quote:
News Update
Please click hereto view recent publication titled ‘Flow Cytometry-Defined CD49d Expression in Circulating T-Lymphocytes Is a Biomarker for Disease Progression in Duchenne Muscular Dystrophy’
ANP is planning to undertake a clinical trial of its drug ATL1102 that targets CD49d (VLA-4) in patients with Duchenne Muscular Dystrophy and will be using flow cytometry measurements as described in the publication to assess the activity of ATL1102 in the proposed study.
Contact Information:
Website: www.antisense.com.au
Antisense Therapeutics office: +61 (0)3 9827 8999
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Abstract they are referring to:
Quote
Flow Cytometry-Defined CD49d Expression in Circulating T-Lymphocytes Is a Biomarker for Disease Progression in Duchenne Muscular Dystrophy.
Savino W1,2,3, Pinto-Mariz F4, Mouly V5,6,7.
Author information
Abstract
Duchenne muscular dystrophy (DMD) affects 1:3500-1:5000 male births, and is caused by X-linked mutations in the dystrophin gene, manifested by progressive muscle weakness and wasting due to the absence of dystrophin protein, leading to degeneration of skeletal muscle. DMD patients are clinically heterogeneous and the functional phenotype often cannot be correlated with the genotype. Therefore, defined reliable noninvasive biomarkers aiming at predicting if a given DMD child will progress more or less rapidly will be instrumental to better design inclusion of defined patients for future therapeutic assays. We recently showed that CD49d expression levels in blood-derived T-cell subsets can predict disease progression in DMD patients. Herein we describe in detail the methodology to be applied for defining, through four-color flow cytometry, the membrane expression levels of the CD49d (the α4 chain of the integrins α4β1 and α4β7) in circulating CD4+ and CD8+ T cell subsets. Since we have also shown that this molecule can also be placed as a potential target for therapeutics in DMD, we also describe the cell migration functional assay that can be applied to test potential CD49d inhibitors that can modulate their ability to cross endothelial or extracellular matrix (ECM) barriers.
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