The cDNA of the human neuromedin B gene (NMB) mapped to 15q11-qter recognizes an XbaI RFLP.
作者信息
Gregory C A, Schwartz J S
机构信息
Department of Human Genetics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
出版信息
Nucleic Acids Res. 1991 Mar 11;19(5):1167. doi: 10.1093/nar/19.5.1167.
Abstract
摘要
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1
The cDNA of the human neuromedin B gene (NMB) mapped to 15q11-qter recognizes an XbaI RFLP.定位于15q11 - qter的人类神经介素B基因（NMB）的cDNA可识别一种XbaI限制性片段长度多态性。
Nucleic Acids Res. 1991 Mar 11;19(5):1167. doi: 10.1093/nar/19.5.1167.
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Detection of molecular rearrangements in Prader-Willi syndrome patients by using genomic probes recognizing four loci within the PWCR.通过使用识别普拉德-威利综合征关键区域（PWCR）内四个位点的基因组探针检测普拉德-威利综合征患者的分子重排。
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Quantitative calibration and use of DNA probes for investigating chromosome abnormalities in the Prader-Willi syndrome.用于研究普拉德-威利综合征染色体异常的DNA探针的定量校准及应用
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An SstI RFLP detected by the probe pKE2.1 (D19S116) localized to human chromosome 19q13.3.
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Long-range restriction mapping and linkage analysis of the Prader-Willi chromosome region (PWCR).普拉德-威利染色体区域（PWCR）的远距离限制性图谱绘制与连锁分析。
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RFLP identified by the probe pKE0.6 (D19S117) at human chromosome 19q13.3.通过探针pKE0.6（D19S117）在人类19号染色体q13.3处鉴定出的限制性片段长度多态性。
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Molecular study of the Prader-Willi syndrome: deletion, RFLP, and phenotype analyses of 50 patients.普拉德-威利综合征的分子研究：50例患者的缺失、限制性片段长度多态性及表型分析
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Somatic recombination rather than uniparental disomy suggested as another mechanism by which genetic imprinting may play a role in the etiology of Prader-Willi syndrome.体细胞重组而非单亲二体被认为是基因印记可能在普拉德-威利综合征病因学中发挥作用的另一种机制。
Hum Genet. 1991 Nov;88(1):42-8. doi: 10.1007/BF00204927.
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