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in ES Cells\nAtrxnull ES cells could not be recovered by direct targeting and were eventually generated by adopting a conditional targeting approach. This is consistent with our observation that Atrx is highly expressed in ES cells, and that the absence of full-length Atrx imparts a growth disadvantage relative to cells bearing a functional Atrx allele. At present, the cause of the proliferative delay in Atrxnull ES cells is not known. Interestingly, we demonstrated that apoptosis is not significantly up-regulated in ES cells lacking Atrx and is only mildly elevated in Atrxnull 7.5 dpc mouse embryos. In contrast, it was recently shown that the loss of Atrx markedly increased the apoptotic population in the differentiating cells of the embryonic cortex and postnatal hippocampus, when Atrx expression was ablated in the developing mouse forebrain using the Atrx flox allele described here [20]. The human ATRX protein has been shown to associate in a complex with Daxx [8], a protein that has been implicated in multiple pathways for the regulation of apoptosis [21]. It is possible that disruption of the mouse Atrx-Daxx complex (by ablation of the Atrx protein) could have triggered a universal proapoptotic response. However, our observations in ES cells demonstrate that the induction of apoptosis is not an automatic response triggered by the removal of Atrx in all cell types, and suggest that the inappropriate apoptosis observed in the Atrx-mutant forebrain may reflect a requirement for Atrx during terminal differentiation."}

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in ES Cells\nAtrxnull ES cells could not be recovered by direct targeting and were eventually generated by adopting a conditional targeting approach. This is consistent with our observation that Atrx is highly expressed in ES cells, and that the absence of full-length Atrx imparts a growth disadvantage relative to cells bearing a functional Atrx allele. At present, the cause of the proliferative delay in Atrxnull ES cells is not known. Interestingly, we demonstrated that apoptosis is not significantly up-regulated in ES cells lacking Atrx and is only mildly elevated in Atrxnull 7.5 dpc mouse embryos. In contrast, it was recently shown that the loss of Atrx markedly increased the apoptotic population in the differentiating cells of the embryonic cortex and postnatal hippocampus, when Atrx expression was ablated in the developing mouse forebrain using the Atrx flox allele described here [20]. The human ATRX protein has been shown to associate in a complex with Daxx [8], a protein that has been implicated in multiple pathways for the regulation of apoptosis [21]. It is possible that disruption of the mouse Atrx-Daxx complex (by ablation of the Atrx protein) could have triggered a universal proapoptotic response. However, our observations in ES cells demonstrate that the induction of apoptosis is not an automatic response triggered by the removal of Atrx in all cell types, and suggest that the inappropriate apoptosis observed in the Atrx-mutant forebrain may reflect a requirement for Atrx during terminal differentiation."}

{"project":"2_test","denotations":[{"id":"16628246-15668733-85799759","span":{"begin":903,"end":905},"obj":"15668733"},{"id":"16628246-12953102-85799760","span":{"begin":983,"end":984},"obj":"12953102"},{"id":"16628246-15077145-85799761","span":{"begin":1076,"end":1078},"obj":"15077145"},{"id":"T69494","span":{"begin":903,"end":905},"obj":"15668733"},{"id":"T51832","span":{"begin":983,"end":984},"obj":"12953102"},{"id":"T83532","span":{"begin":1076,"end":1078},"obj":"15077145"}],"text":"Atrx in ES Cells\nAtrxnull ES cells could not be recovered by direct targeting and were eventually generated by adopting a conditional targeting approach. This is consistent with our observation that Atrx is highly expressed in ES cells, and that the absence of full-length Atrx imparts a growth disadvantage relative to cells bearing a functional Atrx allele. At present, the cause of the proliferative delay in Atrxnull ES cells is not known. Interestingly, we demonstrated that apoptosis is not significantly up-regulated in ES cells lacking Atrx and is only mildly elevated in Atrxnull 7.5 dpc mouse embryos. In contrast, it was recently shown that the loss of Atrx markedly increased the apoptotic population in the differentiating cells of the embryonic cortex and postnatal hippocampus, when Atrx expression was ablated in the developing mouse forebrain using the Atrx flox allele described here [20]. The human ATRX protein has been shown to associate in a complex with Daxx [8], a protein that has been implicated in multiple pathways for the regulation of apoptosis [21]. It is possible that disruption of the mouse Atrx-Daxx complex (by ablation of the Atrx protein) could have triggered a universal proapoptotic response. However, our observations in ES cells demonstrate that the induction of apoptosis is not an automatic response triggered by the removal of Atrx in all cell types, and suggest that the inappropriate apoptosis observed in the Atrx-mutant forebrain may reflect a requirement for Atrx during terminal differentiation."}

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