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由于编码线粒体精氨酰-tRNA 合成酶(RARS2)的基因突变导致的桥脑小脑发育不全 6 型的进一步描述。

Further delineation of pontocerebellar hypoplasia type 6 due to mutations in the gene encoding mitochondrial arginyl-tRNA synthetase, RARS2.

机构信息

Department of Metabolic Medicine, Great Ormond Street Hospital for Children, London, UK.

出版信息

J Inherit Metab Dis. 2012 May;35(3):459-67. doi: 10.1007/s10545-011-9413-6. Epub 2011 Nov 16.

Abstract

Pontocerebellar hypoplasia type 6 (PCH6) (MIM #611523) is a recently described disorder caused by mutations in RARS2 (MIM *611524), the gene encoding mitochondrial arginyl-transfer RNA (tRNA) synthetase, a protein essential for translation of all mitochondrially synthesised proteins. This case confirms that progressive cerebellar and cerebral atrophy with microcephaly and complex epilepsy are characteristic features of PCH6. Additional features of PCH subtypes 2 and 4, including severe dystonia, optic atrophy and thinning of the corpus callosum, are demonstrated. Congenital lactic acidosis can be present, but respiratory chain dysfunction may be mild or absent, suggesting that disordered mitochondrial messenger RNA (mRNA) translation may not be the only mechanism of impairment or that a secondary mechanism exists to allow some translation. We report two novel mutations and expand the phenotypic spectrum of this likely underdiagnosed PCH variant, where recognition of the characteristic neuroradiological phenotype could potentially expedite genetic diagnosis and limit invasive investigations.

摘要

脑桥小脑发育不良 6 型(PCH6)(MIM#611523)是一种最近描述的疾病,由 RARS2(MIM*611524)基因突变引起,该基因编码线粒体精氨酰-tRNA(tRNA)合成酶,是所有线粒体合成蛋白翻译所必需的蛋白质。本病例证实,小脑和大脑进行性萎缩伴小头畸形和复杂癫痫是 PCH6 的特征性表现。PCH 亚型 2 和 4 的其他特征,包括严重的肌张力障碍、视神经萎缩和胼胝体变薄,也得到了证实。可能存在先天性乳酸酸中毒,但呼吸链功能障碍可能较轻或不存在,这表明异常的线粒体信使 RNA(mRNA)翻译可能不是损伤的唯一机制,或者存在第二种机制以允许一些翻译。我们报告了两个新的突变,并扩展了这种可能被低估的 PCH 变异的表型谱,特征性的神经放射影像学表型的识别可能会加速基因诊断并限制有创性检查。

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