Figure 4
Figure 4. PF-04691502 inhibits anti-IgM–induced signaling. CLL cells were treated with (A) soluble anti-IgM beads (n = 9) and (B) immobilized (Imm) anti-IgM beads (n = 5) prior to evaluation of downstream signaling in the presence and absence of PF-04691502 (0.0025-2.5 μM) by immunoblot analysis. Representative cases are shown. CLL cells were treated for 1 hour with PF-04691502 prior to soluble/immobilized anti-IgM addition. pAKTT308 and pS6KT389 were used as markers of PI3K signaling, pAKTS473 and pS6S235/236 were used as markers of mTOR signaling, and pERKT202/Y204 was used as a marker of mitogen-activated protein kinase signaling. HSC70 was used as a loading control.

PF-04691502 inhibits anti-IgM–induced signaling. CLL cells were treated with (A) soluble anti-IgM beads (n = 9) and (B) immobilized (Imm) anti-IgM beads (n = 5) prior to evaluation of downstream signaling in the presence and absence of PF-04691502 (0.0025-2.5 μM) by immunoblot analysis. Representative cases are shown. CLL cells were treated for 1 hour with PF-04691502 prior to soluble/immobilized anti-IgM addition. pAKTT308 and pS6KT389 were used as markers of PI3K signaling, pAKTS473 and pS6S235/236 were used as markers of mTOR signaling, and pERKT202/Y204 was used as a marker of mitogen-activated protein kinase signaling. HSC70 was used as a loading control.

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