Genomic organisation and chromosomal localisation of two members of the KCND ion channel family, KCND2 and KCND3

To follow a candidate gene approach for the involvement of the KCND2 and KCND3 genes (Kv4.2 and Kv4.3) in the pathogenesis of the long QT syndrome (LQTS) and Brugada syndrome, it is necessary to determine the genomic organisation of KCND2 and KCND3. We therefore resolved the intron-exon boundaries a...

Full description

Saved in:
Bibliographic Details
Published inHuman genetics Vol. 106; no. 6; pp. 614 - 619
Main Authors POSTMA, A. V, BEZZINA, C. R, DE VRIES, J. F, WILDE, A. A. M, MOORMAN, A. F. M, MANNENS, M. M. A. M
Format Journal Article
LanguageEnglish
Published Heidelberg Springer 01.06.2000
Berlin
New York, NY
Subjects
Biological and medical sciences
Cardiac dysrhythmias
Cardiology. Vascular system
Chromosome Walking
Chromosomes, Human, Pair 1 - genetics
Chromosomes, Human, Pair 7 - genetics
Exons
Genomic Library
Heart
Humans
Introns
Long QT Syndrome - genetics
Medical sciences
Physical Chromosome Mapping
Polymerase Chain Reaction
Potassium Channels - genetics
Potassium Channels, Voltage-Gated
Sequence Analysis, DNA
Shal Potassium Channels
Human
Arrhythmia
Nucleotide sequence
Prolonged QT interval
Chromosome A1
Cardiovascular disease
Gene organization
Ionic channel
Chromosome C7
Conduction disorder
Blood cell
Heart block
Heart disease
DNA
Genome
Lymphocyte
Online AccessGet full text

Cover

More Information
Summary:To follow a candidate gene approach for the involvement of the KCND2 and KCND3 genes (Kv4.2 and Kv4.3) in the pathogenesis of the long QT syndrome (LQTS) and Brugada syndrome, it is necessary to determine the genomic organisation of KCND2 and KCND3. We therefore resolved the intron-exon boundaries and flanking intronic sequences and found that KCND2 consisted of six exons and KCND3 of seven exons. Subsequently, we designed the oligonucleotide primers needed for amplifying the coding exons of both KCND2 and KCND3 and established conditions for polymerase chain reaction amplification of each exon from genomic DNA. Furthermore, the chromosomal localisation of KCND2 and KCND3 was determined as 7q31 and 1p13.2, respectively. This information should facilitate the systematic screening of KCND2 and KCND3 exons for mutations in (inherited) arrhythmia syndromes, such as LQTS and Brugada.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0340-6717
1432-1203
DOI:10.1007/s004390000308