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. 2009 Oct 27;4(10):e7572. doi: 10.1371/journal.pone.0007572

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Wang et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Mice with different genotypes were induced to disrupt RBP-J, and BM and the peripheral blood (PB) cells were analyzed by FACS. (A, B) The expression of CXCR4 on CD133⁺Flk-1⁺ EPCs in BM (A) and PB (B) of the RBP-J deficient and the control mice was analyzed by FACS. (C, D) FACS analyses shown in (A) and (B) were repeated, and MFI of the CXCR4 expression was analyzed statistically (bars = mean±SD; n = 5; * P<0.05). (E, F) The number of CD133⁺Flk-1⁺ EPCs in BM (E) and PB (F) of the RBP-J deficient and the control mice was determined by cell counting and FACS analysis (bars = mean±SD; n = 5; *P<0.05; ** P<0.01).