| SGS101 antisense RNAi | Antisense RNA interference of SAG101 in transgenic plants delays the onset of leaf senescence for approximately 4 days [11971136]. | — | — | — | — |
| SGS101 chemical induced overexpression | Chemical induced overexpression of SAG101 causes precocious senescence in both attached and detached leaves of transgenic plants [11971136]. | — | — | — | — |
| SCP1 overexpression | Overexpression of SCP1 leads to elevuated ROS levels and reduces chronological lifespan [15024029]. | Yeast | — | — | — |
| SGS1 overexpression | Overexpression of SGS1 extends the maximum lifespan of cells lacking SRS2, but not the mean lifespan [11861900]. | Yeast | — | — | — |
| SOD1 overexpression | The overexpression of Sods, mitochondrial Sod2 and cytosolic CuZnSod (Sod1), in combination delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends chronological lifespan by 30% [12586694]. Overexpression of SOD1 with CCS1 levuates the level of Cn, Zn-Sod activity and increased chronological lifespan. However overexpression of SOD1 without high cooper or simultonous overexpression of CCS1 shortened both chronological and replicative lifespan [15659212]. Overexpression of SOD1 has no effect on replicative lifespan [10224252].
| Yeast | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| Gh antagonist overexpression | Overexpression of a growth hormone antagonist (a mutated bovine growth hormone that competes with the endogenous one) has no effect on lifespan [12933651]. | 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 | — | — | — |
| atf1 overexpression | Overexpressing atf1 is not sufficient to promote chronological lifespan extension in cells lacking sty1 [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 | — | — | — |
| HST2 overexpression | HST2 overexpression extends replicative lifespan. 0.5% glucose restriction does not increase lifespan of sir2;fob1;hst2 triple mutants [16051752]. DR increases lifespan of all four sir2;fob1;hstX(X = sirtuin) triple mutants [16741098; 17129213]. | Yeast | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
GenAge
GenDR
