Mostrando 1 - 20 Resultados de 48 Para Buscar '"ATTAC"', tiempo de consulta: 0.52s Limitar resultados
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    “…Here, we present a mouse model for inducible and reversible ablation of pancreatic β-cells named the PANIC-ATTAC (pancreatic islet β-cell apoptosis through targeted activation of caspase 8) mouse. …”
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    “…To address this question, a novel transgenic animal model was developed by crossing MMTV-NeuT mice containing a constitutively active ErbB2 gene into the FAT-ATTAC (fat apoptosis through targeted activation of caspase 8) background, which expresses an inducible caspase 8 fusion protein targeted to mammary adipose tissue. …”
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    “…In order to achieve specific neutrophil depletion, we cloned the ATTAC construct under the human migration inhibitory factor-related protein 8 (hMRP8) promotor. …”
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    “…To address this question, we developed an inducible suicidal knock-in mouse allele of Pd-l1 (PD-L1(ATTAC)) which allows for the tracking and specific elimination of PD-L1-expressing cells in adult tissues. …”
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    Publicado 2007
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    “…We constructed a novel lenti-INK-ATTAC viral vector to introduce INK-ATTAC genes to the ipsilateral brain and locally eliminate senescent brain cells by administering AP20187 to activate caspase-8 apoptotic cascade. …”
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    “…Next, we used the p21‐ATTAC mouse and the established p16‐INK‐ATTAC mouse to directly compare the contributions of p21(Cip1) versus p16(Ink4a) in driving cellular senescence in a condition where a tissue phenotype (bone loss and increased marrow adiposity) is clearly driven by cellular senescence—specifically, radiation‐induced osteoporosis. …”
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    Publicado 2002
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    “…We previously found genetic clearance of senescent cells from progeroid INK-ATTAC mice prevents lipodystrophy. Here we show that primary human senescent fat progenitors secrete activin A and directly inhibit adipogenesis in non-senescent progenitors. …”
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    “…Induction of fibrosis in NeuT/ATTAC mice led to more rapid tumor development and an inflammatory and fibrotic stromal environment. …”
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    “…In particular, we used either genetic (i.e., the INK-ATTAC “suicide” transgene encoding an inducible caspase 8 expressed specifically in senescent cells(2–4)) or pharmacological (i.e., “senolytic” compounds(5,6)) means to eliminate senescent cells. …”
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    “…Reduced collagen deposition and improved functional recovery over time was also identified in KidVD mice. In KidVD‐POD‐ATTAC mice, an increased number of podocytes were counted at 28 days post‐injury. …”
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