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  1. 21
    “…RNA sequencing analyses of lungs from non-tumor-bearing p16-INK-ATTAC mice identified that palbociclib downregulates immune-related gene sets and gene expression related to leukocyte migration. …”
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    Stromal Senescence following Treatment with the CDK4/6 Inhibitor Palbociclib Alters the Lung Metastatic Niche and Increases Metastasis of Drug-Resistant Mammary Cancer Cells
  2. 22
    “…Studies clearing senescent cells from mice using the p16-based transgene INK-ATTAC have shown that senescent cells can impact both organismal aging and lifespan. …”
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    Senolytics: A Translational Bridge Between Cellular Senescence and Organismal Aging
  3. 23
    “…Using single cell sequencing, we identified a putative senescent microglial population, which increased in abundance with age and was characterized by increased expression of p16 and chemotactic senescence associated secretory phenotype (SASP) factors. Using p16-INK-ATTAC transgenic mice to eliminate p16ink4a-positive senescent cells and mass cytometry, we show that p16ink4a-positive cell targeting reduced the abundance of activated inflammatory cells in the aged female brain. …”
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    Cell Senescence as a Mediator of Age-Dependent Brain Inflammation
  4. 24
    “…METHODS: Herein, we evaluated whether blockade of endotrophin through neutralizing antibodies protects from renal fibrosis in the podocyte insult model (the “POD-ATTAC” mouse). We determined the therapeutic effects of endotrophin targeted antibody through assessing renal function, renal inflammation and fibrosis at histological and transcriptional levels, and podocyte regeneration. …”
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    Endotrophin neutralization through targeted antibody treatment protects from renal fibrosis in a podocyte ablation model
  5. 25
    “…In this article, we investigated the association between M. tuberculosis infection, adipose tissue, and TB disease progression using a transgenic inducible “fatless” model system, the FAT-ATTAC (fat apoptosis through targeted activation of caspase 8) mouse. …”
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    Adipose Tissue Regulates Pulmonary Pathology during TB Infection
  6. 26
    “…To investigate the role of senescence in obesity-related neuropsychiatric dysfunction, we used the INK-ATTAC mouse model, from which p16(Ink4a)-expressing senescent cells can be eliminated, and senolytic drugs dasatinib and quercetin. …”
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    Obesity-Induced Cellular Senescence Drives Anxiety and Impairs Neurogenesis
  7. 27
    “…Global elimination of senescent cells in aged mice (INK‐ATTAC or wild‐type mice treated with D + Q senolytics) in vivo activates resident CPCs and increased the number of small Ki67‐, EdU‐positive cardiomyocytes. …”
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    Aged‐senescent cells contribute to impaired heart regeneration
  8. 28
    “…Adipocyte death was induced using an established transgenic mouse model of inducible adipocyte apoptosis (FAT-ATTAC). Metabolic, biochemical, histologic and flow cytometric analyses were performed. …”
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    Deletion of TNF-Like Weak Inducer of Apoptosis (TWEAK) Protects Mice From Adipose and Systemic Impacts of Severe Obesity
  9. 29
    “…METHODS & RESULTS: Using PANIC-ATTAC mice, a model of titratable, acute β-cell apoptosis capable of autonomous, and effective islet mass regeneration, we demonstrate that an extended washout of residual tamoxifen activity is crucial for β-cell lineage tracing studies using the tamoxifen-inducible Cre/loxP systems. …”
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    Autonomous interconversion between adult pancreatic α-cells and β-cells after differential metabolic challenges
  10. 30
    “…Based on this an investigation was undertaken during both acute and chronic T. cruzi infection utilizing the FAT-ATTAC murine model (that allows modulation of fat mass) to understand the consequences of the loss of adipocytes in the regulation of cardiac parasite load, parasite persistence, inflammation, mitochondrial stress, ER stress, survival, CCC progression and CCC severity. …”
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    Fat tissue regulates the pathogenesis and severity of cardiomyopathy in murine chagas disease
  11. 31
