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Search results 401 to 479 out of 479 for Kcne1

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0.012s
Type Details Score
Publication  
First Author: Moumne O
Year: 2018
Journal: Front Cardiovasc Med
Title: Mechanism Sharing Between Genetic and Gestational Hypoxia-Induced Cardiac Anomalies.
Volume: 5
Pages: 100
Publication
First Author: Wu Y
Year: 2024
Journal: Theranostics
Title: Transcriptome analysis reveals EBF1 ablation-induced injuries in cardiac system.
Volume: 14
Issue: 12
Pages: 4894-4915
Publication
First Author: Dykes IM
Year: 2014
Journal: Circ Res
Title: HIC2 is a novel dosage-dependent regulator of cardiac development located within the distal 22q11 deletion syndrome region.
Volume: 115
Issue: 1
Pages: 23-31
Publication  
First Author: Van Wauwe J
Year: 2024
Journal: Life Sci Alliance
Title: PRDM16 determines specification of ventricular cardiomyocytes by suppressing alternative cell fates.
Volume: 7
Issue: 12
Publication  
First Author: Zinina VV
Year: 2023
Journal: Cells
Title: TCF7L1 Controls the Differentiation of Tuft Cells in Mouse Small Intestine.
Volume: 12
Issue: 11
Publication
First Author: Jones SM
Year: 2005
Journal: J Assoc Res Otolaryngol
Title: A quantitative survey of gravity receptor function in mutant mouse strains.
Volume: 6
Issue: 4
Pages: 297-310
Publication      
First Author: JAX Neuroscience Mutagenesis Facility
Year: 2004
Journal: MGI Direct Data Submission
Title: Heritable mouse mutants from JAX NMF ENU Mutagenesis Program
Publication
First Author: Gómez-Del Arco P
Year: 2024
Journal: Nat Commun
Title: The G4 resolvase Dhx36 modulates cardiomyocyte differentiation and ventricular conduction system development.
Volume: 15
Issue: 1
Pages: 8602
Publication      
First Author: JAX Neuroscience Mutagenesis Facility
Year: 2003
Journal: MGI Direct Data Submission
Title: Heritable mouse mutants from JAX NMF ENU Mutagenesis Program
Publication
First Author: Reeves RH
Year: 1997
Journal: Genomics
Title: High-resolution recombinational map of mouse chromosome 16.
Volume: 43
Issue: 2
Pages: 202-8
Publication
First Author: Zhou B
Year: 2009
Journal: J Clin Invest
Title: Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart.
Volume: 119
Issue: 6
Pages: 1462-76
Publication
First Author: Menendez-Montes I
Year: 2016
Journal: Dev Cell
Title: Myocardial VHL-HIF Signaling Controls an Embryonic Metabolic Switch Essential for Cardiac Maturation.
Volume: 39
Issue: 6
Pages: 724-739
Publication
First Author: Gitton Y
Year: 2002
Journal: Nature
Title: A gene expression map of human chromosome 21 orthologues in the mouse.
Volume: 420
Issue: 6915
Pages: 586-90
Publication
First Author: Reymond A
Year: 2002
Journal: Nature
Title: Human chromosome 21 gene expression atlas in the mouse.
Volume: 420
Issue: 6915
Pages: 582-6
Publication
First Author: Harrell MD
Year: 2007
Journal: Physiol Genomics
Title: Large-scale analysis of ion channel gene expression in the mouse heart during perinatal development.
Volume: 28
Issue: 3
Pages: 273-83
Publication
First Author: Visel A
Year: 2004
Journal: Nucleic Acids Res
Title: GenePaint.org: an atlas of gene expression patterns in the mouse embryo.
Volume: 32
Issue: Database issue
Pages: D552-6
Publication      
First Author: International Knockout Mouse Consortium
Year: 2014
Journal: Database Download
Title: MGI download of modified allele data from IKMC and creation of new knockout alleles
Publication      
First Author: Lennon G
Year: 1999
Journal: Database Download
Title: WashU-HHMI Mouse EST Project
Publication      
First Author: Velocigene
Year: 2008
Journal: MGI Direct Data Submission
Title: Alleles produced for the KOMP project by Velocigene (Regeneron Pharmaceuticals)
Publication      
First Author: International Mouse Strain Resource
Year: 2014
Journal: Database Download
Title: MGI download of germline transmission data for alleles from IMSR strain data
Publication      
First Author: Mouse Genome Informatics and the International Mouse Phenotyping Consortium (IMPC)
Year: 2014
Journal: Database Release
Title: Obtaining and Loading Phenotype Annotations from the International Mouse Phenotyping Consortium (IMPC) Database
Publication      
First Author: Helmholtz Zentrum Muenchen GmbH
Year: 2010
Journal: MGI Direct Data Submission
Title: Alleles produced for the EUCOMM and EUCOMMTools projects by the Helmholtz Zentrum Muenchen GmbH (Hmgu)
Publication        
First Author: The Gene Ontology Consortium
Year: 2014
Title: Automated transfer of experimentally-verified manual GO annotation data to mouse-rat orthologs
Publication        
First Author: UniProt-GOA
Year: 2012
Title: Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Publication
First Author: Kawai J
Year: 2001
Journal: Nature
Title: Functional annotation of a full-length mouse cDNA collection.
