Description:
MENKES SYNDROME
ATPASE, CU(2+)-TRANSPORTING, ALPHA POLYPEPTIDE; ATP7A
Repository
|
NIGMS Human Genetic Cell Repository
|
Subcollection |
Heritable Diseases |
Class |
Disorders of Metal Metabolism |
Cell Type
|
Fibroblast
|
Transformant
|
Untransformed
|
Relation to Proband
|
proband
|
Confirmation
|
Molecular characterization before cell line submission to CCR
|
Species
|
Homo sapiens
|
Common Name
|
Human
|
Remarks
|
|
Passage Frozen |
10 |
|
IDENTIFICATION OF SPECIES OF ORIGIN |
Species of Origin Confirmed by Nucleoside Phosphorylase, Glucose-6-Phosphate Dehydrogenase, and Lactate Dehydrogenase Isoenzyme Electrophoresis |
|
Gene |
ATP7A |
Chromosomal Location |
Xq21.1 |
Allelic Variant 1 |
; MENKES DISEASE |
Identified Mutation |
IVS20AS-2, A>G |
Remarks |
Line S1488; has normal level of mRNA; donor subject has a splice acceptor mutation in the ATP7A gene, agAA>ggAA junction 4150/4151, in the 5' flanking region of exon 21 (IVS20AS-2, A>G), resulting in a frameshift and a cryptic splice site |
Das S, Levinson B, Whitney S, Vulpe C, Packman S, Gitschier J, Diverse mutations in patients with Menkes disease often lead to exon skipping. Am J Hum Genet55:883-889 1994 |
PubMed ID: 7977350 |
Passage Frozen |
10 |
Split Ratio |
1:3 |
Temperature |
37 C |
Percent CO2 |
5% |
Medium |
Eagle's Minimum Essential Medium with Earle's salts and non-essential amino acids with 2mM L-glutamine or equivalent |
Serum |
15% fetal bovine serum Not inactivated |
Substrate |
None specified |
Subcultivation Method |
trypsin-EDTA |
Supplement |
- |
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