    “…Thus, we developed a mouse model (p16-LOX-ATTAC) that allowed for inducible SnC elimination (senolysis) in a cell-specific manner and compared the effects of local versus systemic senolysis during aging using bone as a prototype tissue. …”
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    Local senolysis in aged mice only partially replicates the benefits of systemic senolysis
  12. 32
    “…AP20187 was used to specifically eliminate senescent cells and proven to alleviate CNV progression in INK-ATTAC transgenic mice. Senescent adult RPE cell line-1 cells produced elevated levels of senescence-associated secretory phenotypes, including VEGFs; they also demonstrated increased proliferation, migration, invasion, and tube formation in human umbilical vein endothelial cells. …”
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    Dasatinib Plus Quercetin Alleviates Choroid Neovascularization by Reducing the Cellular Senescence Burden in the RPE–Choroid
  13. 33
    “…A beta-lactamase gene ctx-m-14 with its surrounding insertion elements (ISEcp1, truncated IS903 and a 20 bp inverted repeat sequence) may compose an active transposon which is directly bordered by two putative target repeats “ATTAC.” CONCLUSIONS/SIGNIFICANCE: The K. pneumoniae plasmid pKF3-70 carries an extended-spectrum beta-lactamase gene, ctx-m-14. …”
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    Sequence Analysis of pKF3-70 in Klebsiella pneumoniae: Probable Origin from R100-Like Plasmid of Escherichia coli
  14. 34
    “…To explore the physiological relevance and consequences of naturally occurring senescent cells, we used a previously established transgene, INK-ATTAC, to induce apoptosis in p16(Ink4a)-expressing cells of wild-type mice by injection of AP20187 twice a week starting at one year of age. …”
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    Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan
  15. 35
    “…Genetic clearance of senescent cells in aged normocholesterolemic INK‐ATTAC mice phenocopied changes elicited by D+Q. Senolytics tended to reduce aortic calcification (alizarin red) and osteogenic signaling (qRT–PCR, immunohistochemistry) in aged mice, but both were significantly reduced by senolytic treatment in hypercholesterolemic mice. …”
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    Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice
  16. 36
    “…Recent groundbreaking studies demonstrate that senescent cell depletion through INK-ATTAC transgene-mediated or cell-penetrating FOXO4-DRI peptide induced forced apoptosis, reduced age-associated damage and dysfunction in multiple organs, in particular the kidney, and increased performance and lifespan. …”
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    Cellular senescence in the aging and diseased kidney
  17. 37
    “…The elimination of p16‐expressing cells in old mice, using the INK‐ATTAC transgene, increases bone mass indicating that senescent cells contribute to skeletal aging. …”
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    Elimination of senescent osteoclast progenitors has no effect on the age‐associated loss of bone mass in mice
  18. 38
    “…We observed an age‐dependent increase in p16(Ink4a) senescent cells, which was more pronounced in microglia and oligodendrocyte progenitor cells and characterized by a SASP. We then aged INK‐ATTAC mice, in which p16(Ink4a)‐positive senescent cells can be genetically eliminated upon treatment with the drug AP20187 and treated them either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin. …”
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    Whole‐body senescent cell clearance alleviates age‐related brain inflammation and cognitive impairment in mice
  19. 39
    “…Ab-4 promoted β-cell survival and enhanced the recovery of insulin(+) islet mass with concomitant increases in circulating insulin and C peptide. In PANIC-ATTAC mice, an inducible model of β-cell apoptosis which allows for robust assessment of β-cell regeneration following caspase-8–induced diabetes, Ab-4 drove a 6.7-fold increase in β-cell mass. …”
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    Glucagon blockade restores functional β-cell mass in type 1 diabetic mice and enhances function of human islets
  20. 40
    “…Consistently, depletion of senescent cells prevented podocyte loss in old p16 INK‐ATTAC transgenic mice. Importantly, these experimental findings are relevant to humans. …”
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    Glomerular endothelial cell senescence drives age‐related kidney disease through PAI‐1
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