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A recent study also demonstrated mislocalization of APE1 from the nucleus to the cytoplasm as a possible trigger of oxidative DNA damage in spinal motor neurons expressing mutant SOD1 G93A , despite upregulation of multiple DNA repair enzymes, suggesting that restricted localization of APE1 could inhibit redox homeostasis (Li J

The presence of neural markers in neuroblastic cells and vanillylmandelic acid (VMA) in urine supports a neuroectodermal origin [1,8,12-15,18-21]

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