Fig. 2.
Fig. 2. (A) The EPOR fails to support proliferation signaling in HT-2 cells. HT-2 ⊡), HT-2.EPOR.3 (⧫), and HT-2EPOβγ () cells were incubated with no cytokine, various doses of EPO, or 10 nmol/L IL-2 and incorporation of [3H]thymidine was measured at 48 hours. Data are presented as percent of [3H]thymidine incorporation relative to IL-2. (B) The EPOR supports proliferation signaling in 32D cells. 32D (⊡) and 32D.EPOR (⧫) cells were incubated with no cytokine, various doses of EPO, or 10%WEHI-CM (IL-3). Data are presented as percent of [3H]thymidine incorporation relative to IL-3. (C) The EPOR can pair with EPOβ to support EPO-dependent proliferation signaling in HT-2 cells. HT-2.EPOR.3 cells were transfected with 20 μg of pCMV4 vector with no insert (control, ⧫) or pCMV4.EPOβ (EPOβ, ⊡) and [3H]thymidine incorporation measured on days 6-16, as indicated.

(A) The EPOR fails to support proliferation signaling in HT-2 cells. HT-2 ⊡), HT-2.EPOR.3 (⧫), and HT-2EPOβγ () cells were incubated with no cytokine, various doses of EPO, or 10 nmol/L IL-2 and incorporation of [3H]thymidine was measured at 48 hours. Data are presented as percent of [3H]thymidine incorporation relative to IL-2. (B) The EPOR supports proliferation signaling in 32D cells. 32D (⊡) and 32D.EPOR (⧫) cells were incubated with no cytokine, various doses of EPO, or 10%WEHI-CM (IL-3). Data are presented as percent of [3H]thymidine incorporation relative to IL-3. (C) The EPOR can pair with EPOβ to support EPO-dependent proliferation signaling in HT-2 cells. HT-2.EPOR.3 cells were transfected with 20 μg of pCMV4 vector with no insert (control, ⧫) or pCMV4.EPOβ (EPOβ, ⊡) and [3H]thymidine incorporation measured on days 6-16, as indicated.

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