| daf-2 |
IGFR-1 |
Caenorhabditis elegans |
14.9 ± 0.1 d |
83.0% |
Gene inactivation leads to disruption of insulin signaling |
N/A |
118 |
| age-1 |
PI3K |
Caenorhabditis elegans |
16 ± 2 d |
~1000% |
Gene inactivation leads to disruption of insulin signaling |
N/A |
41 |
| bec-1 |
beclin |
Caenorhabditis elegans |
22.4–31.1 d (mean lifespan) |
−15–30% (across six trials) |
Gene inactivation leads to disruption of autophagy |
N/A |
119 |
| hsf-1 |
HSF |
Caenorhabditis elegans |
13.8 ± 0.5 d |
22.0% |
Gene overexpression leads to activation of the heat shock promoter |
N/A |
120 |
| daf-16 |
FOXO |
Caenorhabditis elegans |
23.2 ± 0.8 d |
−27.0% |
Gene inactivation leads to disregulation of stress response machinnery |
N/A |
120 |
| let-363 |
TOR |
Caenorhabditis elegans |
10 d |
250.0% |
Gene inactivation leads to disruption of insulin signaling |
N/A |
121 |
| sgk-1 |
SGK |
Caenorhabditis elegans |
14.7 ± 0.3 d |
61.0% |
Gene inactivation leads to disruption of insulin signaling (as sgk-1 acts in parallel with AKT kinases) and better stress response. |
N/A |
122 |
| hcf-1 |
HCFC1 |
Caenorhabditis elegans |
14.3 ± 0.1 d |
28.0% |
Gene inactivation leads to activation of stress response by daf-16/FOXO |
N/A |
123 |
| jnk-1 |
JNK |
Caenorhabditis elegans |
16.8 ± 0.2 d |
−21.7% |
Gene inactivation leads to disruption of stress response by daf-16/FOXO |
N/A |
124 |
| jkk-1 |
JKK1 |
Caenorhabditis elegans |
16.8 ± 0.2 d |
−20.9% |
Gene inactivation leads to disruption of stress response by daf-16/FOXO |
N/A |
124 |
| akt-1 akt-2 |
AKT1 AKT2 |
Caenorhabditis elegans |
14.7 ± 0.3 d |
19.0% |
Simultaneous inactivation of these genes leads to disruption of insulin signaling |
N/A |
122 |
| sod1 |
SOD1 |
Caenorhabditis elegans |
18 d |
33% (averaged across trials 1 and 2) |
Overexpression of sod1 activates longevity-promoting transcription factors. |
N/A |
125 |
| sod2 |
SOD2 |
Caenorhabditis elegans |
19 d |
10% (averaged across trials 5 and 6) |
Overexpression of sod2 activates longevity-promoting transcription factors. |
N/A |
125 |
| dSir2 |
SIRT1 |
Drosophila melanogaster |
37 d |
57.0% |
Overexpression of dSir2 enhances energy metabolism |
female |
126 |
| dSir2 |
SIRT1 |
Drosophila melanogaster |
41 d |
32.0% |
Overexpression of dSir2 enhances energy metabolism |
male |
126 |
| chico |
InRS |
Drosophila melanogaster |
44 d |
47.7% |
Gene inactivation leads to disruption of insulin signaling |
female |
38 |
| InR |
InR |
Drosophila melanogaster |
N/A |
85.0% |
Gene inactivation leads to disruption of insulin signaling |
female |
127 |
| dFOXO |
FOXO |
Drosophila melanogaster |
Varies across trials |
19.4% (averaged across trials) |
Overexpression of dFOXO leads to disruption of insulin signaling |
female |
128 |
| dFOXO |
FOXO |
Drosophila melanogaster |
Varies across trials |
15.5% (averaged across trials) |
Overexpression of dFOXO leads to disruption of insulin signaling |
male |
128 |
| dPTEN |
PTEN |
Drosophila melanogaster |
57 d |
17.4% |
Overexpression of dPTEN leads to disruption of insulin signaling |
female |
128 |
| dPTEN |
PTEN |
Drosophila melanogaster |
51 d |
19.6% |
Overexpression of dPTEN leads to disruption of insulin signaling |
male |
128 |
| hsp22 |
HSP22 |
Drosophila melanogaster |
60 ± 3 d |
32.0% |
Overexpression of hsp22 increases cell-protection against oxidative injuries |
male |
78 |
| sod2 |
SOD2 |
Drosophila melanogaster |
77.8 ± 5.7 d and 74.7 ± 5.1 d |
−9.5% and −7.4% |
Overexpression of SOD2 caused decrease of mitochondrial H2O2 release and enhancement of free methionine content essential for normal biological processes. |
male |
129 |
| sod1 |
SOD1 |
Drosophila melanogaster |
27 d |
>66% |
Overexpression of sod1 in motorneurons enhances RO metabolism |
male |
130 |
| mTOR |
TOR |
Drosophila melanogaster |
N/A |
30.0% |
Overexpression of dominant negative form of TOR alters stress responses translation and/or mitochondrial function |
male |
131 |
| dS6K |
S6K |
Drosophila melanogaster |
N/A |
29.0% |
Overexpression of dominant negative form of S6 kinase alters stress responses translation and/or mitochondrial function |
male |
131 |
| IGFR-1 |
IGFR-1 |
Mus musculus |
568 ± 49 d |
33.0% |
Gene inactivation leads to disruption of insulin signaling |
female |
37 |
| IGFR-1 |
IGFR-1 |
Mus musculus |
585 ± 69 d |
16.0% |
Gene inactivation leads to disruption of insulin signaling |
male |
37 |
| p66shc |
p66 |
Mus musculus |
761 ± 19.02 d |
30.0% |
Disactivation of p66 contributes to increased cellular and organism oxidative stress resistance |
male and female |
88 |
| Klotho |
KLOTHO |
Mus musculus |
715 ± 44 d |
20.0 and 30.8% (transgenic lines EFmKL46 and EFmKL48) |
Gene inactivation leads to disruption of insulin signaling |
male |
48 |
| Klotho |
KLOTHO |
Mus musculus |
697 ± 45 d |
18.8 and 19.0% (transgenic lines EFmKL46 and EFmKL48) |
Gene inactivation leads to disruption of insulin signaling |
female |
48 |
| Arf |
p19 |
Mus musculus |
113.8 ± 2.4 wk |
16.0% |
Hypothetically activation of Arf/p53 module provides anti-cancer and anti-aging effect detecting cellular damage. |
male and female |
132 |
| SIRT6 |
SIRT6 |
Mus musculus |
851.3 ± 24.9 and 724.0 ± 35.0 d (transgenic lines 55 and 108) |
14.8% and 16.9% (transgenic lines 55and 108) |
Overexpression leads to higher levels of IGF-binding protein 1 and altered phosphorylation levels of major components of IGF1 signaling |
male |
133 |
| p63 |
p63 |
Mus musculus |
121 wk (median lifespan) |
−21.5% |
p63 deficiency activates widespread cellular senescence with enhanced expression of senescent markers SA-β-gal PML and p16INK4a |
male and female |
134 |
| Brca1 |
Brca |
Mus musculus |
713 ± 146 d |
−8.0% |
Gene inactivation leads to hypersensitivity to DNA damaging agents and consequently genomic instability of cells |
female |
135 |
