Interventions

  • name effect species mean median maximum
    Bax knockout Inactivation of proapoptotic Bax extends fertile potential and minimized age-related health problems, including bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and selective attention deficit. Bax deficiency does not lead to an increase in tumor incidence. Despite the apparently increased quality of life of aging females lacing Bax, there is no significant differences in overall lifespan [17360389]. Mouse
    bchs mutation Loss of function mutation in bchs results in a 40-45% decrease in mean lifespan and is associated with age-related neurodegenerative phenotype with reduced CNS size and altered morphology as well as accumulation of insoluble ubiquinated proteins and amyloid precursor-like proteins along with an increase in neuronal apoptosis. No pronounced developmental defects were observed and young adults have normal behaviours, indicating that the bchs gene is essential for normal adult survival and longevity [12598614]. bchs mutation reduces mean lifespan by 28 - 54% and maximum lifespan by 24 - 46% [17435236]. Fly -28 to -54 -24 to -46
    BCY1 deletion Disruption in BCY1 by mutation results decreases mean and maximum replicative lifespan by 37 and 16% and is associated with increased PKA activity [8195187]. Yeast -37 -16
    BLM mutation BLM mutation cuases Bloom syndrom. Individuals with Bloom syndrome have a shortend life expectancy []. Death is primary due to cancer, particulary leukemia and lymphoma [German, 1992]. Bloom syndrome is not a premature aging disease. Bloom syndrome characteristics are grwoth deficiency, sun-snesitivity, telangiectatic hypo- and hyperpigmented skin, predisposition to malignancy, and chromosomal instability [5770175]. Human
    Bmcp knockout Bmcp knockout flies live longer on low-calorie diets, have a decreased fertility, and gain less weight on high-calorie diets. Bmcp (ucp5) knockout mutants live longer than wild-type on low-calorie diets, but no longer on starvation or high-calorie diets. Ectopic neuronal expression of Bmcp transgene rescues starvation sensitive phenotype of Bmcp knockout mutants [16387864]. Fly
    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
    bra-1 mutation bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. Worm -6 to -25
    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
    Bub1b mutation Bub1b mutation decreases median lifespan by 60% (from 15 to 6 months). Bub1b mutant mice develop many phenotypes suggestive of accelerated aging, including: progressive bilateral cataracts, substantial loss of sub dermal adipose tissue, spinal kyphosis, muscle atrophy, and decreased wound healing. Moreover, there is a pronounced increase in senescent associated Beta-galactosidase expression in late generation Bub1b mutant mice, indicative of increased rate of cellular senscence. Homozyogous knockout of Bub1b results in lethality, while heterozygous animals exhibit no aging phenotypes [15208629]. Mouse -60
    Bub1b mutation The median and maximum lifespan of mice with a nonsense mutation 2211insGTTA in BubR1 is significantly reduced. BubR1(+/GTTA) mice develop several aging-related phenotypes at an accelerated rate, including catarct formation, lordokyphosis, skeletal muscle wasting, impaired exercise ability, and fat loss. Further BubR1(+/GTTA) mice develop mild anaplodies and exhibit enhanced growth of carcinogen-induced tumors [Wijshake et al. 2012]. Mouse
    BUL1 deletion Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    bwa mutation bwa (alias Dacer) inactivation increases Drosophila pre-adult development time and anti-oxidative stress capacity. Mean lifespan is increased by 16% in females, by 21% in males and by 19% in total. Maximum lifespan of females, males is also extended by 20 and 12%, respectively [20112046]. Fly +16 to +21 +12 to +20
    C26B2.2 knockout C26B2.2 knockout mutations extend lifespan [15253933]. Worm
    car mutation Loss-of-function mutation in car results in reduction of mean lifespan by 34 - 53% and maximum lifespan by 28 - 29% [17435236]. Fly -34 to -53 -28 to -29
    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
    cdc-25.3 knockout cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. Worm +40
    CDC25 mutation The CDC25-10 allele extends mean and maximum replicative lifespan by 34% and 18%, respectively, at 30 degree Celsius. cdc25-10 mutants have an extended replicative lifespan under AL. Growth on 0.5% glucose restriction does not further extend replicative lifespan of cdc25-10 mutants. CDC25 null mutant is not viable. CDC25 appears to act in the same genetic pathway as SIR2 and NPT1 and is suggested to be genetic model of DR [11000115]. Yeast +34 +18
    CDC6 mutation The CDC6-1 conditional allele results in an approximately 20% increase in mean replicative life span. This allele is defective for replicative initiation form the rDNA ARS at 27 degree Celsius, resulting in a reduced rate of extrachromosomal rDNA circle accumulation [9428525]. The cdc6-1 allele results in genomic instability at the permissive temperature [8552037]. Yeast +20
    Cdk5 mutation Cdk5 loss-of-function mutations result in defective axon guidance, age-dependent behavioral deficits and reduced lifespan by about one third [17368005]. Fly
    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
    Interventions are an extension of GenAge and GenDR.