Genomic structure of the human PLZF gene

The human PLZF (promyelocytic leukaemia zinc finger) gene encodes a Krüppel-like zinc finger protein, which was identified via the reciprocal translocation t(11;17)(q23;q21) fusing it to the retinoic acid receptor alpha ( RARα) gene in promyelocytic leukaemia. To determine its complete genomic organ...

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Bibliographic Details
Published in:Gene 1999-08, Vol.236 (1), p.21-24
Main Authors: van Schothorst, E.M., Prins, D.E.M., Baysal, B.E., Beekman, M., Licht, J.D., Waxman, S., Zelent, A., Cornelisse, C.J., van Ommen, G.J.B., Richard, C.W., Devilee, P.
Format: Article
Language:English
Subjects:
Base Sequence
Chromosome 11
Chromosomes, Artificial, Yeast
Chromosomes, Human, Pair 11
Cosmids
DNA-Binding Proteins - genetics
Exons
Gene organisation
Genetic Markers
Germ-Line Mutation
Humans
Introns
Kruppel-Like Transcription Factors
Models, Genetic
Molecular Sequence Data
paraganglioma
Physical map
PLZF gene
Polymerase Chain Reaction
Polymorphic markers
Promyelocytic Leukemia Zinc Finger Protein
Retinoic acid receptor ^a
Transcription Factors - genetics
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Summary:The human PLZF (promyelocytic leukaemia zinc finger) gene encodes a Krüppel-like zinc finger protein, which was identified via the reciprocal translocation t(11;17)(q23;q21) fusing it to the retinoic acid receptor alpha ( RARα) gene in promyelocytic leukaemia. To determine its complete genomic organisation, we constructed a cosmid-map fully containing the hPLZF gene. The gene has seven exons, including a novel 5′ untranslated exon, varying in size from 87 to 1358 bp and spans at least 120 kb. Flanking intronic sequences were identified and all splice acceptor and donor sites conformed to the gt/ag rule. Five polymorphic markers could be fine located in its vicinity. These data will facilitate mutation analysis of hPLZF in t(11;17) leukaemia cases, as well as assist mapping and loss-of-heterozygosity analysis. Here we have tested hPLZF as a possible candidate for the PGL1 locus involved in hereditary head and neck paragangliomas. However, mutation analysis revealed no aberration in 12 paraganglioma patients from different families.
ISSN:0378-1119
1879-0038
DOI:10.1016/S0378-1119(99)00277-2