Erratum to: Thrombospondin 1 is a key mediator of transforming growth factor b-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism
© Chen et al.; licensee BioMed Central. 2015
Received: 20 November 2014
Accepted: 18 December 2014
Published: 14 March 2015
The original article was published in Fibrogenesis & Tissue Repair 2011 4:9
Figure Two panel A (Figure 1 here) - Experiment assessing the influence of blocking thrombospopndin- 1 on normal and scleroderma fibroblasts in 3-dimensional collagen gels was performed and western blot for loading control GAPDH as well as total ERK and phospho-ERK were completed.
Figure Five panel B (Figure 2 here) - Role of PDGF, IFNb and TFGb and the influence of the kinase inhibitor Gleevac on MAPK activation by normal fibroblasts was carried out and the levels of total ERK and phospho-ERK assessed.
Figure Six panel B (Figure 3 here) - The effect of the ERK inhibitor (U0126) and IFNb on the expression of thrombospondin-1 compared to the loading control (GAPDH) was re-examined in normal and scleroderma fibroblasts.
- Yunliang C, Andrew L, Abraham DJ, Laura K, Xu S-w, Denton CP, et al. Thrombospondin 1 is a key mediator of transforming growth factor b-mediated cell contractility in systemic sclerosis via a mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)-dependent mechanism. Fibrogenesis and Tissue Repair. 2011;4:9.View ArticleGoogle Scholar
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.