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Blood, Vol. 110, Issue 1, 305-312, July 1, 2007 This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef Ubp43 regulates BCR-ABL leukemogenesis via the type 1 interferon receptor signaling Blood Yan et al. 110: 305 Supplemental materials for: Yan et al, Vol 110, Issue 1, 305-312 Files in this Data Supplement: Figure S1. Ubp43-deficient bone marrow cells are suitable for bone marrow cell retroviral infection and transplantation (PDF, 11.4 KB) - The mean and the standard deviation of the percentage of WBCs expressing retrovirally transduced EGFP+ after bone marrow transplantation (BMT) are shown. Figure S2. The expression and phosphorylation of BCR-ABL are not affected by the presence of Ubp43 or IFN-β (PDF, 48.6 KB) - Protein extracts were prepared from parental Ubp43+/+, Ubp43–/–, and Ubp43-reconstituted Ubp43–/– (Ubp43reconst) MEFs and BCR-ABL–expressing MEFs. (A) Ten µg protein from each sample was used to Western blot sequentially with -ABL and -tubulin antibodies. (B) The same protein samples were used to Western blot with the antibody against phosphorylated tyrosine. BCR-ABL–transduced lines showed a high-molecular-weight band (indicated by the arrow, > 175 kDa) corresponding to phosphorylated BCR-ABL, which is reduced upon STI571 treatment (data not shown). A constitutively phosphorylated protein (indicated by *) served as a loading control. This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef

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