| Literature DB >> 32718094 |
Roberta Gualdani1, Marie de Clippele1, Ikram Ratbi1, Philippe Gailly1, Nicolas Tajeddine1.
Abstract
The authors wish to make the following corrections to this paper [...].Entities:
Year: 2020 PMID: 32718094 PMCID: PMC7463690 DOI: 10.3390/cancers12082023
Source DB: PubMed Journal: Cancers (Basel) ISSN: 2072-6694 Impact factor: 6.639
Figure 2Effects of STIM1 and TRPC1 depletion on apoptosis-associated mitochondrial transmembrane potential (ΔΨm) dissipation and plasma membrane permeabilization. (A) Following transient transfection (for 72 h) with either siRNA downregulating STIM1 (siSTIM1) or TRPC1 (siTRPC1) or with a control siRNA (siCTRL), A549 cells were left untreated or treated for additional 24 h with 25 µM CDDP, and labeled for the cytofluorometric assessment of ΔΨm [with the ΔΨm-sensitive probe DiOC6(3)] and plasma membrane integrity (with propidium iodide, i.e., PI). (B) Quantification of data presented in A. White and grey columns represent the percentage of cells exhibiting ΔΨm loss alone [DiOC6(3)low] or in association with plasma membrane breakdown (PI+), respectively. Data are means of triplicate experiments ± S.D. and are representative of three independent experiments. Student’s t test was employed to assess statistical significance. *** p < 0.001. (C) Immunoblot analysis of STIM1 expression 96 h after transfection of A549 cells with siCTRL, siSTIM1 or siTRPC1. β-actin was used as loading control.