Cell Microbiol 11:1179C1189. determine the percentage of cells with places indicating the colocalization of EGFR with GPB2, EEA1, or DSG3. Email address details are the mean SD from three 3rd party experiments. Orgs, microorganisms. Download FIG?S1, PDF TNFSF10 document, 0.3 MB. Copyright ? 2021 Phan et al. This article is distributed beneath the conditions of the Innovative Commons Attribution 4.0 International license. FIG?S2. Surface-expressed gC1qR offers minimal effects on the number of cells that are associated with oral epithelial cells. Sulfasalazine (A) Effects of two different anti-gC1qR monoclonal antibodies on the number of cell-associated cells. (B) Effects of the anti-gC1qR antibody 74.5.2 and the EGFR kinase inhibitor gefitinib on the quantity of cell-associated cells. (C and D) Quantity of cells that are cell associated with NIH/3T3 cells expressing human being gC1qR and/or human being EGFR. (C) Effects of EGFR and gC1qR manifestation on cell association. (D) Effects of inhibiting surface-expressed gC1qR with the anti-gC1qR antibody 74.5.2. Results are the mean SD from three self-employed experiments, each performed in triplicate. The data were analyzed using one-way analysis of variance with Dunnetts test for multiple comparisons. ns, not significant; Orgs/HPF, organisms per high-power field; *, 0.05. Download FIG?S2, PDF file, 0.3 MB. Copyright ? 2021 Phan et al. This content is distributed under the terms of the Creative Commons Attribution 4.0 International license. FIG?S3. Inhibition of gC1qR does not block EGFR phosphorylation in response to 40 M candidalysin (A) or 1 ng/ml epidermal growth element (EGF) (B). Representative Western blots from three self-employed experiments. Download FIG?S3, PDF file, 0.02 MB. Copyright ? 2021 Phan et al. This content is distributed under the terms of the Creative Commons Attribution 4.0 International license. FIG?S4. Effects of anti-gC1qR antibodies and gC1qR siRNA within the relationships of with human being oral epithelial cells and main mouse oral epithelial cells. (A and B) Effects of the indicated anti-gC1qR antibodies on adherence to main mouse (A) and main human being (B) oral epithelial cells. (C-E) Effects of siRNA knockdown of gC1qR within the phosphorylation of EGFR in main mouse oral epithelial cells. (C) Representative Western blot. (D) Densitometric analysis of four Western blots, such as Sulfasalazine the one demonstrated in panel C. Results in panels A and B are the mean SD from three self-employed experiments, each performed in triplicate. The data were analyzed using one-way analysis of variance with Dunnetts test for multiple comparisons. 0.05; **, 0.01. Download FIG?S4, PDF file, 0.3 MB. Copyright ? 2021 Phan et al. This Sulfasalazine content is distributed under the terms of the Creative Commons Attribution 4.0 International license. FIG?S5. Effects of siRNA knockdown of IFITM3 within the response of human being and mouse oral epithelial cells to to main human being Sulfasalazine oral epithelial cells (C), endocytosis Sulfasalazine by main mouse oral epithelial cells (D), and adherence to main mouse oral epithelial cells (E). Results in panels C to E are the mean SD from three self-employed experiments, each performed in triplicate. The data were analyzed using one-way analysis of variance with Dunnetts test for multiple comparisons. 0.05; **, 0.01. Download FIG?S5, PDF file, 0.3 MB. Copyright ? 2021 Phan et al. This content is distributed under the terms of the Creative Commons Attribution 4.0 International license. ABSTRACT During oropharyngeal candidiasis, activates the epidermal growth element receptor (EGFR), which induces oral epithelial cells to endocytose the fungus and synthesize proinflammatory mediators. To elucidate EGFR signaling pathways that are stimulated by Als3 invasin, gC1qR was required for the fungus to induce autophosphorylation.