Fig. 2.
Fig. 2. Specific 35S-Ad2 binding to HeLa cells; to OCI-My5, RPMI 8226, ARH-77, HS Sultan, and IM-9 MM cells; to patient MM1 cells; to normal B splenocytes; to CESS and JY EBV-transformed B cells; and to normal BM MNCs. HeLa cells; OCI-My5, RPMI 8226, ARH-77, HS Sultan, and IM-9 MM cells; patient MM1 cells; normal B splenocytes; CESS and JY EBV-transformed B cells; and normal BM MNCs (1 × 106) were incubated with either RmcB anti-CAR MoAb (1:100) or 5E2B4 mouse MoAb (IgG2; 1:100; isotype control), followed by incubation with 35S-labeled Ad2, and then washed, solubilized, and analyzed on a β-counter. The percentage of specific Ad2 binding (difference in Ad2 binding by 5E2B4-treated versus RmcB-treated cells) relative to control HeLa cells (100% specific Ad2 binding) was determined. RD PCR3 and RD CAR transfectants served as negative and positive controls, respectively.

Specific 35S-Ad2 binding to HeLa cells; to OCI-My5, RPMI 8226, ARH-77, HS Sultan, and IM-9 MM cells; to patient MM1 cells; to normal B splenocytes; to CESS and JY EBV-transformed B cells; and to normal BM MNCs. HeLa cells; OCI-My5, RPMI 8226, ARH-77, HS Sultan, and IM-9 MM cells; patient MM1 cells; normal B splenocytes; CESS and JY EBV-transformed B cells; and normal BM MNCs (1 × 106) were incubated with either RmcB anti-CAR MoAb (1:100) or 5E2B4 mouse MoAb (IgG2; 1:100; isotype control), followed by incubation with 35S-labeled Ad2, and then washed, solubilized, and analyzed on a β-counter. The percentage of specific Ad2 binding (difference in Ad2 binding by 5E2B4-treated versus RmcB-treated cells) relative to control HeLa cells (100% specific Ad2 binding) was determined. RD PCR3 and RD CAR transfectants served as negative and positive controls, respectively.

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