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. 2009 Jan 26;184(2):281–296. doi: 10.1083/jcb.200806121

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© 2009 Mao et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 1. — Characterization of PIP5K-γ in BMM. (A) Western blot of endogenous proteins in WT BMM. (B) Quantitative RT-PCR. The PIP5K level in WT BMM was normalized against cyclophilin (n = 3). (C) Recruitment of PIP5K-γ to the phagocytic cup. WT BMM exposed to IgG-opsonized particles were stained with anti–PIP5K-γpan antibody. The middle and right panels show enlarged views of regions marked by asterisks. Bars, 10 µm. (D) Western blot of PIP5K-γ−/− BMM. (E) FACs analysis of surface accessible FcγR. Black peaks, surface FcγR fluorescence; white peak, background. (F) CSF-1–induced ERK activation. CSF-1–stimulated BMM were extracted for Western blotting with anti-ERK and -pERK. (G) Phosphoinositide analyses. The PIP₂ or PIP value in PIP5K-γ−/− BMM was expressed as the percentage of WT cells. Left, TLC (n = 3). Right, HPLC (n = 4). Error bars indicate SEM. n.s., not significant.