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

  • Species: + -
  • Types: + -
  • symbol name observation species
    MIR106A microRNA 106A MIR106A is downregulated in senescent cells as it has a good correlation with p21 transcription, while p53 represses mir17-92 cluster [20437201; 20089119]. Human
    miR17 microRNA 17 miR17 is downregulated in senescent cells and has a good correlation with p21 transcription, while p53 represses mir17-92 cluster [20437201; 20089119] Human
    CCL2 chemokine (C-C motif) ligand 2 CCL2 levels in plasma increase with age and it is part of the senescence-associated secretory phenotype [19648977]. Human
    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
    MIR373 microRNA 373 miR-373 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. Human
    MIR372 microRNA 372 miR-372 expression is able to bypass RAS-induced senescence in presence of wild-type p53 [16564011]. 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
    hsa-let-7f hsa-let-7f 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
    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
    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
    MIR34C microRNA 34c 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
    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
    • 17 factors
    Factors are an extension of GenAge and GenDR.

    Comment on This Data Unit


    Please log in for making a comment without the need to specify any credentials.