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Dystonia associated with mutation of the neuronal sodium channel Scn8a and identification of the modifier locus Scnm1 on mouse chromosome 3 总被引:2,自引:1,他引:1
Sprunger LK; Escayg A; Tallaksen-Greene S; Albin RL; Meisler MH 《Human molecular genetics》1999,8(3):471-479
The mouse mutant medJ contains a splice site mutation in the neuronal
sodium channel Scn8a that results in a very low level of expression. On a
C57BL/6J genetic background, medJ homozygotes exhibit progressive paralysis
and juvenile lethality. The C3H genetic background has an ameliorating
effect, producing viable adults with a novel dystonic phenotype. The
dystonic mice exhibit movement-induced, sustained abnormal postures of the
trunk and limbs. A dominant modifier locus responsible for the difference
between strains was mapped to a 4.5 +/- 1.3 cM interval on mouse chromosome
3. Our findings establish a role for ion channels in dystonia and
demonstrate the impact of genetic background on its severity and
progression. This new model suggests that SCN8A on chromosome 12q13 and
SCNM1 on chromosome 1p21-1q21 may contribute to human inherited dystonia.
相似文献
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K KAWAKAMI MH QURESHI T ZHANG Y KOGUCHI K SHIBUYA S NAOE A SAITO 《Clinical and experimental immunology》1999,117(1):113-122
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目的研究电离辐射对ConA激活的脾细胞内游离钙离子([Ca2+]i)动员的影响,以探讨电离辐射免疫抑制作用的发生机理。方法采用Fura2/AM双波长荧光测定法检测了X射线全身照射后的小鼠脾细胞内[Ca2+]i对ConA反应性的变化。结果小鼠接受0、05、1、2、4和6Gy吸收剂量的X射线全身照射后24小时,脾细胞内[Ca2+]i对ConA反应性呈剂量依赖性下降,表现为[Ca2+]i上升幅度减小、上升至峰值时间延长。2GyX射线全身照射后的时程观察表明,照后2小时细胞内[Ca2+]i对ConA反应性开始下降,24小时达最低点,照后5天才略有回升。结论电离辐射所致免疫功能抑制与其抑制淋巴细胞内[Ca2+]i动员等信息传递过程有关 相似文献
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MH Sun G Mechtersheimer P Moellera CH Herfarth MV Knebel Doeberitz HK Scharkert T Lehnert J Gebert 《World journal of gastroenterology : WJG》2000,6(3)
AIM To study the clonality of the esophageal carcinosarcoma by using molecular approaches.METHODS Two esophageal carcinosarcomas were included in the study. Tumor area from dysplasticlesion, squamout cell carcinoma, basaloid cell carcinoma and spindle cell elements were microdissectedseparately. Each element was analyzed with 14 microsatellite markers and direct sequenced for p53 gene andras gene mutation.RESULTS Both tumors displayed a typical histologic feature of carcinosarcoma. Both cases showed thedivergent differentiation by immunohistochemistry study. In case 1 the identical LOH at p53 and hMLH1 lociwas detected. The heterogenous LOH was detected only in carcinosarcoma at RB1 and BRCA1 loci, whilethe LOH at ACTC locus was seen only in sarcoma. The same mutation of the splice site of exon 6-intron 6displayed in the two tumor elements. In case 2, a coordinate LOH at RB locus was demonstrated in threetypes of tumor elements: sqamous carcinoma, basaloid carcinoma and spindle cell element. A heterogenousLOH was seen only in spindle cells at TAP1 locus. No mutation in exon 5-8 of p53 gene has been found incase 2. No mutation of K-ras gene was found.CONCLUSION Although the different differentiation, the two elements of esophageal carcinosarcoma mayhave a single clonality. The p53 gene mutation occurred before the two differentiation directions switched.The distinct molecular genotype can be determined through molecular biological analysis. The microsatelliteprofiling can serve as an approach to find out which genetic alteration occurs before or after thedifferentiation is determines. 相似文献