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Histone H2AX is integral to hypoxia-driven neovascularization - pp553 - 5583 W6 {( f7 N" l1 C$ q0 ^/ w
Matina Economopoulou, Harald F Langer, Arkady Celeste, Valeria V Orlova, Eun Young Choi, Mingchao Ma, Athanassios Vassilopoulos, Elsa Callen, Chuxia Deng, Craig H Bassing, Manfred Boehm, Andre Nussenzweig & Triantafyllos Chavakis
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doi:10.1038/nm.1947( G$ Q& u. `2 f8 o( S/ W0 G
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Hypoxia-triggered neovascularization occurs in many types of disease. Endothelial cells must be able to cope with hypoxic stress, which in other cell types can induce a DNA repair response and inhibit replication. Matina Economopoulou et al. now show that hypoxia induces the generation of a hallmark of the DNA repair response, phosphorylated histone H2AX, in proliferating endothelial cells and that H2AX function is required for neovascularization under hypoxic or ischemic conditions in vivo
9 X$ b1 t Q# i5 C! shttp://www.nature.com/nm/journal/v15/n5/full/nm.1947.html |
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