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

. 2013 Jun 7;17(7):901–913. doi: 10.1111/jcmm.12079

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

Copyright © 2013 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.

Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

PMC Copyright notice

Fig. 2 — Identification of cellular JNK-regulated proteins in H₂O₂-exposed HCEC. (A) Immunoblot analysis following JNK inhibition by the JNK inhibitor SP600125 revealed p21^WAF¹, γ-H2AX, as well as caspases 3, 8 and 9 as cellular JNK-regulated proteins. The effective inhibition of JNK was ensured through missing phosphorylation of the transcription factor c-jun at serine residues 63 and 73. (B) Immunoblot analysis showed an overexpression of the death receptor TRAIL-R1/DR4 after H₂O₂. (C) Immunoblot analysis of subcellular fractionated cellular proteins of H₂O₂-treated HCEC. Each extract was analysed using specific antibodies against proteins from various cellular compartments, including cytoplasmic (GAPDH, HSP90), plasma membrane (TRAIL-R1/DR4), nuclear soluble (Sp1) and chromatin-bound (histone 3). (D) Analysis of the membrane extracts of HCEC and H₂O₂-exposed HCEC by immunoblotting showed accumulation of the TRAIL-R1/DR4 in H₂O₂-exposed cells.