• name effect species mean median maximum
    sptf-3 Overexpression Overexpression of sptf-3 extends lifespan [18059442]. Worm
    ectopic Trp53 overexpression Mutant mice with activated Trp53 display enhanced resistance to spontaneous tumours and signs of premature ageing including reduced lifespan, osteoporosis, organ atrophy and a diminished stress tolerance [11780111]. Mouse
    super-Trp53 super-p53 mice generate by integrating a transgenic copy of a large genomic segment containing an intact and complete copy of p53 have an ehanced response to DNA damage, are significantly protected from cancer and had no indication of accelerated aging [12426394]. Mouse
    super-Ink4a/Arf super-Ink4a/Arf mice carrying a transgenic copy of a large genomic segment containing an intact and complete copy of the Cdkn2a (a.k.a. Ink4a/Arf) gene are significantly protected from cancer and had no indication of accelerated aging. Cells derived from super-Ink4a/Arf mice have increased resistance to in vitro immortalization and oncogenic transformation [15520276]. Mouse
    super-Ink4a/Arf/p53 super-Ink4a/Arf/p53 mice have a synergic protection against cancer and delayed aging [Workshop RoSyBa 2011]. Mouse
    Pink1 overexpression Overexpression of Pink1 and overexpression of Pink1 with alpha-synclein results in an increase in lifespan which is accompanied by an increase in healthspan (as measured by mobility) when driven by a dopaminergic cells targeting TH-Gla4 transgene [22653599]. Fly
    cup-4 overexpression cup-4 overexpession reduces oxidative stress resistance and shortens lifespan of wild-type under AL [19783783]. Worm
    nlp-7 overexpression nlp-7 overexpression reduces oxidative stress resistance and shortens lifespan of wild-type under AL [19783783]. Worm
    Cisd2 overexpression A persistent level of Cisd2 achieved by transgenic expression extends mean, median and maximum lifespan without any apparent deleterious side effects [22661501]. Mouse
    CIT2 overexpression Overexpression of CIT2 has no effect on replicative lifespan [10224252]. Yeast
    clk-1 overexpression Overexpression of clk-1 shortens lifespan and is associated with increased mitochondrial activity [10202142]. Worm
    daf-18 overexpression Overexpression increases adult lifespan in individual tissues [16153634]. Worm
    Down syndrom Individuals with Down syndrome develop the neuropathological lesions of Alzheimer disease significantly earlier than those without [3158266] and have a shorter lifespan. Down syndrome is cuased by duplication of small regions of chromosome 21 [8197171]. The major features of Down syndrome are mental retardation, characteristic facial features, congenital malformations of the heart and gastrointestinal tract, thyroid disease, and an increased incidence of leukaemia [Epstein, 1989]. Neurons cultured in vivo form individuals with Down syndrome degenerate and exhibit apoptosis [8524410]. Down syndrome neurons also display increased generation of reactive oxygen species and treatment with antioxidants can prevent degeneration. Human
    Mt2 overexpression Overexpression of Mt2 extends mean and maximum lifespan [15533947]. Fly
    FPS1S overexpression Plants overexpressing FPS1S exhibit a cell death/senescence-like phenotype and grw vigorously than wild-type [12000449]. In plants with increased FPS activity, the expression of senescence activated gene SAG12 is prematurely induced.
