Description:
NEUROPATHY, HEREDITARY SENSORY AND AUTONOMIC, TYPE III; HSAN3
INHIBITOR OF KAPPA LIGHT POLYPEPTIDE GENE ENHANCER IN B CELLS, KINASE-COMPLEX ASSOCIATED PROTEIN; IKBKAP
Repository
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NIGMS Human Genetic Cell Repository
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Subcollection |
Heritable Diseases |
Class |
Disorders of the Nervous System |
Quantity |
25 µg |
Quantitation Method |
Please see our FAQ |
Biopsy Source
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Peripheral vein
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Cell Type
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B-Lymphocyte
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Tissue Type
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Blood
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Transformant
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Epstein-Barr Virus
|
Sample Source
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DNA from LCL
|
Race
|
White
|
Ethnicity
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ASHKENAZI
|
Family Member
|
4
|
Relation to Proband
|
mother
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Confirmation
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Clinical summary/Case history
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Species
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Homo sapiens
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Common Name
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Human
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Remarks
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GENE MAPPING & DOSAGE STUDIES - Y CHROMOSOME |
PCR analysis of DNA from this cell culture gave a negative result with a primer for Yq11, DYS227. |
|
Gene |
IKBKAP |
Chromosomal Location |
9q31 |
Allelic Variant 1 |
603722.0001; FAMILIAL DYSAUTONOMIA |
Identified Mutation |
c.2204+6T>C (IVS20+6T>C); Slaugenhaupt et al. (2001) found that more than 99.5% of disease alleles causing familial dysautonomia (223900) in Ashkenazi Jewish individuals carried a donor splice site mutation (IVS20+6T-C) which leads to deletion of exon 20 from mRNA. Haplotype analyses were consistent with a common founder. Anderson et al. (2001) identified the same mutation in Ashkenazi Jewish patients with familial dysautonomia. |
Remarks |
Clinically unaffected; donor subject is heterozygous for a mutation in the IKBKAP gene on one allele: c.2204+6T>C (IVS20+6T>C); this donor splice site mutation leads to deletion of exon 20 from the mRNA; the second allele is negative for the IVS20+6T>C and R696P mutations; negative for both Canavan and Tay-Sachs; affected children are GM05105, GM05106. |
Anderson SL, Coli R, Daly IW, Kichula EA, Rork MJ, Volpi SA, Ekstein J, Rubin BY, Familial dysautonomia is caused by mutations of the IKAP gene. Am J Hum Genet68(3):753-758 2001 |
PubMed ID: 11179021 |
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