Sambuughin N, McWilliams S, de Bantel A, Sivakumar K, Nelson T E
Barrow Neurological Institute, Phoenix, AZ, USA.
Am J Hum Genet. 2001 Jul;69(1):204-8. doi: 10.1086/321270. Epub 2001 May 29.
Malignant hyperthermia (MH) is an anesthetic-drug-induced, life-threatening hypermetabolic syndrome caused by abnormal calcium regulation in skeletal muscle. Often inherited as an autosomal dominant trait, MH has linkage to 30 different mutations in the RYR1 gene, which encodes a calcium-release-channel protein found in the sarcoplasmic reticulum membrane in skeletal muscle. All published RYR1 mutations exclusively represent single-nucleotide changes. The present report documents, in exon 44 of RYR1 in two unrelated, MH-susceptible families, a 3-bp deletion that results in deletion of a conserved glutamic acid at position 2347. This is the first deletion, in RYR1, found to be associated with MH susceptibility. MH susceptibility was confirmed among some family members by in vitro diagnostic pharmacological contracture testing of biopsied skeletal muscle. Although a single-amino-acid deletion appears to be a subtle change in the protein, the deletion of Glu2347 from RYR1 produces an unusually large electrically evoked contraction tension in MH-positive individuals, suggesting that this deletion produces an alteration in skeletal-muscle calcium regulation, even in the absence of pharmacological agents.
恶性高热(MH)是一种由麻醉药物诱发的、危及生命的高代谢综合征,由骨骼肌中异常的钙调节引起。MH通常作为常染色体显性性状遗传,与RYR1基因中的30种不同突变有关,该基因编码一种在骨骼肌肌浆网膜中发现的钙释放通道蛋白。所有已发表的RYR1突变均仅代表单核苷酸变化。本报告记录了在两个不相关的MH易感家族的RYR1基因第44外显子中,一个3碱基对的缺失导致2347位保守谷氨酸的缺失。这是首次在RYR1中发现与MH易感性相关的缺失。通过对活检骨骼肌进行体外诊断性药理挛缩试验,在一些家庭成员中证实了MH易感性。虽然单个氨基酸的缺失在蛋白质中似乎是一个细微的变化,但从RYR1中缺失Glu2347会在MH阳性个体中产生异常大的电诱发收缩张力,这表明即使在没有药理试剂的情况下,这种缺失也会导致骨骼肌钙调节的改变。