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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 1 Rheb1 upregulates β cell mass and mTORC1 signaling.
A: Rheb1 expression in the islets isolated from people with different age; B: Immunofluorescence staining of Rheb1 (red) and insulin (as a β-cell marker; green) in pancreatic sections of 8-week-old male pRheb1KO mice (n = 3) and wild-type (WT) mice (n = 3). Scale bars: 10 μm; C and D: Average β-cell mass and β-cell size in pancreatic sections of 2-month-old male pRheb1KO (n = 4) and WT mice (n = 5) subjected to insulin staining; E: Anti-apoptotic genes from RNA-seq of islets of bRheb1KO mice (n = 3) and WT mice (n = 3), of which is reanalyzed from our previous RNA-seq data[3]. All data are represented as the mean ± SD, aP < 0.05, bP < 0.01. WT: Wild-type.
- 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