 increases survival during the first 15 days during chronologocal aging, but does not increase chronological lifespan. FBP1 deletion reduces production of reactive oxygen species while overexpression of FBP1 shortens chronological lifespan [16199065]. Budding yeast
    CLN3 CycLiN 3 Overexpression shortens chronological lifespan together with age-dependent increases in genome instability and apoptosis. While around 80% of wild-type cells are alive almost non CLN3 overexpressers are alive (under condition that avoids adaptive regrowth) [17710147]. Budding yeast
    Factors are an extension of GenAge and GenDR.

    Comment on This Data Unit