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尿苷二磷酸葡萄糖脱氢酶变体导致糖基化肌营养不良症。

UDP-glucose dehydrogenase variants cause dystroglycanopathy.

作者信息

Reelfs Anna M, Stephan Carrie M, Czech Theresa M, Cox Mary O, Joseph Soumya, Darbro Benjamin W, Moore Steven A, Campbell Kevin P, Mathews Katherine D

机构信息

University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.

Department of Pediatrics, University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.

出版信息

Ann Clin Transl Neurol. 2025 Jun;12(6):1302-1308. doi: 10.1002/acn3.70002. Epub 2025 Apr 17.

Abstract

UDP-glucose dehydrogenase (UGDH) variants have been associated with hypotonia, developmental delay, and epilepsy. We report the first pathologic evidence of dystroglycanopathy in siblings with UGDH variants. Both presented around 6 months with developmental delay and elevated creatinine kinase. Sibling A developed epilepsy at age 9 years. Muscle biopsy from sibling A showed necrotizing myopathy with reduced matriglycan immunostaining. Western blot revealed α-dystroglycan with abnormally low molecular weight. The siblings shared pathogenic UGDH variants in trans: c.305G>A p.(R102Q) is predicted to disrupt protein structure and function; c.265-6C>G is deleterious to splicing. We propose that UGDH is an additional dystroglycanopathy gene.

摘要

UDP-葡萄糖脱氢酶(UGDH)变体与肌张力减退、发育迟缓及癫痫有关。我们报告了首例携带UGDH变体的同胞患糖基化肌营养不良症的病理证据。两人均在6个月左右出现发育迟缓及肌酸激酶升高。同胞A在9岁时患癫痫。对同胞A进行的肌肉活检显示为坏死性肌病,基质糖蛋白免疫染色减少。蛋白质印迹法显示α-肌营养不良聚糖分子量异常低。这对同胞携带反式排列的致病性UGDH变体:c.305G>A p.(R102Q)预计会破坏蛋白质结构和功能;c.265-6C>G对剪接有害。我们提出UGDH是糖基化肌营养不良症的另一个致病基因。

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