Interventions

  • name effect species mean median maximum
    vab-1 RNAi vab-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    CG3776 underexpression Underexpression of CG3776 (alias Jhebp29) reduces the mean lifespan, where the reduction in males is slightly higher. The lifespan of females and male flies underexpressed CG3776 is reduced by 31.6% and 38.8%, respectively when compared with Oregon R flies [18275960].. Fly -31.6 to -38.8
    ARO7 deletion Under starvation/extreme DR deletion of ARO7 increases mean chronological lifespan and confers higher resistance to heat-shock, but made cell more sensitive to acetic acid and leads to growth defects. In W303-1A background ARO7 deletion causes an even more severe growth defect and mutants are short-lived [20657825]. Yeast
    VPS27 deletion Under starvation conditions VPS27 deletion mutants have a dramatically reduced lifespan [20953148]. Yeast
    VPS25 deletion Under starvation conditions VPS25 deletion mutants have a dramatically reduced lifespan [20953148]. Yeast
    l(3)neo18 RNAi Under rich nutritional conditions lifespan of l(3)neo18 (alias CG9762) RNAi knockout animals is indistinguishable from wild-type, while upon DR, lifespan extension is diminished in males and females [19804760]. Fly
    CG11015 RNAi Under rich nutritional conditions lifespan of CG11015 RNAi treated animals is indistinguishable from that of controls, while upon DR, lifespan extension is diminished in males and females [19804760].
    ATG16 deletion Under AL atg16 mutation shortens chronological, but not replicative lifespan. 0.5% glucose DR extends chronological lifespan of atg16 mutants, but amino-acid DR does not extend the short chronological lifespan of atg16 mutants (similar to several other autophagy mutants). ADE4 deletion in atg16 mutants results only in a partial extension of chronological lifespan by 0.5% glucose DR. The long chronological lifespan of tor1 mutants requires ATG16 [20421943]. Yeast
    unc-76 mutation unc-76(e911) allele extends male lifespan by about 50%, but has no effect on hermaphrodite lifespan [10747056]. unc-76 mutants are uncoordinated [4366476]. Worm +50
    unc-51 mutation unc-51(e369) mutation reduces mean but extends maximum lifespan. unc-51(e369) mutation reduces lifespan of eat-2(ad1116) mutants to that of wild-type [18219227]. Worm
    unc-46 mutation unc-46(e177) allele has no significant effect on lifespan [9789046]. unc-46 mutants are uncoordinated [4366476]. Worm
    unc-35 mutation unc-35(e259) has no effect on male or hermaphrodite lifespan [10747056]. unc-35 mutants are uncoordinated [4366476]. Worm
    unc-32 mutation unc-32 mutation extends male lifespan by about 170%, but has no effect on hermaphrodite lifespan [10747056]. unc-31 mutants are uncoordinated [4366476]. Worm +170
    UCHL1 mutation UCHL1 is assoicated with Parkinson's disease [9774100]. UCHL1 belongs to a family of de-ubiquitinating enzymes responsible for the hydrolysis of bonds between ubiquitin molecules and small adducts [11084366]. Decreased activity due to mutation may result in decreased labeling of abnormal proteins for clearance. Human
    Thor overexpression Ubiquitously overexpression of wild-type Thor (alias d4E-BP) causes no change under AL, but an activated allele (with more than 3-fold increased binding activity to delF4E) significantly extends lifespan of females (weak allele) and females as well as males (strong allele). Mean lifespan is extended by 11 to 40%. Median lifespan of males and females is enhanced by by 11 and 22%, respectively. Maximum lifespan is extended by 16 and 18% for males and females, respectively. Under DR (0.25% YE) there is no lifespan extension, beyond the effect of DR alone, in all (wild-type, weak and strong) Thor alleles [19804760]. Lifespan of animals with increased Pten and 4E-BP activity in muscle exhibit and extended mean and maximum lifespan by 20% and 15.8% [21111239]. Fly +11 to +40 +11 to +22 +16 to +18
    Tsc1 overexpression Ubiquitously overexpression of UAS constructs (via the daughterless (da)-GAL-4 driver) containing dTSC1 extends mean lifespan at 29°C by 14% [15186745]. Fly +14
    Ubiquitinous SOD1 overexpression Ubiquitous overexpression of SOD1 does not extend lifespan in mice. Homozygous transgenic mice with two- to five-fold overexpression of SOD1 in various tissues exhibit a light reduction in lifespan. Hemizygous transgenic mice, with 1.5- to 3-fold overexpression of SOD1 display no difference in lifespan compared with nontransgenic litermate controls [10719757]. Transgenic mice with a mutant SOD1 transgene develop neuronal cytoskeletal lesions resembling the human amytrophic lateral sclerosis (ALS) phenotype [8610185]. Transgenic mice overexpressing SOD1 (and having 3.1-fold higher cellular Cu,Zn SOD activity in the brain) have reduced infarct size following experimental cerebral ischemia [1763030]. Mouse
    Dominant-negative S6k Ubiquitous overexpression of a dominant-negative form of S6k (alias dS6K) increases mean lifespan by 22%. Overexpression of a dominant-negative form of S6k protects mutants from deleterious effects of rich food, as if mimicking the effect of DR [15186745]. Fly +22
    Cbs overexpression Ubiquitous or neuron-specific transgenic overexpression of Cbs enhances longevity in fully-fed animals. Adult-specific ubiquitous expression of Cbs is sufficient to increase female mean and maximum lifespan by 12 - 43% and 10%, respectively. Males, whose lifespan is relatively less affected by DR, exhibite a smaller, but still significant increase in lifespan by 7% upon Cbs overexpression. Neuronal overexpression also increases lifespan, albeit modestly (approximately 12% mean and 15% maximum lifespan extension), whereas overexpression in the fat body and in the gut has no effect [21930912]. Fly +12 to +43 +10 to +15
    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
    Sod2 overexpression Two-fold overexpression of Sod2 in young (4-6 months) and old (26-28 months) throughout the life results in decreased lipid peroxidation, increased resistance against paraquat-induced oxidative stress, and decreased age-related decline in mitochondrial ATP production, without any change on lifespan or age-related pathology [19633237]. Mouse
    rut mutation Two rutabaga mutants, rut1 and rut2080, have significantly shortened lifespans [17369827]. Fly
    Trx-2 mutation Trx-2 mutants have a 25% reduction in maximum lifespan and exhibit lower tolerance to oxidative stress while animals carrying multiple copies of Trx-2 exhibit higher tolerance [17567437]. Fly -25
    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
    TRM9 deletion TRM9 deletion almost triples mean chronological lifespan under starvation/extreme DR, increases heat resistance, but reduces resistance to acetic acid. Similar effect were present in the BY746 background in SDC medium [20657825]. Yeast
    Interventions are an extension of GenAge and GenDR.