|mrpl-37 ||— ||Knockdown of mrpl-37 increases lifespan by 41% . ||Nematode |
|mrpl-2 ||— ||Knockdown of mrpl-2 increases lifespan by 54% . ||Nematode |
|mrpl-1 ||— ||Knockdown of mrpl-1 increases lifespan by 57% . ||Nematode |
|nkcc-1 ||Na-K-Cl Cotransporter homolog ||Knockdown of nkcc-1 throughout the entire life increases the lifespan by 23% . ||Nematode |
|mrps-5 ||— ||Knockdown of mrps-5 throughout the entire life increases the lifespan by 60%. mrps-5 RNAi prevents aging-associated functional decline and alters mitochondrial function. Knocking down mrps-5 after early development no longer affects nematode lifespan. When RNAi of mrps-5 was performed during the larval stages only, lifespan increases by 48%, whereas RNAi started from the L4 stage has no effect. mrps-5 RNAi results in fragmented mitochondria. mrps-5 RNAi increases lifespan by 40% in widltype, 37% in daf-16(mu86), 40% in sir-2.1(ok434) 69% in aak-2(ok524) and 112% in mev-1(kn1). Knockdown of cco-1 does not extend the lifespan of mrps-5 RNAi . ||Nematode |
|snz ||snazarus ||Mutation in snz increases maximum lifespan of both sexes by up to 66%, while the median female lifespan is approximately 85% higher and that of males around 72% . ||Fruit fly |
|Loco ||locomotion defects ||Reduced expression of Loco due to hetero-deficient results in a 17-20% longer mean lifespan for both male and females, besides the fact that the homozygous deficiency of loco is lethal. Several of these long-lived mutants are more resistant to stresses such as starvation, oxidation and heat. Additionally, mutants have higher Manganese-containing superoxide dismutase (MnSOD) activity, increased fat content an diminished cAMP levels. Loco's RGS domain is required for the regulation of longevity as deletion analysis suggest . ||Fruit fly |
|Lnk ||— ||Loss of Lnk function results in increased median (14% in females and 17.5 in males) and maximum lifespan, reduced female fecundity and improves survival under conditions of oxidative stress and starvation. Heterozygousity does not result in any significant differences in lifespan in either males or females. Moreover, lifespan extension in one of the female homozygous mutant is fully rescued by the introduction of a Lnk genomic rescue construct . ||Fruit fly |
|Gr63a ||Gustatory receptor 63a ||Gr63a loss-of-function in female flies leads to 30% extended mean lifespan, increased fat deposition, and enhanced resistance to some (but not all) environmental stresses. Lifespan of males is not extended .
Overexpression of Gr63a has modest negative effect on lifespan . ||Fruit fly |
|esc ||extra sexcombs ||Males heterozygous for the null esc4 or the dominant negative esc9 mutation that are progeny of an out-cross to a O-R wild-type strain have median lifespan that is, respectively, 47% and 60% longer than the O-R control. When derived from an out-cross to a longer-lived C-S wild-type strain, heterozygous esc9 flies have a median lifespan that is 43% longer than the C-S control . ||Fruit fly |
|Edem1 ||— ||The mean lifespan of Edem1 mutants of both male and female is increased by more than 30% . ||Fruit fly |
|E(z) ||Enhancer of zeste ||Flies heterozygous for the protein null E(z)63 or the catalytically inactive E(z)731 mutation that are progeny of an out-cross to an Oregon-R (O-R) wild-type strain exhibit a substantially greater median lifespan than the O-R control (71% and 76%, respectively). When derived from an out-cross to a longer-lived Canton-S (C-S) wild-type strain, the median lifespan of E(z)63 heterozygous is 33% longer than the C-S control . ||Fruit fly |
|CG9172 ||— ||RNAi against CG9172 increases mean lifespan in females by up to 4-12% when applied in both development and adulthood, and up to 46% when applied in adult neurons only. For males the effect is variable . ||Fruit fly |
