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Glauber B. Pereira, Fanxue Meng, Neriman T. Kockara, Baoli Yang and Patricia A. Wight Targeted deletion of the antisilencer/enhancer (ASE) element from intron 1 of the myelin proteolipid protein gene (Plp1) in mouse reveals that the element is dispensable for Plp1 expression in brain during development and remyelination Journal of Neurochemistry 124

Article first published online: 21 DEC 2012 | DOI: 10.1111/jnc.12092

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Removal of the antisilencer/enhancer (ASE) element from Plp1 intron 1 shows that it is essential for robust activation of Plp1-lacZ constructs in oligodendroglial cell lines, but dispensable for activation of the native gene in mouse during development and remyelination. Perhaps the ASE does not function in vivo, or its loss can be compensated for by other regulatory elements in Plp1.

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