T cell-specific deletion of the inositol phosphatase SHIP reveals its role in regulating Th1/Th2 and cytotoxic responses -- Tarasenko et al. 104 (27): 11382 Data Supplement - HTML Page - index.htslp -- Proceedings of the National Academy of Sciences

Tarasenko et al. 10.1073/pnas.0704853104.

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SI Figure 7
SI Table 1
SI Figure 8
SI Figure 9

SI Figure 7

Fig. 7. Greatly reduced SHIP mRNA expresion in DP and SP thymocytes from CD4creSHIP^fl/fl mice. DP and SP cell populations were sorted by flow cytometry. and SHIP mRNA was quantified by real-time PCR. Values are relative to L32 RNA in the same cells.

SI Figure 8

Fig. 8. SHIP deletion in T cells does not affect Akt or Gsk3b activation on CD28 stimulation. Lymph nodes and splenic CD4⁺ T cells were stimulated with plate-bound anti-CD28 (10 mg/ml) for the indicated time periods. Phosphorylation of Akt and Gsk3b were detected by immunoblotting cell lysates with phospho-Akt and phospho-Gsk3b antibodies. Immunoblots were stripped off and reprobed with ERK1/2 and Gsk3b, respectively, for protein quantification.

SI Figure 9

Fig. 9. T-bet mRNA stability in CD4cre SHIPfl/fl (filled squares) and SHIPfl/fl (empty triangles) T cells. After 3 days culture in Th1-skewing conditions, actinomycin D was added and T-bet mRNA levels assessed at the indicated times. (A) Relative amount of T-bet mRNA relative to L32 rRNA. (B) Percent decreases from the nontreated samples. Experiment was repeated twice with similar results.