|CG18809 ||— ||RNAi of CG18809 results in a 7-19% increase in mean lifespan of females, while neural RNAi results in an increased mean lifespan of up to 12% in females. For males the results are variable . ||Fruit fly |
|CG17856 ||— ||RNAi of CG17856 results in an increase in mean lifespan of 13-18% in females. In the case of males and post-developmental experiments the results are variable . ||Fruit fly |
|alpha-Man-I ||alpha Mannosidase I ||alpha-Man-I mutant fly exhibit enhanced resistance to paraquat and starvation an a 60% increase in mean lifespan for both sexes. After outcrossing, the mutant exhibit, under normal conditions, an increase in mean lifespan of 22% for females and 38% for males. Maximum lifespan is increased by 15%. alpha-Man-I RNAi knockdown results in a 39% increase in mean lifespan . ||Fruit fly |
|14-3-3epsilon ||CG31196 gene product from transcript CG31196-RA ||Loss of 14-3-3ε results in increased stress-induced apoptosis, growth repression and extended lifespan of flies, in a foxo-dependent manner. Mean lifespan of males and females is increased by 25% and 49%, respectively. Increased 14-3-3ε expression also reverts foxo-induced growth defects. No effect of lifespan is observed when overexpressing 14-3-3ε in adipose tissue, indicating that endogenous foxo activity in this tissue is low under normal conditions . ||Fruit fly |
|frh-1 ||FRataxin (involved in human Friedrich's ataxia) Homolog ||Complete absence of frataxin,the mitochondrial protein defective in individuals with Friedreich ataxia is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively .
Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression. Frataxin expression modulates autophagy in the absence of p53 . ||Nematode |
|mir-239 ||— ||Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively, whereas overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively . ||Nematode |
|Ctf1 ||Cardiotrophin 1 ||Absence of Ctf1 is associated with decreased arterial fibrosis, stiffness mad senescence and increased longevity. Ctf1-null mice have a decrease in arterial stiffness and decrease in levels of inflammatory, apoptotic and senescence, whereas telomere-linked and DNA repair proteins as well as antioxidant enzyme activities are increased. The median lifespan of Ctf1-null mice is increased by 5 month (18%) .
Wild-type and Ctf1-null mice exhibit an increase of senescence markers (p53, Mdm2, p21, and p16) with age but are lower in Ctf1-null mice.
Ctf1-null mice have a diminished vascular NFκB signaling, lower inflammation and oxidative stress and reduced senescence. Ctf1-null mice have a 12% increase in body weight, 130% increased adiponectin levels and 51% decreased leptin concentrations .
Treatment of cells with CT-1 increases SA-β-galactosidase, and apotosis and senescence makers (p53, p21 and p16), without modifying Mdm2 expression . ||House mouse |
|HAC1 ||Homologous to Atf/Creb1 1 ||Deletion of HAC1 decreases mean, median and maximum replicative lifespan by 10, 8 and 5%, respectively . ||Budding yeast |
|l(3)DTS3 ||lethal (3) DTS3 ||Female, but not male, heterozygous mutants exhibit a 42% increase in mean lifespan and resistance to various stresses, with no apparent deficit in fertility or activity . ||Fruit fly |
|let-23 ||LEThal 23 ||Postdevelopmental inactivation of let-23 by RNA interference extends the lifespan by 5.6% [New Longevity Regulators]. ||Nematode |
|cyc-2.1 ||CYtochrome C 2.1 ||RNA interference of cyc-2.1 increases mean lifespan by 80% . cyc-2.1 RNAi has no significant effect on lifespan of eat-2 mutants, although CYC-2.1 levels are elevated in eat-2 mutants . ||Nematode |
|icl-1 ||IsoCitrate Lyase homolog 1 ||RNAi knockdown of icl-1 (alias gei-7) starting at hatching or only during the adulthood significantly extends lifespan of wild-type, but does not alter, or even shortens the lifespan of eat-2 mutants . ||Nematode |