Denigma

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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  • Species: + -
    Nematode (7)   Fruit fly (3)   Human (27)   House mouse (5)  
  • Classifications: + -
    Aging Associated (4)   Aging Differential (1)   Aging‑Suppressed (1)   Aging‑Suppressor (8)   Negative Aging‑Suppressor (8)   Positive Aging‑Suppressor (4)   Gerontogene (2)   Negative Gerontogene (2)   Positive Gerontogene (1)   Longevity‑Associated (1)   Longevity‑Differential (1)   Senescence‑Associated (15)   Senescence‑Differential (1)   Senescence‑Induced (8)   Senescence‑Suppressed (1)   Cancer‑Related (12)   Oncogene (5)   Tumor‑Suppressor (9)   Stem Cell Related (2)  
  • Types: + -
    miRNA «  Gene « 
    • symbol name observation species
    MIR20A microRNA 20a Overexpression of MiR-20a in mouse embryonic fibroblasts induces senescence by lowering Lrf (a transcriptional repressor of the Mdm2 inhibitor p19ARF [15662416; 9529248]) protein levels and in turn increasing p19ARF levels [18596985]. House mouse
    MIR21 MIRN21; hsa-mir-21; miR-21; miRNA21 MIR21 is the most highly expressed microRNA gene in octogenarians and centenarians. MIR21 expression is higher under cardiovascular diseases and lower in centenarian offspring. MIR21 is correlated with C-reactive protein and fibrinogen levels. TGF-βR2 mRNA, a MIR21 target, exhibits the highest expression in leukocytes form a subset of octogenarians. MIR-21 may be a biomarker of inflammation [23041385]. Human
    MIR217 microRNA 217 MIR217 (alias hsa-miR-217) is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC, but overall had very low expression levels [18493317]. Human
    miR221 microRNA 221 miR221 and miR222 downregulate PTEN, a major tumor suppressor and TIMP3, which induces activation of caspases 8 and 9 [19962668]. Thus miR221 and miR222 enhance tumorigenecity in cell lung cancer, gastric cancer and hepatocarcinoma cells [20618998] Human
    miR222 microRNA 222 miR221 and miR222 downregulate PTEN, a major tumor suppressor and TIMP3, which induces activation of caspases 8 and 9 [19962668]. Thus miR221 and miR222 enhance tumorigenecity in cell lung cancer, gastric cancer and hepatocarcinoma cells [20618998]. Human
    MIR27A microRNA 27a MIR27A can be both a tumor-suppressor and an oncogene. For instance, the expression of miR-27a is significantly lower in acute leukemia compared to normal cells. It has been shown that miRNA-27a inhibits cell growth and promotes apoptosis by targeting 14-3-3θ, a member of 14-3-3 family of anti-apoptotic proteins. [23236401]. Therefore, it acts as a tumor-suppressor in leukemia. However, in gastric cancer mir-27a acts as an oncogene by targeting inhibiting and thus promoting cancer cell growth [18789835]. Human
    MIR29A microRNA 29a miR-29a reduces the amount of methylation and upregulates a long non-coding RNA form a region called MEG3 that is responsible for inducing apoptotic pathway. Thus reducing tumorgensis in non-malignant hepatocytes [21625215]. Human
    MIR34A microRNA 34a mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. Human
    MIR34B microRNA 34b mir-34 family, particularly miR-34a, as downstream effectors of p53 involved in cell cycle [17656095], leads to cell cycle arrest, increased expression of Beta-galactosidase [17554337] and downregulation of E3F family target genes [17875987]. MDM2 inhibiting drug Nutlin-3, leads to p53 activation, induced up-regulation of primarily miR-34a and later miR-34b and miR-34c [18451145]. Human
    MIR34C microRNA 34c — 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
    MIR372 microRNA 372 miR-372 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. Human
    MIR373 microRNA 373 miR-373 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. 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
    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
    MIRC29 microRNA 29c hsa-miR-29c is significantly upregulated in senescent human mesenchymal stem cells (hMSCs) when compared to early passage hMSC [18493317]. Human
    Factors are an extension of GenAge and GenDR.

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