Blair I P, Dawkins J L, Nicholson G A
Molecular Medicine Laboratory, University of Sydney, Clinical Sciences Building, Concord Hospital, NSW, Australia.
Cytogenet Cell Genet. 1997;78(2):140-4. doi: 10.1159/000134649.
The peripheral neuropathy, hereditary sensory neuropathy type I (HSN-I) is an autosomal dominant degenerative disorder of sensory and motor neurons. The disease leads to distal sensory loss, distal muscle wasting and weakness, and variable neural deafness. The HSN-I locus was recently mapped to a large genetic interval on chromosome 9q22 that includes the candidate genes GAS1 and XPA. XPA mutations have been shown to cause peripheral neuropathy, and GAS1 is related to the PMP22 gene, which is critical in the pathogenesis of two other peripheral neuropathies. By undertaking extensive genetic linkage analysis within the candidate region, we have refined the HSN-I locus to a critical interval of 3-4 cM. GAS1, XPA, and several other genes that map within the interval initially identified for the disease locus have been investigated and excluded from playing a pathogenic role in HSN-I.
遗传性感觉神经病I型(HSN-I)是一种常染色体显性遗传的感觉和运动神经元退行性疾病。该疾病导致远端感觉丧失、远端肌肉萎缩和无力,以及不同程度的神经性耳聋。HSN-I基因座最近被定位到9号染色体q22上的一个大的遗传区间,该区间包含候选基因GAS1和XPA。已证明XPA突变会导致周围神经病变,并且GAS1与PMP22基因相关,PMP22基因在另外两种周围神经病变的发病机制中起关键作用。通过在候选区域内进行广泛的遗传连锁分析,我们已将HSN-I基因座精确定位到一个3-4厘摩的关键区间。已对GAS1、XPA以及最初确定为疾病基因座区间内定位的其他几个基因进行了研究,并排除了它们在HSN-I中发挥致病作用的可能性。