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. 2021 Sep 30;130(8):498–508. doi: 10.1055/a-1608-0607

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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Fig. 7 — Intracellular ATP contributed to FAM3A-induced proliferation of pancreatic β cells. ( a ) The cell cycle analysis was performed after Ad-FAM3A infection in HIT-T15 cells. The left panel shows a representative image and the right panel shows a statistical graph. ( b ) MTT assay to analyze the effect of FAM3A overexpression on cell viability in HIT-T15 cells. In a MIN6 cell line, analysis of cell cycle showed the effect of suramin on FAM3A-induced cell proliferation. ( c ) Representative images of the cell cycle, ( d ) statistical graphs of panel ( c ). ( e ) Cells exposed to suramin and nifedipine for 24 h weakened the effect of FAM3A on cell viability. Immunohistochemical staining of PCNA in ( f ) acute FAM3A knockdown mice and ( g ) β cell-specific FAM3A gene knockout (BKO) mice. N=4–5, *P<0.05 vs. Ad-GFP, #P<0.05 vs. Ad-FAM3A.