Human bronchial epithelial
BEAS-2B cells were purchased from the China Center for Type Culture Collection (CCTCC, Wuhan, China) and cultured in Dulbecco’s Modified Eagle Medium (DMEM, Invitrogen, San Diego, CA, USA) supplemented with 10% fetal bovine serum (FBS, Gibco, NY, USA). ATF3 KO
BEAS-2B cells were custom developed by using a CRISPR/Cas9 gene-editing method by Cyagen Biosciences (Suzhou, China). Sodium meta-arsenite (NaAsO
2) was purchased from Sigma (St Louis, MO, USA). The inhibitors,
SB203580,
SP600125,
U0126 and
LY294002, were purchased from Santa Cruz Biotechnology (Dallas, TX, USA). Antibodies against ATF3 (33593), DR5 (3696), JNK (9252),
p-JNK (4668), p38 (8690), p-p38 (9215), Bcl-xL (2764), caspase 8 (9746), cleaved caspase 8 (8592), caspase 3 (14220), cleaved caspase 3 (9664), caspase 9 (9502), cleaved caspase 9 (9509), α-tubulin (2125), AKT (C67E7), p-AKT (4060T), ERK (4695), p-ERK (91015) and
β-actin (4970) were purchased from Cell Signaling Technologies (Danvers, MA, USA).
Shi Q., Hu B., Yang C., Zhao L., Wu J, & Qi N. (2021). ATF3 Promotes Arsenic-Induced Apoptosis and Oppositely Regulates DR5 and Bcl-xL Expression in Human Bronchial Epithelial Cells. International Journal of Molecular Sciences, 22(8), 4223.