Based on the graph, it can be seen that clone 68 had a much lower level of HbF expression compared to clones 65 and 73, which were treated with the same combination of sgRNAs. This suggests that the deletion of BCL11A in clone 68 may not have been as effective in inducing fetal hemoglobin expression as in the other clones.
It is important to further investigate the reasons for this difference in HbF expression levels among the clones in order to optimize the targeted deletion strategy for lowering hemoglobin gamma expression. This could involve exploring variations in the editing efficiency of sgRNAs, the impact of off-target effects, or potential differences in genetic background that may influence the response to BCL11A deletion.
they are tyring to lower hemoglobin y expression but in this graph when clone og ga+gc was much hihger except for number 68 compared with untreated.
Fig. 3. Consequences of targeted deletion on the protein level. Knockdown
of BCL11A expression leads to fetal hemoglobin induction. Western blot analysis was performed to determine HbF expression levels in BCL11A-edited K562
clones #65, #68, and #73 treated by the combination of sgRNAs A and C (A).
Quantification of western blots derived from 3 independent experiments using
ImageJ software (B). Data represent the mean ± S.D. of densitometric analysis
of immunoblots. g; guide RNA.
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