Figure 1.
p66Shc deficiency enhances the ability of leukemic Eμ-TCL1 cells to promote the contact-independent expression of homing chemokines in stromal cells. qRT-PCR analysis of CXCL9 (A), CXCL10 (B), CXCL11 (C), CCL2 (D), CXCL13 (E), and CCL19 (F) mRNA in OP9 murine stromal cells kept in culture medium (OP9; n ≥ 6), cocultured with B cells purified from spleens of WT mice (OP9+WT; n = 3) or p66Shc−/− (OP9+p66−/−, n = 3) mice, cocultured with leukemic B cells purified from spleens of Eμ-TCL1 mice (OP9+TCL1; n ≥ 5) or Eμ-TCL1/p66Shc−/− mice (OP9+TCL1/p66−/−; n ≥ 6) with overt disease (cells), or with the respective conditioned media (SN). The relative gene transcript abundance was determined on triplicate samples using the dCt method and normalized to GAPDH. Data are mean ± standard deviation. ***P ≤ .001, **P ≤ .01, *P ≤ .05, 1-way analysis of variance, multiple comparison.

p66Shc deficiency enhances the ability of leukemic Eμ-TCL1 cells to promote the contact-independent expression of homing chemokines in stromal cells. qRT-PCR analysis of CXCL9 (A), CXCL10 (B), CXCL11 (C), CCL2 (D), CXCL13 (E), and CCL19 (F) mRNA in OP9 murine stromal cells kept in culture medium (OP9; n ≥ 6), cocultured with B cells purified from spleens of WT mice (OP9+WT; n = 3) or p66Shc−/− (OP9+p66−/−, n = 3) mice, cocultured with leukemic B cells purified from spleens of Eμ-TCL1 mice (OP9+TCL1; n ≥ 5) or Eμ-TCL1/p66Shc−/− mice (OP9+TCL1/p66−/−; n ≥ 6) with overt disease (cells), or with the respective conditioned media (SN). The relative gene transcript abundance was determined on triplicate samples using the dCt method and normalized to GAPDH. Data are mean ± standard deviation. ***P ≤ .001, **P ≤ .01, *P ≤ .05, 1-way analysis of variance, multiple comparison.

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