Deletion of the developmentally essential gene ATR in adult mice leads to age-related phenotypes and stem cell loss.

By Yaroslava Ruzankina, C. Pinzon-Guzman, Amma Asare, Tony Ong, Laura L. Pontano, G. Cotsarelis, Valerie P. Zediak, Marielena Velez, A. Bhandoola, E. Brown. Cell Stem Cell, 2007

795 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ab4fb2452f2a430b8692a668a76540a57facd1e1

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Citations in the corpus

Critical Role for CD103+/CD141+ Dendritic Cells Bearing CCR7 for Tumor Antigen Trafficking and Priming of T Cell Immunity in Melanoma (2016, positive): “Ubc-CreERT2 mice (Ruzankina et al., 2007) were crossed to themTmG reporter strain (Muzumdar et al., 2007) to generate Ubc-CreERT2 mTmG mice.”
How stem cells age and why this makes us grow old (2007, methodology): “, who used a conditional allele for the DNA-damage response gene Atr (ataxia telangiectasia and Rad3-related), are worth considering in this regar”
Mechanisms of stem cell self-renewal. (2009, background): “Conditional deletion of the DNA damage response gene, ATR, in all tissues of adult mice leads to widespread stem cell depletion, defects in tissue regenerative capacity, and phenotypes that resemble premature aging (Ruzankina et al. 2007).”
Stems cells and the pathways to aging and cancer. (2008, background): “, 2000), it seems likely that the loss of LSK cells in aged ATR mosaic mice may be a result of lasting consequences of ATR deficiency in niche cells (Ruzankina et al., 2007).”
Signaling through BMPR-IA regulates quiescence and long-term activity of neural stem cells in the adult hippocampus. (2010, background): “when forced to proliferate (Cheng et al., 2000; Kippin et al., 2005; Ruzankina et al., 2007), and quiescence may function as a protective mechanism that counteracts stem cell exhaustion.”
The DNA Damage Response: Making it safe to play with knives (2010, background): “Deletion of ATR in adult mice was also shown to lead to stem cell loss and premature aging (Ruzankina et al., 2007).”
Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, methodology): “Because of the stochastic nature of the inducible Cre system, HK2 expression was still detectable in some tumors arising in tamoxifen-treated KRasLA2-G12D;Hk2f/f;UBCCreERT2 mice, especially in larger size tumors (Figure 6G).”
Metabolic regulation of hematopoietic stem cells in the hypoxic niche. (2011, background): “Inducible ATR knockout mice show dramatic reductions in tissue-specific stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity (Ruzankina et al., 2007).”
Leptin Receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow (2014, neutral): “Mice All mice were maintained in a C57BL/6 background, including Lepr-cre (DeFalco et al., 2001), Leprfl/fl (Cohen et al., 2001), Ptenfl/fl (Groszer et al., 2001), Scf-GFP (Ding et al., 2012), Cxcl12-DsRed (Ding and Morrison, 2013), Ubc-creER (Ruzankina et al., 2007), Rosa26-CAG-loxp-stop-loxp-tdTom”
SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, methodology): “We backcrossed tamoxifen-inducible cre-ERT2 mice (Ruzankina et al., 2007) to C57BL/ 6J and combined this with floxed SIRT1 mice (Cheng et al.”