Correction to: Modulation of Rab7a-mediated growth factor receptor trafficking inhibits islet beta cell apoptosis and autophagy under conditions of metabolic stress (Scientific Reports, (2020), 10, 1, (15741), 10.1038/s41598-020-72939-y)

Nirun V. Hewawasam, Fadel Lhaf, Henry A. Taylor, Katrina Viloria, Amazon Austin, Aileen King, Peter Jones, Lucy Jones, Mark D. Turner, Natasha J. Hill*

*Corresponding author for this work

Research output: Contribution to journalComment/debate

Abstract

Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-020-72939-y, published online 25 September 2020 This Article contains an error in Figure 6b, where the image for active Caspase-3/7 in control siRNA cells treated with 0.1mM palmitic acid (PA) was a duplication of the image for Rab7 siRNA cells treated with 0.3mM PA. The correct Figure 6 and its accompanying legend appear below. (Figure presented.) Rab7a attenuation protects against metabolic stress-induced beta cell death. INS-1 cells were treated with control- or Rab7a-siRNA for 3 days, then treated with the indicated concentration of palmitic acid (PA). (a) Cells were imaged using an IncucyteZoom system to determine cell area. (b) Representative images using 5 µM of Caspase-3/7 apoptosis reagent (Essen bioscience), which shows caspase-3/7 activation. Scale bar = 300 µm. (c) Cell lysates were prepared and analysed by western blot to quantify the amount of active (17 kDa) and inactive (35 kDa) Caspase-3. Representative blots are shown. (d) Relative mean expression of active caspase-3 is shown from three independent experiments. (e, f) Western blot analysis was used to determine expression of the autophagy marker LC3-I/II, with representative blots shown in (e), and relative mean expression of LC3-II from three independent experiments shown in (f). Values standardised to untreated control siRNA sample. Error bars indicate SEM, and Students’ t-test was used for statistical analysis.

Original languageEnglish
Article number32621
JournalScientific Reports
Volume15
Issue number1
DOIs
Publication statusPublished - Dec 2025
Externally publishedYes

ASJC Scopus subject areas

  • Multidisciplinary

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