Interventions

  • Species: + -
  • name effect species mean median maximum
    sptf-3 Overexpression Overexpression of sptf-3 extends lifespan [18059442]. Worm
    old-2 overexpression Overexpression of old-2 increases slightly, although statistically significant mean and maximum lifespan by 19 and 44% [9768365]. Worm +19 +44
    old-1 overexpression Overexpression of old-1 in transgenic animals increases mean and maximum lifespan by 40-100% (average 65%) and 97%, respectively. old-1 overexpression of increases stress resistance (to heat by 20% and ultraviolet irradiation by 33%) without altering development or fertility. Effects of old-1 on lifespan and stress resistance is under regulation of daf-16 [9768365]. Worm +40 to +100 +97
    cup-4 overexpression cup-4 overexpession reduces oxidative stress resistance and shortens lifespan of wild-type under AL [19783783]. Worm
    nlp-7 overexpression nlp-7 overexpression reduces oxidative stress resistance and shortens lifespan of wild-type under AL [19783783]. Worm
    clk-1 overexpression Overexpression of clk-1 shortens lifespan and is associated with increased mitochondrial activity [10202142]. Worm
    daf-18 overexpression Overexpression increases adult lifespan in individual tissues [16153634]. Worm
    hsp-6 overexpression Overexpression of hsp-6 from a muscle-specific promoter extends lifespan mean and maximum lifespan by 43 and 45% relatively to animals expressing GFP from the same promoter [11959102]. Worm +43 +45
    INS overexpression Expression of human insulin under an inducible heat shock promoter increases nematode lifespan by 25% and is also able to enhance the lifespan of daf-2 mutants [11274053]. Worm +25
    ins-1 overexpression Increased dosage of ins-1 under its own promoter as well as a heat shock promoter increases lifespan by 25% and is also able to increase the lifespan of daf-2 mutants. Overexpression of ins-1 also causes an increase in dauer formation and can enhance the dauer formation of daf-2 mutants [11274053]. Worm +25
    SNCA overexpression Transgenic lines overexpressing either human wild-type or mutant (A53T) forms of the SNCA (alpha-synclein) gene under a pan-neuronal promoter live on average about 25% longer, even in weak (m577) and strong (e1370) daf-2 mutant backgrounds, and exhibited decreased pharyngeal pumping and egg-laying. Wild-type SNCA crossed into eat-2(ad1113) does not significantly effect lifespan compared to that of the background strain. Pumping rate in wild-type SCNA and A53T SCNA overexpression mutants were less than control already at day 1 of adulthood. The attenuation of lifespan exptesion by SNCA overexpression by growing on thick bacterial lawns, suggests that DR may explain some fo the effects on lifespan. SCNA overexpression increases average lifespan by 21.3% (wild-type) and 16.3% (A53T) [16782295]. Worm +26 to +34 +19 to +31
    uba-1 overexpression Overexpression of uba-1 does not result in significant increase in median lifespan [22737090]. Worm
    lys-1 overexpression Overexpression of lys-1 increases mean and maximum lifespan by 5 and 26%, but has no significant effect on median lifespan [22737090]. Worm +5 +26
    ucp-4 overexpression Overexpression reduces mean lifespan by 5%, has no significant effect on median lifespan, and slighlty increases maximum lifespan by 12% [22737090]. Worm -5 +12
    pnc-1 overexpression Overexpression of pnc-1 increases adult survival under oxidative stress but does not extend the lifespan [17335870]. Worm
    Overexpression of ucp2 and aakg-2 Overexpression of aakg-2 toegther with D. rerio ucp2 was non-additive with sDR [22737090]. Worm
    ubc-18 overexpression ubc-18 overexpression is unable to extend lifespan (possibly, UBC-18 is not limiting for WWP-1 function in lifespan) [19553937]. Worm
    aqp-1 overexpression Overexpression of aqp-1::GFP rescues short lifespan of aqp-1 deletion mutants and partially prevented glucose from shortening lifespan. Worm
    cbp-1 overxpression Overexpression of cbp-1 does not significantly affect lifespan [19924292]. Worm
    faah-1 overexpression faah-1 overexpression reduces eicosapentaenoyl ethanolamide (EPEA), palmitoleyol ethanolamide, linoleyol ethanolamide, as well as arachidonoyl ethanolamide (AEA) levels, delays development, increases thermal stress resistance, and was associated with mean and maximum adult lifespan extension by 19 and 35%, respectively, in presence of abundant food but not under (two different protocols of) DR. Overexpression in pharynx was largely sufficient for this lifespan extension [21562563]. Worm +19 +35
    trx-1 overexpression trx-1 overexpression extends lifespan in wild-type but not in eat-2 mutants. Ectopic expression of trx-1 in ASJ neurons (but not in the intestine) in trx-1 mutants rescues the lifespan-extension conferred by eat-2 mutation. trx-1 overexpression extends lifespan of wild-type but not in eat-2 mutants. trx-1 deletion almost completely suppresses lifespan extension induced by dietary deprivation (DD). DD upregulates trx-1 expression in ASJ neurons. DR activates trx-1 in ASJ neurons which in turn triggers a trx-1-dependent non-cell autonomous mechanism to extend adult lifespan [21334311]. Worm
    daf-16 overexpression Overexpression of wild-type DAF-16 modestly increases lifespan by 20% [11747825]. Worm +20
    Overexpression of constitutive nuclear SKN-1 skn-1 transgenes that overexpress a constitutive nuclear form of SKN-1 in the intestine extend the mean lifespan by 5-21%, independently of DAF-16 [18358814]. Worm +5 to +21
    sir-2.1 overexpression sir-2.1 overexpression extends lifespan by about 50% and this lifespan extension depends on DAF-16 activity as it is suppressed by mutation in daf-16 and it does not synergize with daf-2 [11242085]. Overrexpression of sir-2.1 synergizes with TGF-beta mutation (daf-4 and daf-1) for dauer formation [11242085]. Worm +50
    pha-4 overexpression pha-4 overexpression increases longevity of wild-type only slightly, but significant that of daf-16 mutants [17476212]. Worm
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    • 25 of 47 interventions
    Interventions are an extension of GenAge and GenDR.