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
    MIR34C microRNA 34c Human
    hsa-let-7c microRNA let-7c let-7c is downregulated in prostate cancer, which increases cell proliferation [22479342]. More specifically, let-7c is a regulator of androgen receptor (AR), which plays a role in the development of prostate cancer [22128178]. Human
    lin-4 abnormal cell LINeage 4 A loss-of-function mutation in lin-4 shortens lifespan and accelerated tissue ageing while overexpressing lin-4 extends lifespan by redarding aging [16373574]. lin-4 is regulated by DAF-16 in L1 arrest. Nematode
    hsa-let-7a microRNA let-7a A tumor-suppressor downregulated in different types of cancer. Let-7a binds to 3'-UTR region of RAB40C, thus leading to a decrease in cell proliferation and an increase of G1 arrest in human gastric carcinomas [20809749, 21349817]. In human breast cancer, evidence suggests that members of let-7 family inhibit breast cancer cell migration by targeting genes responsible for actin dynamics [23339187]. Moreover, let-7a directly targets CCR7, a receptor that promotes invasiveness of cancer cells [23335963] Human
    mir-277 Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype. Transgenic inhibition with a miRNA sponge construct also shortens lifespan [23669073]. miR-277 is downregulated during adult life [23669073]. mir-277 controls branched-chain amino acid catabolism and as a result it can modulate the activity of TOR kinase [23669073]. Fruit fly
    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
    ENSRNOG00000044316 is transcriptional downregulated 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
    miR-214 microRNA 214 Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. House mouse
    Mir669c microRNA 669c Expression increases with age in mouse liver. The miRNA downregulates detoxification and regeneration genes, which may contribute to aging [18561983]. House mouse
    hsa-let-7f hsa-let-7f is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    MIRC29 microRNA 29c hsa-miR-29c is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    MIR369 microRNA 369 hsa-miR-369-5p is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    MIR371A microRNA 371a hsa-miR-371 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    MIR499 microRNA-449 hsa-miR-499 is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    Mir27a MicroRNA 27a In Ames dwarf mice (which displays delayed Aging), Mir27a expression is significantly higher than in control mice. Mir27a may be responsible for delayed Aging in dwarf mice: it suppresses the expression of ODC1 and SRM, which in turn suppresses polyamine synthesis in dwarf mice liver. Part of the ability of dwarf mice to suppress or avoid tumor or Cancer growth may be attributed to the decreased Polyamine biosynthesis. [19878148] House mouse
    Mir34a microRNA mir-34a Increases in aging rat liver, which suppresses the expression of such proteins as Sirt1 and Mgst1, resulting in dysfunction of oxidative stress defense and regulation [21216258] Norway rat
    Mir93 microRNA mir-93 Increases in Aging rat Liver, which suppresses the expression of such proteins as Sirt1 and Mgst1, resulting in dysfunction of oxidative stress defense and regulation [21216258] Norway rat
    hsa-let-7b microRNA let-7b Let-7b, a member of the let-7 group, appears to be a tumor-suppressor. In acute lymphoblastic leukemia, let-7b is severely downregulated and its overexpression inhibits cancer cells growth [22918121]. In melanoma cells, the miRNA downregulates the expression of cell cycle regulators such as cyclin D1, D3, and A and Cdk4, which inhibits cell cycle progression. [18379589] Human
    mir-71 Loss and gain-of-function of mir-71 decreases and increases lifespan, respectively [21129974]. mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan, while extra copies of mir-71 extend the lifespan with an increase in lifespan by 15 - 25% [22482727], Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants [22482727], During adulthood mir-71 is strongly expressed in the intestine, body wall muscles and neurons. mir-71 is upregulated in aging adults [22482727], Nematode
    mir-124 Loss of mir-124 increases reactive oxygen species formation and accumulation of the aging marker lipofuscin, reduces whole body ATP levels and results in reduction in lifespan [23075628]. Supplementation of vitamin C normalizes the reduced median lifespan of mir-124 mutants [23075628]. The expression of the conserved mir-124 in whole wrn-1 mutants (which premature age) is significantly reduced [23075628]. Nematode
    Mir1 miR-1 is associated with stem cell differentiation in mouse and human ESCs [18371447]. House mouse
    Mir133 miR-133 is associated with stem cell differentiation in mouse and human ESCs [18371447]. House mouse
    MIR146B microRNA 146b miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. Human
    MIR146A microRNA 146a miR-146a/b is significantly elevated during senescence as a compensatory response to restrain inflammation via the suppression of IL-6 and IL-8 secretion and downregulation of IRAK1 (component of IL-1 receptor signaling). Ectopic expression of miR-146a/b in primary fibroblasts suppresses IL-6 and IL-8 secretion and downregulation of IRAK1 [20148189]. Human
    MIR155 microRNA 155 mir-155 is significantly overexpressed in human breast cancer while targeting the miRNA could induce apoptosis and cell cycle arrest as well as inhibit cell growth. [18719391]. Mir155 acts by repressing socs1, a tumor suppressor. In addition, inflammatory signals may activate miR155, thus suggesting that the miRNA serves as a link between inflammation and malignancy formation [20354188]. It is also upregulated in lung cancer and acts an oncogene by targeting Apaf1 and thus reducing apoptosis rate [22996741]. Inhibition of mir-155 radiosensitizes cancer cells [22027557]. Human
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    • 25 of 52 factors
    Factors are an extension of GenAge and GenDR.

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