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. 2021 Jul 25;11(17):8535–8549. doi: 10.7150/thno.61452

Figure 4.

Figure 4

Gab1 is a key adaptor protein of NLGN3 signaling. The primary human glioma cells (“P1”) (A) or U251MG cells (B), with Gab1 shRNA or the scramble control shRNA (“scr-shRNA”), were treated with or without NLGN3 (50 ng/mL) for applied time periods, listed proteins in total cell lysates were tested by Western blotting. Wild-type (WT) and Gab1 knockout (Gab1-KO) MEFs were treated with NLGN3 (50 ng/mL) for applied time, tested by Western blotting of listed proteins in total cell lysates (C). U251MG cells were treated with NLGN3 (50 ng/mL) for 5 min, association of Gαi1/3-Gab1-SHP2-p85 was tested by co-IP assays (D). WT, Gαi1/3 DKO (E), Gαi1 or Gαi3 SKO (F), as well as WT MEFs with Gαi1 plus Gαi3 CRISPR/Cas9 DKO constructs (F) or Gαi1 shRNA plus Gαi3 shRNA (“Gαi1/3 DshRNA”) (G) were treated with NLGN3 (50 ng/mL) for applied time, total- and p-Gab1 were tested. Gαi1/3 DKO MEFs were transfected with the adenovirus Gαi1 construct (“Ad-Gαi1”), the adenovirus Gαi3 construct (“Ad-Gαi3”) or the empty vector (“Ad-Vec”), treated with NLGN3 (50 ng/mL) for applied time periods, total- and p-Gab1 were tested (H). Quantifications were from five replicate blot data. #P < 0.05.