Fig. 5: siRNA-mediated suppression of CRTAM, FOXP4, GRIN2C, LILRA3, PIBF1, SCGB3A1, and TXNDC12 in SH-SY5Y human neuroblastoma cells reduces inflammation-induced pS199/pS202 (AT8) and/or pT231 (AT180) tau phosphorylation. | Communications Biology

Fig. 5: siRNA-mediated suppression of CRTAM, FOXP4, GRIN2C, LILRA3, PIBF1, SCGB3A1, and TXNDC12 in SH-SY5Y human neuroblastoma cells reduces inflammation-induced pS199/pS202 (AT8) and/or pT231 (AT180) tau phosphorylation.

From: Machine learning prediction and tau-based screening identifies potential Alzheimer’s disease genes relevant to immunity

Fig. 5

SH-SY5Y cells were transiently transfected with either targeted GOI or scrambled siRNAs. After 48 h, cells were treated with CM (at 50%) derived from BV2 microglial cells. After 24 h, the lysates from SH-SY5Y cells were prepared and Western blot was performed for AT8 and AT180 antibodies and actin as loading control. Note that the levels of AT8 and/or AT180 are significantly altered in SH-SY5Y cells upon knockdown of MPxgb(AD) predicted CRTAM, FOXP4, GRIN2C, LILRA3, PIBF1, SCGB3A1, and TXNDC12 genes. (Raw blots are shown in Supplementary Fig. 11). Data shown are mean ± s.e.m; unpaired t tests; *p < 0.05; **p < 0.01, ***p < 0.005, n = 3 biological replicates and n = 3 technical replicates).

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