Chromosomal mapping in the mouse of eight K + -channel-genes representing the four Shaker -like subfamilies Shaker, Shab, Shaw , and Shal

Klocke, Rainer; Roberds, Steven L.; Tamkun, Michael M.; Gronemeier, Monika; Augustin, Andrei; Albrecht, Barbara; Pongs, Olaf; Jockusch, Harald

doi:10.1016/s0888-7543(05)80358-1

Cited by 27 publications

(9 citation statements)

References 48 publications

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“…PCR-generated fragments corresponding to nt 1-297 of hKv,I3 were amplified from a rodent/human chromosome mapping panel derived from 18 hybrid cell lines with various amounts of individual human chromosome contents, as described in Materials and Methods. (41). However, a fourth loci for long QT syndrome is known to exist but has yet to be localized (40).…”

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confidence: 99%

Characterization of a voltage-gated K+ channel beta subunit expressed in human heart.

England

Uebele

Shear

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

135

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Voltage-gated K+ channels are important modulators of the cardiac action potential. However, the correlation of endogenous myocyte currents with K+ channels cloned from human heart is complicated by the possibility that heterotetrameric av-subunit combinations and functionaltering .8 subunits exist in native tissue. Therefore, a variety of subunit interactions may generate cardiac K+ channel diversity. We report here the cloning of a voltage-gated K+ channel 13 subunit, hK4,83, from adult human left ventricle that shows 84% and 74% amino acid sequence identity with the previously cloned rat Kv31 and Kv32 subunits, respectively.Together these three KvI3 subunits share >82% identity in the carboxyl-terminal 329 aa and show low identity in the aminoterminal 79 aa. RNA analysis indicated that hKv.I3 message is 2-fold more abundant in human ventricle than in atrium and is expressed in both healthy and diseased human hearts.Coinjection of hKv483 with a human cardiac delayed rectifier, hKv1.5, in'Xenopus oocytes increased inactivation, induced an 18-mV hyperpolarizing shift in the activation curve, and slowed deactivation (T = 8.0 msec vs. 35.4 msec at -50 mV).hKvI33 was localized to human chromosome 3 by using a human/rodent cell hybrid mapping panel. These data confirm the presence of functionally important K+ channel 13 subunits in human heart and indicate that 18-subunit composition must be accounted for when comparing cloned channels with endogenous cardiac currents.Potassium channels play an essential role in most excitable cells and are responsible for many diverse physiological functions (1-3). In the heart, voltage-gated K+ channels (Kvs) are responsible for establishing the resting membrane potential and modulating the frequency and duration of action potentials, as well as being the targets of several antiarrhythmic drugs. At present, whole-cell and patch-clamp studies have characterized at least five distinct K+ currents in mammalian myocardium (4-14), while molecular cloning efforts have yielded at least seven cardiac K+ channel genes expressed in rat or human heart (15-18). Six of these cloned genes represent Shaker-like K+ channels from either the K1, KV2, or K,4 gene subfamilies. The diversity of K+ channels in the heart is readily apparent. Nevertheless, correlation of cloned channels with endogenous myocyte currents has been difficult because most heterologously expressed channels display either a fastinactivating or a delayed-rectifier-type current, often with similar pharmacology. Although the human K,1.5 isoform (hK,1. We report here the cloning and characterization of a cDNA from human heart that encodes another K+ channel , subunit, designated hKV,33, adopting proposed nomenclature (26). ¶ This subunit is present in both healthy and cardiomyopathic heart tissue and alters the functional properties of hKvl.5, converting it from a delayed rectifier to a channel with rapid, but partial, inactivation. In addition, this current activates at lower voltages and has dramatically slower deactivati...

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mentioning

confidence: 99%

Characterization of a voltage-gated K+ channel beta subunit expressed in human heart.

England

Uebele

Shear

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

135

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“…Subsequently, a Kv channel gene ( Kcna1 ) exhibiting amino acid sequence similarity to Shaker was cloned in mice and humans (Curran et al 1992; Tempel et al 1988) and shown to encode the Kv1.1 α-subunit, a member of the Kv1 subfamily of voltage-gated potassium channels (Curran et al 1992; Klocke et al 1993). The Kv1 subfamily, also known as the Shaker -related family, consists of eight different genes (Kv1.1–1.8) (Gutman et al 2005).…”

Section: Adar Substrates In the Central Nervous Systemmentioning

confidence: 99%

Editing of Neurotransmitter Receptor and Ion Channel RNAs in the Nervous System

Hood

Emeson

2011

Current Topics in Microbiology and Immunology

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The central dogma of molecular biology defines the major route for the transfer of genetic information from genomic DNA to messenger RNA to three-dimensional proteins that affect structure and function. Like alternative splicing, the post-transcriptional conversion of adenosine to inosine (A-to-I) by RNA editing can dramatically expand the diversity of the transcriptome to generate multiple, functionally distinct protein isoforms from a single genomic locus. While RNA editing has been identified in virtually all tissues, such post-transcriptional modifications have been best characterized in RNAs encoding both ligand- and voltage-gated ion channels and neurotransmitter receptors. These RNA processing events have been shown to play an important role in the function of the encoded protein products and, in several cases, have been shown to be critical for the normal development and function of the nervous system.

