Skip to main content
. 2021 May 18;296:100789. doi: 10.1016/j.jbc.2021.100789

Figure 1.

Figure 1

Inactivation of SLC35A1 compromises sialylation and assembly of the laminin-binding glycan of α-dystroglycan.A, schematic representation of tools used to assess sialylation and the assembly of the laminin-binding glycan. B–G, flow cytometry with MAL II lectin, peanut agglutinin (PNA), and the antibody IIH6 was performed on wildtype or SLC35A1 KO HAP1 cells that were transduced with a lentivirus driving expression of murine Slc35a1 complementary DNA or an empty vector control. Two independent clones (#1 and #2) were analyzed. Bar graphs underneath flow cytometry histograms represent means ± SEM of the mean fluorescence intensity (MFI) observed in three independent experiments. Note that the presented experiment was performed in parallel to the experiment presented for Figure 3, explaining why the empty vector controls are identical. H, samples from the indicated HAP1 cell lines were subjected to laminin overlay or β-dystroglycan Western blot. MAL II, Maackia amurensis lectin II.