| 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 | — | — | — |
| SOD2 overexpression | Combined overexpression of SOD1 and SOD2 extends chronological lifespan by 30% in EG103 strain [12586694].
| Yeast | — | — | — |
| 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 | — | — | — |
| SSD1-V overexpression | Overexpression of SSD1 (addition of a SSD1-V allele) increases replicative lifespan by 50%, independently of SIR2 and SIR2 further extends the lifespan, although SIR2 is necessary for SSD1-V cells to attain maximal lifespan [15126388]. SSD1-V also dramatically increases chronological lifespan with lifespan twice as long as ssd1-d cells [19570907].
Addition of SSD1-V allele to an ssd1-d strain suppresses the short lifespan of an MPT5 deletion mutant [11805047] and extend wild-type lifespan [Kaeberlein and Guarente, unpublished].
SSD1-V slightly extends the lifespan of swi4 and ccr4 mutant strains and suppresses the temperature sensitive growth phenotype of mpt5, ccr3, swi4, and swi6 single mutants [11805047]. SSD1-V also suppresses the synthetic lethality caused by deletion of MPT5 in combination with a mutation in SWI4, SWI6, or CCR4 [11805047]. SSD1-V suppresses mutations that affect cell wall stability [1545797; 8386319], RNA polymerase III activity [8510644], RNA splicing [10446233], and PKA activity [1848673; 8200529]. | Yeast | +50 to +100 | — | — |
| sug overexpression | Overexpression of sug (from a doxycycline-inducible promoter) results in a 5-9% increase in mean lifespan [12620118]. | Fly | +5 to +9 | — | — |
| CKIepsilon mutation | A mutation in CKIepsilon called tau, if homozygous, shortens the circadian period (by 20%), increases metabolic rate (by 20%), and increases lifespan by 14-16% under conditions of constant darkness [12054192].
Male and female wild-type hamsters are heavier than homozygous mutants throughout the entire lifespan, and heterozygous mutants have intermediate weight [12054192]. | Hamster | +14 to +16 | — | — |
| Heterozyogus Trp53 truncation mutation | Mice heterozyogous for an allele of p53 that removes the 5' portion of the protein demonstrate decreased cancer, permature aging phenotypes, and shortened lifespan in the mixed inbred C57BL/6â129/Sv background. It has been proposed that the this allele of p53 results in increased activity/overexpression [11780111]. | Mouse | — | — | — |
| unc-78 mutation | Mutation in unc-78 has no effect on lifespan [9789046].
unc-78 mutants move slowly [7190524]. | Worm | — | — | — |
| VhaSFD overexpression | Overexpression of VhaSFD (from a doxycycline-inducible promoter) results in a 5-10% increase in mean lifespan [12620118]. | Fly | +5 to +10 | — | — |
| IME1 transient overexpression | Transient overexpression of IME1 resets the replicative lifespan of old cells back to that of young cells [21700873]. | Yeast | — | — | — |
| NDT80 transient overexpression | Transient overexpression of NDT80 rejuvenates old cells [21700873]. | Yeast | — | — | — |
| Elevation of histone expression | The elevation of histone expression promotes replicative lifespan extension [20832724]. | Yeast | — | — | — |
| Tert re-activation | Re-activation of telomerase in a model of premature aging caused by accelerated telomere shortening (duo to telomerase deficiency) was enough to revert some age-associated phenotypes [21113150].
Mice lacking telomerase age more rapedely and died earlier, as an abundance of critically short telomeres developed. Reawakening of Tert, leads to disappearment of age-related symptoms and rejuvenation occurred in several organs including their brains [http://www.isagenixhealth.net/blog/2012/05/16/telomerase-stimulation-extends-lifespan-in-mice/]. | Mouse | — | — | — |
| Dnmt gene therapy | Injecting a virus that contains extra copies of a Dnmt into elderly mice restored their faulty memories to it oiriganal capacity of young ones. Halving the amount of Dnmt produced by younger mice, deteriotes their memory to that of non-treated older mice [http://www.medicaldaily.com/news/20120702/10573/aging-memory-dna-enzyme-forgetfulness-young-old.htm]. | Mouse | — | — | — |
| uba-1 overexpression | Overexpression of uba-1 does not result in significant increase in median lifespan [22737090]. | Worm | — | — | — |
| Mir20a Overexpression | 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]. | Mouse | — | — | — |
| Trxr-1 overexpression | Overexpression of Trxr-1 (alias GSR; glutathione reductase) in transgenic flies results in increased lifespan and oxidative stress resistance, but only under hyperoxia [10506576]. | Fly | — | — | — |
| pnc-1 overexpression | Overexpression of pnc-1 increases adult survival under oxidative stress but does not extend the lifespan [17335870]. | Worm | — | — | — |
| git3 constitutive activative mutation | Constitutive activation of the G-alpha subunit acting downstream of Git3 accelerates aging and inhibits the effect of DR [19266076]. | | — | — | — |
| atf1 overexpression | Overexpressing atf1 is not sufficient to promote chronological lifespan extension in cells lacking sty1 [20075862]. | | — | — | — |
| wis1 constitutive active mutation | Constitutive active mutation of wis1 extends chronological lifespan and there is no further beneficial effect of DR [20075862]. | | — | — | — |
| ERG2 overexpression | Overexpression of ERG2 with the promoter of ERG6 (Perg6-ERG2) extends replicative lifespan and this effect was overlapping with moderate DR, because DR can not extend the lifespan of this mutant [Tang et al., unpublished]. | Yeast | — | — | — |
| TSA1 activating mutation | A gain-of-function allele of peroxiredoxin (thioredoxin peroxidase, Tsa1) causes a dominant oxidative stress-resistance and robust premature aging phenotype with reduced mean lifespan. These effect is not provoked by altered Tsa1 levels, nor can it be stimulated by deletion, haploinssufficiency or overexpression of wild-type allele [20729566]. | Yeast | — | — | — |
| NPT1 overexpression | Increased dosage of NPT1 increases SIR2-dependent silencing, stabilizes the rDNA locus and extends replicative lifespan by up to 60%. 0.5% glucose restriction does not significantly further increase replicative lifespan of NPT1 overexpression [11884393]. NPT1 deletion decreases replicative lifespan by 50% [17482543] as well as chronological lifespan [17110466]. Deletion of NPT1 shortens the lifespan in W303R. Replicative lifespan extension of cdc25-10 mutation (assumed to act as a genetic DR-mimetic) is cancelled out by NPT1 deletion [11000115]. | Yeast | +60 | — | — |
| MDH1 overexpression | Overexpression of MDH1 extends replicative lifespan by 25% and does not synergize with 0.5% glucose restriction [18381895]. | Yeast | +25 | — | — |
GenAge
GenDR
