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Opening an iso Image with winrar. Mac OS X 10.6.1 or newer and Firestorm.rp.html Download first. Fusrodatin. to a single nucleotide polymorphism (SNP) within *JMY* \[[@CR11]\]. In the present study, SNP12 was revealed to be associated with the JHS phenotype, while SNP1 and SNP11 were not. Among the 3 SNPs, SNP12 was a missense mutation, resulting in the substitution of alanine (A) by threonine (T) at position 404 (A404T). The A404T substitution is located in the BRCA2-binding domain (amino acid 392--454), and has been shown to be associated with breast cancer risk in women \[[@CR20]\]. It is possible that in the present study, SNP12 was associated with JHS because of its effect on BRCA2 binding.
SNP12 was identified by homozygosity mapping in a large Japanese family, and the proband was affected by JHS \[[@CR11]\]. In the present study, homozygosity mapping showed that the proband had only two homozygous SNPs in chromosome 7, and three SNPs in chromosome 16. All of these SNPs were found to be linked to *JMY* using linkage disequilibrium mapping.
The evidence for an association between *JMY* and JHS was obtained by (1) confirming that SNP12 was associated with JHS using a case--control study and (2) confirming that SNP12 was linked to *JMY* using linkage disequilibrium mapping. Furthermore, by screening DNA from family members of the two affected patients, we found that SNP12 was in strong linkage disequilibrium with *JMY*. All these findings suggest that SNP12 is a causative mutation for JHS.
Our data suggest that the presence of SNP12 is linked to JHS in two ways: (1) SNP12 is linked to an unidentified causative gene for JHS, and (2) SNP12 is linked to *JMY* on the basis of its position and linkage disequilibrium with the causative gene for JHS. SNP12 is, therefore, possibly the causative mutation for JHS in our patient. However, we could not exclude the possibility that SNP12 is not the causative mutation for JHS in our patient, but is in strong linkage dise 0b46394aab
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