    hep overexpression Overexpression of hey significantly extends median (50%) and maximum (25%) lifespan [14602080]. Fly +50 +25
    HSP104 overexpression Overexpression of HSP104 driven by GAL promoter is insufficient to extend replicative lifespan [9851879]. Overproduction of HSP104 in wild-type cells has no effect on replicative life span, but suppresses the reduced lifespan of Sir2-deficient cells [17908928]. HSP104 overproduction is sufficient to induce thermotolerance [8643570]. Yeast
    MAPT overexpression Expression of wild-type human MAPT (tau) moderately shortened lifespan. Expression of a mutant form of human MAPT (Arg406 Trp), associated with an early onset familial form of demetia, results in a several shortened lifespan. MAPT is implicated in the pathogenesis of Alzeimer's disease and related disorders in humans. Transgenic flies exhibit key features of the human disorders: adult onset, progressive neurodegeneration, early death, enhanced toxicity of mutant tau, accumulation of abnormal tau, and relative anatomic selectivity. However, neurodegeneration occurred without the neurofibrillary formation that is observed in humans disease and some rodent taupathy models [11408621]. Fly
    TXN overexpression Overexpression of TXN1 in transgenic C57BL/6 mice resulted in extended median (35%) and maximum (22%) lifespan. Telomerase activity in spleen tissues of TXN1 overexpressing mice is higher than tha in wild-type [12230882]. Mouse +35 +22
    Klotho overexpression Klotho overexpression leads to lifespan extension [16123266]. Mouse
    Activating let-60 mutation The let-60(n1046gf) activating mutation greatly reduces lifespan of wild-type, weakly suppresses constitutive dauer diapause in daf-2 and age-1 mutants and extends lifespan induced by mutation of daf-2 [16164423]. Worm
    LMNA mutation Dominant mutation in LMNA (lamin A/C) gene cause Hutchinson-Gilford progeria syndrome (HGPS) which is rare and characterized by prematurly senile appearing skin and hair, with death from coronary artery disease often by age 10 [Gilford 1904; Hutchinson 1886; OMIM]. The median age of death in HGPS individuals is 13.4 years. A C to T transition at nucleotide 1824 is associated with HGPS [Sandra-Giovannoli et al., 2003; Eriksson et al., 2003]. The 1824C-T allele appears to act in a dominant negative manner by interfering with normal splicing, resulting in production of both the normal transcript and a transcript deleted for 150 bp at the 3' end [Sandre-Giovannoli et al, 2003]. Cultured skin fibroblasts from individuals with progeria exhibit an increased fraction of hat-labile proteins [1128606]. Gilford (1904). Ateleiosis and progeria: continuous youth and premature old age. Brit Med J 2, 914-918. Hutchinson, J. (1886). Case of congenital absence of hair, with atrophic condition of the skin and its appendages, in a boy whose mother had been almost wholly bald from alopecia areata from the age of six. Lancet 1, 923. Human
    SIR2RP1 overexpression Overexpression of SIR2RP1 (alias LmSIR2) results in a significant increase in survival of the vertebrate stage under normla axenic culture conditions, but has no effect on survival of the insect stage of the parasite. SIR2RP1 is mainly localized within the cytoplasm [12383511].
    MORF4 overxpression Overexpression of MORF4 reverses the immortal phenotype of immortal cell lines in complementation group B [9891081]. Cellular senescence is dominant over immortality in fused hybrids of normal and immortal human cell in culture [6879195]. Fusion of immortal cell lines with each other led to the idenetification of four complementation groups for immortality [3413074]. MORF4 rescues the immortal phenotype [9891081]. Human
    HSPA9 overexpression Overexpression of HSPA9 (mortalin) increases the proliferation potential of normal fibroblasts [11959102]. Transfection of normal human fibroblasts with human HSPA9 (or the murine Hspa9) overexpression vectors led to an increase in the number of population doublings the cells could sustain before senescing (increase varying from 32-60%, depending on the exact construct used). Transfected cells retain a youthful morphology longer than the controls cells, and there is an dealy in appearance of senescence associated beta-galactosidase activity [10838077]. Mot-2 overexpressing cells exhibit a reduction in p53 transcriptional activation (as measured by expression from vectors containing either luciferase or beta-glactosidase driven by p53 binding sites) [10838077], which might partially or wholly explain the effects of Mot-2 on proliferative potential. HSPA9 is differentially distributed and/or translated in normal vs. transformed cells [8454632]. Human
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    • 25 of 226 interventions
    Interventions are an extension of GenAge and GenDR.