Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Nov 6;10(11):73. doi: 10.1038/s41389-021-00363-6

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 4 — A Western blot to confirm ATRX ablation in Cas9 control (Ctrl) and ATRX KO (C-1, C-2, and C-3) SK-N-AS cells. Growth curves show that cell viability was unchanged between Ctrl and ATRX KO SK-N-AS cells. Data are expressed as means ± standard deviation (SD), N = 3. B Colony formation assays were performed to assess the proliferative abilities of Ctrl and ATRX KO SK-N-AS cells. Lower panel, representative images for clonogenic formation. Error bars represent SD from three technical replicates. *p < 0.05; A one-way ANOVA with Dunnett’s and Tukey’s test were used for statistical analyses. C Immunoblot and IF analyses of γH2AX in ATRX-intact (Ctrl) and ATRX KO SK-N-AS cells with a positive control (parental SK-N-AS cells treated with doxorubicin, 0.5 μg/mL for 24 h). D Immunoblots for the expression of p53-ATM checkpoint proteins in cell lysates prepared from Ctrl and ATRX KO SK-N-AS cells. Doxorubicin (0.5 μg/mL)-treated two NB cell lines (SK-N-SH and NGP) were used as a positive control. E IF staining of G4 (1H6) revealed that ATRX deficiency did not cause G4 formation in ATRX KO SK-N-AS cells. The DNA G-quadruplex stabilizer CX-5461 (50 nM, 24 h) was used as a positive control to stain G4 (1H6). F Whole-cell extracts from Ctrl and ATRX KO SK-N-AS cells were analyzed by western blotting with the p-KAP1 (Ser-824), KAP1, p-Chk1 (Ser-345), Chk1, p-RPA32 (Ser-33), and RPA32 antibodies. β-Tubulin was used as a loading control. Doxorubicin (0.5 μg/mL, 24 h)-treated NGP cells were used as a positive control.