Publication Date:
1982-02-19
Description:
Nondeletion forms of hereditary persistence of fetal hemoglobin may result from regulatory disorders of globin gene expression. The defects in two such conditions were localized by demonstrating a tight genetic linkage between the disorders and polymorphic restriction endonuclease sites within the beta-like globin gene complex. In one instance, the defect probably occurred outside the region of DNA between the epsilon- and beta-globin genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Old, J M -- Ayyub, H -- Wood, W G -- Clegg, J B -- Weatherall, D J -- New York, N.Y. -- Science. 1982 Feb 19;215(4535):981-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6186021" target="_blank"〉PubMed〈/a〉
Keywords:
Chromosome Deletion
;
DNA Restriction Enzymes
;
Female
;
Fetal Hemoglobin/*genetics
;
Genetic Linkage
;
Globins/genetics
;
Humans
;
Male
;
Pedigree
;
Polymorphism, Genetic
;
Thalassemia/*genetics
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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