Interventions

  • name effect species mean median maximum
    AVO2 deletion Deletion of AVO2 extends chronological lifespan [21641548]. Yeast
    AVT1 deletion Deletion of AVT1 accelerates the development of age-induced mitochondrial dysfunction without effecting the kinetics of vacuolar acidity decline and prevents the suppression of mitochondrial dysfunction by VMA1 and VPH2 overexpression without affecting vacuolar acidity. AVT1 deletion decreases mean, median and maximum lifespan by 21, 22, and 12%, respectively [23172144]. Yeast -20.6 -22.4 -11.8
    BAS1 deletion Deletion of BAS1 increases replicative lifespan by 30% in the alpha strain [16293764; 19030232]. Yeast +30
    BMH1 deletion Deleting BMH1 extends chronological lifespan by 25% and is associated with activated stress response, decreased ROS levels and increased heat-shock-element-driven transcription activity. BMH1 deletion was non-additive with the genetic DR mimetic cdc25 and tor1. Water starvation (a form of extreme DR) extends chronological lifespan of BMH1 mutant even more as it does in wild-type [19805817]. Yeast +25
    BNA6 deletion Deletion of BNA6 (alias QPT1) has no effect on replicative lifespan and is not required for lifespan extension by DR, but is lethal with mutation of NPT1 [11000115]. Deletion of BNA6 decreases chronological lifespan [17110466]. Yeast
    Brca1 deletion Deletion of Brca1 causes senescence in mutant embryos and cultured cells and tumorigenesis and signs of premature aging in adults [12533509]. Brca1 heterozygous seem to have shortened lifespan with 70% of tumor incidence. Lymphoma, but not ovarian and mammary gland tumors, occurs commonly in these animals. After a whole-body exposure to ionizing radiation, Brca1 heterozygous mice have a 3-5-fold higher incidence to ovarian tumors, but not lymphoma, when compared with Brca1(+/+) mice [17420720]. Mouse
    BRE5 deletion Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] Yeast +30
    BUL1 deletion Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    Casp-2 deficiency Loss of caspase-2 resulted in a shortened (10%) maximum lifespan and in enhanced aging-related traits such as impaired hair growth, increased bone loss, and reduced body fat content [17188333]. Mouse -10
    CAT5 deletion Deletion of CAT5 decreases chronological lifespan by up to 50% [17492370] and also decreases replicative lifespan by 30% in the alpha strain [18340043]. Yeast -30 to -50
    CCR4 deletion Deletion of CCR4 increases mean chronological lifespan by 20 - 41% (20, 33, 41) in diploid cells [21447998]. In W303R CCR4 deletion shortens replicative lifespan by approximately 80% and results in temperature sensitivity that is suppressed by SSD1-V. SSD1-V partially suppresses the short-lifespan of ccr4 mutant. CCR4 mutation is synthetically lethal in combination with deletion of MPT5 in the absence of SSD1-V [11805047]. Yeast -80 to +20
    CCS1 deletion Deletion of CCS1 reduces replicative lifespan by 50% [17460215]. Yeast -50
    Cdkn1a knockout Deletion of Cdkna1 (alias p21) prolongs the lifespan of telomerase-deficient mice with dysfunctional telomeres and improves the repopulation capacity and self-renewal of hematopoietic stem cells [17143283]. The p21(-/-) strains like the Cdkn1a(tmi/Tyj) exhibits enormous regenerative capacities as it closes ear holes similar to MRL mice [20231440; 21722344]. Mouse
    che-11 mutation Loss-of-function muation in che-11 increases lifespan up to 40% (in Bristol N2) [10617200]. che-11 mutants are dye filling defective, defective in osmotic avoidance and dauer formation, and have irregular amphid cilia [2428682]. Worm +40
    che-13 mutation Loss-of-function mutation in che-13 increases lifespan up to 40% (in Bristol N2) [10617200]. che-13 Mutants are dye filling defective, have severely shortened axonemes and ectopic assembly of ciliary structures and microtubules in many sensory neurons as well as are defective in osmotic avoidance and dauer defective [2428682]. Worm +40
    che-2 mutation che-2 recessive loss-of-function mutations extend lifespan up to 50% (in Bristol N2) [10617200]. che-2 mutants are chemotactic defective, slightly small, defective for osmotic avoidance, have ciliated neurons with abnormal stunted ultrastructure, and are dauer defective [2428682; 1732156]. Worm +50
    che-2 mutation Loss-of-function in che-3 extends lifespan by 50-100% depending on the allele, but life-extension is suppressed by daf-16 (in Bristol N2) [10617200]. che-3 mutations have defective sensory neurons [2428682; 10508861] and are defective in dye filling [2428682; 7705621] as well as dauer defective [1732156]. Worm +50 to +100
    CHL1 deletion CHL1 deletion mutant exhibits a shortened mean and maximum lifespan by 36 and 29%, respectively, as well as hypersensitivity to heat stress. CHL1 may modulate transcriptional silencing in the presence of Sir proteins [16182251]. Yeast -36 -29
    CIT2 deletion Deletion of CIT2 has no effect on replicative lifespan [10224252]. Yeast
    CKA2 deletion CKA2 deletion approximately doubles mean chronological lifespan under starvation/extreme DR in BY4741 also increases as well as as heat-shock resistance in SDC medium in the W303-1A and DBY746 genetic backgrounds [20657825]. Yeast
    CKB2 deletion Lack of Ckb2 promotes a modest but significant chronological lifespan extension and marked increase in yeat resistance [20657825]. Yeast
    CLA4 deletion Deletion of CLA4 decreases replicative lifespan by 60% in the alpha strain [18340043; 19030232]. Yeast -60
    clk-3 mutation Mutations in clk-3 slow down development and extend adult lifespan (at 20 degree Celsius in Bristol N2). clk-3 mutation slows growth and rhythms similiar to clk-1a and profounds maternal and zygotic rescue [8638122]. Worm
    COQ3 deletion Deletion of COQ3 decreases chronological lifespan and renders cells respiratory deficient and sensitive to hydrogen peroxide [12586694]. Yeast
    COX1 deletion Deletion of mobile group II intron (intron alpha) from COX1 doubles lifespan and prevents accumulation of senescence-associated DNA concatemer corresponding to this of the mitochondrial genome [10330149]. Deletion encompassing COX1's intron alpha and its upstream exon abolishes the senescence process entirely [2999848].
    Interventions are an extension of GenAge and GenDR.