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©The Author(s) 2025.
World J Diabetes. Jun 15, 2025; 16(6): 104973
Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.104973
Published online Jun 15, 2025. doi: 10.4239/wjd.v16.i6.104973
Figure 4 Rheb1 regulates β cell proliferation via mTORC1 and AMPK signaling simultaneously.
A: The expression of AMPK signaling and its downstream in the MIN6 cell treated with GFP or Rheb1OE adenovirus for 48 hours with or without rapamycin treatment; B: The population of 5-ethy-nyl-2’-deoxyuridine + cells of MIN6 cell treated with GFP or Rheb1OE adenovirus for 48 hours with or without rapamycin and AICAR treatment; C: The population of Ki67+ cells of insulin+ islet treated with GFP or Rheb1OE adenovirus with or without rapamycin and AICAR treatment; D: Western blot analysis of MIN6 cell treated with GFP or Rheb1OE adenovirus for 48 hours with or without rapamycin and AICAR treatment; E: Cell vitality analysis of MIN6 cell treated with GFP or Rheb1OE adenovirus for 48 hours with or without rapamycin and AICAR treatment. All data are represented as the mean ± SD, aP < 0.05, bP < 0.01, cP < 0.001.
- Citation: Yang Y, Song WJ, Zhang JJ. Ras homolog enriched in brain 1 regulates β cell mass and β cell function via mTORC1/AMPK/Notch1 pathways. World J Diabetes 2025; 16(6): 104973
- URL: https://www.wjgnet.com/1948-9358/full/v16/i6/104973.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i6.104973