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“…Anchor loci are shown in bold; the figures to the left of the genetic map are genetic distances in cM from the centromere (Hillyard et al 1993). Mapping data were taken from Siracusa & Abbott, 1993;Klocke et al 1993;Matsunami et al 1993;Abbott et al 1994;Laurent et al 1994;Li et al 1994;Lock et al 1994;Malas et al 1994;Peters et al 1994;Williamson et al 1994 and Dutton et al, personal communication. associated with paternal duplication can be rescued by a maternally derived distal Chr 2 and vice versa for a maternal duplication suggests that at least two genes are imprinted in opposite directions . From genetic studies the imprinting region is defined as lying between the breakpoints of two reciprocal translocations T(2; 8) 2Wa in band H3 and T(2; 16)28H in band H4 and is estimated to be about 20 cM in genetic length and probably only 7-5 Mb in physical size (Cattanach et al 1992;Peters et al 1994).…”

Section: Introductionmentioning

confidence: 99%

“…These loci, excluding the simple sequence repeats, are shown in Fig. 1 (mapping data taken from Siracusa & Abbott, 1993;Copeland et al 1993;Klocke et al 1993;Matsunami et al 1993;Abbott et al 1994;Laurent et al 1994;Li et al 1994;Lock et al 1994;Malas et al 1994;Peters et al 1994;Williamson et al 1994 and Dutton et al, personal communication).…”

Section: Introductionmentioning

confidence: 99%

Thirteen genes (Cebpb, E2f1, Tcf4, Cyp24, Pck1, Acra4, Edn3, Kcnb1, Mc3r, Ntsr, Cd40, Plcg1andRcad) that probably lie in the distal imprinting region of mouse Chromosome 2 are not monoallelically expressed

et al. 1995

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SummarySeven imprinted genes are currently known in the mouse but none have been identified yet in the distal imprinting region of mouse Chromosome (Chr) 2, a region which shows striking linkage conservation with human chromosome 20q13. Both maternal duplication/paternal deficiency and its reciprocal for distal Chr 2 lead to mice with abnormal body shapes and behavioural abnormalities. We have tested a number of candidate genes, that are either likely or known to lie within the distal imprinting region, for monoallelic expression. These included 3 genes (Cebpb, E2f1 and Tcf4) that express transcription factors, 2 genes (Cyp24 and Pck1) that are involved in growth, 5 genes (Acra4, Edn3, Kcnb1, Mc3r and Ntsr) where a defect could lead to neurological and probably behavioural problems, and 3 genes (Cd40, Plcg1 and Rcad) that are less obvious candidates but sequence information was available for designing primers to test their expression. On/off expression of each gene was tested by reverse transcription–polymerase chain reaction (RT–PCR) analysis of RNA extracted from tissues of mice with maternal duplication/paternal deficiency and its reciprocal for the distal region of Chr 2. None of the 13 genes is monoallelically expressed in the appropriate tissues before and shortly after birth which suggests that these genes are not imprinted later in development. This study has narrowed down the search for imprinted genes, and valuable information on which genes have been tested for on/off expression is provided. Since there is considerable evidence of conservation of imprinting between mouse and human, we would predict that the 13 genes are not imprinted in human. Five of the genes: E2f1, Tcf4, Kcnb1, Cd40 and Rcad, have not yet been mapped in human. However, because of the striking linkage conservation observed between mouse Chr 2 and human chromosome 20, we would expect these genes to map on human chromosome 20q13.

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Chromosomal mapping in the mouse of eight K + -channel-genes representing the four Shaker -like subfamilies Shaker, Shab, Shaw , and Shal

Cited by 27 publications

References 48 publications

Characterization of a voltage-gated K+ channel beta subunit expressed in human heart.

Characterization of a voltage-gated K+ channel beta subunit expressed in human heart.

Editing of Neurotransmitter Receptor and Ion Channel RNAs in the Nervous System

Thirteen genes (Cebpb, E2f1, Tcf4, Cyp24, Pck1, Acra4, Edn3, Kcnb1, Mc3r, Ntsr, Cd40, Plcg1andRcad) that probably lie in the distal imprinting region of mouse Chromosome 2 are not monoallelically expressed

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