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

. 2007 Nov 22;9(6):R122. doi: 10.1186/ar2330

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

Copyright © 2007 Cailotto et al.; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Contribution of protein kinase C (PKC) pathway to transforming growth factor-beta-1 (TGF-β1)-induced expression of the Ank gene. (a) Effect of PKC inhibitors on Ank expression. Total RNA was extracted from rat chondrocytes stimulated with 10 ng/mL of TGF-β1 in the presence of 10 μM of calphostin C (general PKC inhibitor) or 5 μM of rottlerin (PKCδ inhibitor) or 5 μM of Gö6976 (PKC α/β1 inhibitor) added 1 hour before TGF-β1. (b) Dose-response study of PKC-dependent induction of Ank by TGF-β1. Total RNA was extracted from rat chondrocytes stimulated with 10 ng/mL of TGF-β1 in the presence of 0, 1, 2.5, 5, or 10 μM of Gö6976 added 1 hour before TGF-β1. The mRNA level of Ank obtained from real-time polymerase chain reaction analysis was normalized to that of S29 mRNA and is expressed as mean percentages (± standard deviation) over control values from three independent experiments. Statistically significant differences from the control are indicated as *p < 0.05 and from TGF-β1-treated cells as #p < 0.05.