{'fraction_non_alphanumeric': 0.01603206412825651, 'fraction_numerical': 0.0, 'mean_word_length': 5.756756756756757, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Overexpression of Human PHEX Under the Human β‐Actin Promoter Does Not Fully Rescue the Hyp Mouse Phenotype

XLH in humans and the Hyp phenotype in mice are caused by inactivating Phex mutations. Overexpression of human PHEX under the human β‐actin promoter in Hyp mice rescued the bone phenotype almost completely, but did not affect phosphate homeostasis, suggesting that different, possibly independent, pathophysiological mechanisms contribute to hyperphosphaturia and bone abnormalities in XLH.