5-AMINOLEVULINATE SYNTHASE IS AT 3P21 AND THUS NOT THE PRIMARY DEFECT IN X-LINKED SIDEROBLASTIC ANEMIA
- 1 September 1988
- journal article
- research article
- Vol. 43 (3) , 331-335
Abstract
The gene for 5-aminolevulinate synthase (ALAS) has been mapped to 3pter-3q13.2 by Southern blot hybridization analysis of a mouse/human hybrid cell panel. In situ hybridization maps the gene to 3p21, distal to the common fragile site at 3p14.2 (FRA3B). The mapping of this gene to an autosome makes it improbable that it is the site of the primary defect in X-linked sideroblast anemia.This publication has 17 references indexed in Scilit:
- Further localization of ETS1 indicates that the chromosomal rearrangement in Ewing sarcoma does not occur at fra(11)(q23)Human Genetics, 1988
- Human ?-aminolevulinate dehydratase: chromosomal localization to 9q34 by in situ hybridizationHuman Genetics, 1987
- Nudeotide sequence of the chicken 5-aminolevulinate synthase geneNucleic Acids Research, 1986
- Control of 5-Aminolevulinate Synthase in AnimalsCurrent Topics in Cellular Regulation, 1986
- DNA polymerase ? inhibition by aphidicolin induces gaps and breaks at common fragile sites in human chromosomesHuman Genetics, 1984
- High-resolution chromosomal localization of human genes for amylase, proopiomelanocortin, somatostatin, and a DNA fragment (D3S1) by in situ hybridization.Proceedings of the National Academy of Sciences, 1983
- Assignment of the human coproporphyrinogen oxidase to chromosome 9Human Genetics, 1983
- Regional gene assignment of human porphobilinogen deaminase and esterase A4 to chromosome 11q23 leads to 11qter.Proceedings of the National Academy of Sciences, 1981
- A highly polymorphic locus in human DNA.Proceedings of the National Academy of Sciences, 1980