Mostrando 41 - 48 Resultados de 48 Para Buscar '"ATTAC"', tiempo de consulta: 0.09s Limitar resultados
  1. 41
    “…The elimination of senescent cells by suicide gene-meditated ablation of p16(Ink4a)-expressing senescent cells in INK-ATTAC mice or by treatment with a combination of the senolytic drugs dasatinib and quercetin (D+Q) reduces overall hepatic steatosis. …”
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  2. 42
    “…Genetically reducing highly p16Ink4a-expressing cells in old INK-ATTAC mice or administering the senolytics, Dasatinib plus Quercetin (D+Q) or Fisetin (F), to young mice transplanted with senescent cells, young diet-induced obese (DIO) mice, or naturally-aged mice increased urine, kidney, and/or brain α-Klotho. …”
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  3. 43
    “…We aimed to investigate the effects of p16Ink4a-positive cell removal on the mass and proliferative capacity of remaining β-cells using INK-ATTAC mice as a transgenic model of senolysis. Clearance of p16Ink4a positive subpopulation was tested in mice of different ages, males and females, and with two different insulin resistance models: high-fat diet (HFD) and insulin receptor antagonist (S961). …”
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  4. 44
  5. 45
    “…Adipocyte apoptosis was induced in obese male FAT-ATTAC mice through AP20187 dimerizer-mediated activation of caspase 8 selectively in adipocytes. …”
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  6. 46
  7. 47
    “…METHODS: We used 2 novel genetic murine models to reduce cholangiocyte senescence: (i) p16(Ink4a) apoptosis through targeted activation of caspase (INK-ATTAC)xMdr2(-/-), in which the dimerizing molecule AP20187 promotes selective apoptotic removal of p16-expressing cells; and (ii) mice deficient in both p16 and Mdr2. …”
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  8. 48
    “…METHODS: The impact of cellular senescence on the interaction between RT and P was assessed by harnessing female INK-ATTAC mice, which express a dimerizable form of caspase 8 (CASP8) under the promoter of cyclin dependent kinase inhibitor 2A (Cdkn2a, coding for p16(Ink4)), as host for endogenous mammary tumors induced by the subcutaneous implantation of medroxyprogesterone acetate (MPA, M) pellets combined with the subsequent oral administration of 7,12-dimethylbenz[a]anthracene (DMBA, D). …”
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