Science Advances

Supplementary Materials

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  • Fig. S1. Deletion of FcRL1 gene in CH27 cells and mouse with CRISPR-Cas9.
  • Fig. S2. Flow cytometry analysis of the expression level of BCR and FcRL1 on plasma membrane and intracellular c-Abl fusion protein.
  • Fig. S3. Off-target detection of the sgRNA used for knocking out FcRL1 in CH27 cells.
  • Fig. S4. Off-target detection of the upstream sgRNA used for knocking out FcRL1 in mouse.
  • Fig. S5. Off-target detection of the downstream sgRNA used for knocking out FcRL1 in mouse.
  • Fig. S6. FcRL1 deficiency in primary B cell intrinsically impaired the antigen binding–induced B cell activation in the absence of FcRL1 ligation.
  • Fig. S7. FcRL1 is passively recruited into the B cell immunological synapse upon BCR engagement in CH27-FcRL1-KO B cells expressing HA-FcRL1-YFP.
  • Fig. S8. Sequence alignment of the cytoplasmic tail of FcRL1.
  • Fig. S9. Disruption of FcRL1 gene had no effect on B cell development in FcRL1-KO mice.

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