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Point mutation associated with hereditary persistence of fetal hemoglobin decreases RNA polymerase III transcription upstream of the affected gamma-globin gene.
Author(s) -
David P. Carlson,
Jeffrey Ross
Publication year - 1986
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.6.9.3278
Subject(s) - biology , rna polymerase ii , transcription (linguistics) , microbiology and biotechnology , point mutation , polymerase , rna polymerase iii , fetal hemoglobin , gene , general transcription factor , transcription factor ii d , globin , rna polymerase , genetics , rna , promoter , gene expression , fetus , mutation , pregnancy , linguistics , philosophy
A base substitution in the 5'-flanking region of a human fetal globin gene is associated with abnormal fetal hemoglobin production. It also reduces by 5- to 10-fold in vitro transcription of the gene by RNA polymerase III. We discuss potential links between polymerase III transcription and abnormal hemoglobin production.

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