These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Immunohistochemical studies on disabled-2 protein in the spinal cords of rats with experimental autoimmune encephalomyelitis. Author: Ahn M, Oh H, Lee W, Kim H, Moon C, Shin T. Journal: Brain Res; 2011 Oct 06; 1416():51-60. PubMed ID: 21890121. Abstract: Disabled-2 (Dab-2), an adaptor protein of transforming growth factor beta (TGF-β) signaling, was studied in the spinal cords of rats with experimental autoimmune encephalomyelitis (EAE) to evaluate the possible involvement of Dab-2 in the pathogenesis of EAE using Western blot and immunohistochemical analyses. Western blot analysis showed that two isoforms (p96 kDa and p67 kDa) of Dab-2 were detected in the spinal cords of rats used as controls. Both isoforms of Dab-2 were significantly elevated in the EAE spinal cord at the peak stage of EAE (P<0.05) and declined at the recovery stage. However, only the p96 kDa isoform was markedly phosphorylated in the EAE spinal cord. Immunohistochemistry showed that Dab-2 and p-Dab-2 were detected in some vascular endothelial cells, glial cells, and some neurons in the rat spinal cords of normal and immunized CFA-alone controls. In EAE lesions, Dab-2 and p-Dab-2 were immunodetected in some inflammatory cells (mainly in ED1-positive macrophages and R73-positive T cells), while the enhanced immunoreactivity of Dab-2 in spinal cord cells suggested constitutive expression. Additionally, TGF-β1 immunoreactivity showed a similar expression pattern of Dab-2 in EAE lesions. These findings suggest that Dab-2 is transiently upregulated and phosphorylated (particularly the p96 kDa isoform) in EAE, a CNS autoimmune disease, and may be involved in TGF-β signaling.[Abstract] [Full Text] [Related] [New Search]