Figure 4
Figure 4. On BCR ligation, NFAT2 is differentially activated in B cells from both groups of patients. (A) Nuclear or cytoplasmic extracts from freshly isolated B cells from R (n = 9) and NR (n = 6) cases and from unstimulated or CD3+/CD28+-stimulated Jurkat cell line (horizontal dashed lines) were analyzed for their NFAT2 DNA-binding ability using an ELISA-derived assay. Competition with a specific oligonucleotide was used to ensure binding specificity (P, probe; n = 3). No statistical difference (ns) was observed between NR and R patient extracts. (B) Nuclear extracts from NR (n = 13) and R (n = 12) cells stimulated or not with an anti-IgM antibody (10 μg/mL/106 cells) for 18 hours were used following the same protocol as described in panel A. Results are presented as fold induction of the NFAT2 DNA-binding ability on stimulation.

On BCR ligation, NFAT2 is differentially activated in B cells from both groups of patients. (A) Nuclear or cytoplasmic extracts from freshly isolated B cells from R (n = 9) and NR (n = 6) cases and from unstimulated or CD3+/CD28+-stimulated Jurkat cell line (horizontal dashed lines) were analyzed for their NFAT2 DNA-binding ability using an ELISA-derived assay. Competition with a specific oligonucleotide was used to ensure binding specificity (P, probe; n = 3). No statistical difference (ns) was observed between NR and R patient extracts. (B) Nuclear extracts from NR (n = 13) and R (n = 12) cells stimulated or not with an anti-IgM antibody (10 μg/mL/106 cells) for 18 hours were used following the same protocol as described in panel A. Results are presented as fold induction of the NFAT2 DNA-binding ability on stimulation.

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