Volume: 409
Issue: 6821
Pages: 685-90
Publication
First Author: Adams DJ
Year: 2024
Journal: Nature
Title: Genetic determinants of micronucleus formation in vivo.
Volume: 627
Issue: 8002
Pages: 130-136
Publication        
First Author: MGD Nomenclature Committee
Year: 1995
Title: Nomenclature Committee Use
Publication        
First Author: AgBase, BHF-UCL, Parkinson's UK-UCL, dictyBase, HGNC, Roslin Institute, FlyBase and UniProtKB curators
Year: 2011
Title: Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Publication        
First Author: GOA curators
Year: 2016
Title: Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Publication      
First Author: The Jackson Laboratory Mouse Radiation Hybrid Database
Year: 2004
Journal: Database Release
Title: Mouse T31 Radiation Hybrid Data Load
Publication
First Author: Okazaki Y
Year: 2002
Journal: Nature
Title: Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.
Volume: 420
Issue: 6915
Pages: 563-73
Publication        
First Author: The Gene Ontology Consortium
Year: 2010
Title: Automated transfer of experimentally-verified manual GO annotation data to mouse-human orthologs
Publication
First Author: Diez-Roux G
Year: 2011
Journal: PLoS Biol
Title: A high-resolution anatomical atlas of the transcriptome in the mouse embryo.
Volume: 9
Issue: 1
Pages: e1000582
Publication        
First Author: Mouse Genome Informatics Scientific Curators
Year: 2002
Title: Mouse Genome Informatics Computational Sequence to Gene Associations
Publication      
First Author: Mouse Genome Informatics Scientific Curators
Year: 2010
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Genome U74 Array Platform (A, B, C v2).
Publication      
First Author: MGI Genome Annotation Group and UniGene Staff
Year: 2015
Journal: Database Download
Title: MGI-UniGene Interconnection Effort
Publication        
First Author: Marc Feuermann, Huaiyu Mi, Pascale Gaudet, Dustin Ebert, Anushya Muruganujan, Paul Thomas
Year: 2010
Title: Annotation inferences using phylogenetic trees
Publication      
First Author: Mouse Genome Database and National Center for Biotechnology Information
Year: 2000
Journal: Database Release
Title: Entrez Gene Load
Publication      
First Author: Allen Institute for Brain Science
Year: 2004
Journal: Allen Institute
Title: Allen Brain Atlas: mouse riboprobes
Publication      
First Author: Mouse Genome Informatics Scientific Curators
Year: 2009
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Gene 1.0 ST Array Platform
Publication      
First Author: Mouse Genome Informatics (MGI) and The National Center for Biotechnology Information (NCBI)
Year: 2010
Journal: Database Download
Title: Consensus CDS project
Publication      
First Author: Mouse Genome Informatics Group
Year: 2003
Journal: Database Procedure
Title: Automatic Encodes (AutoE) Reference
Publication      
First Author: Bairoch A
Year: 1999
Journal: Database Release
Title: SWISS-PROT Annotated protein sequence database
Publication        
First Author: Mouse Genome Informatics Scientific Curators
Year: 2005
Title: Obtaining and Loading Genome Assembly Coordinates from Ensembl Annotations
Publication      
First Author: Mouse Genome Informatics
Year: 2010
Journal: Database Release
Title: Protein Ontology Association Load.
Publication        
First Author: Mouse Genome Informatics Scientific Curators
Year: 2005
Title: Obtaining and loading genome assembly coordinates from NCBI annotations
Publication      
First Author: Mouse Genome Informatics Scientific Curators
Year: 2009
Journal: Database Download
Title: Mouse Microarray Data Integration in Mouse Genome Informatics, the Affymetrix GeneChip Mouse Genome 430 2.0 Array Platform
Publication
First Author: Mansén A
Year: 2010
Journal: Acta Physiol (Oxf)
Title: Thyroid hormone receptor alpha can control action potential duration in mouse ventricular myocytes through the KCNE1 ion channel subunit.
Volume: 198
Issue: 2
Pages: 133-42
DO Term
Allele
Name: transgene insertion 1, Ivan P Moskowitz
Allele Type: Transgenic
Attribute String: Inducible, Recombinase
Allele
Name: transgene insertion, Bjorn Vennstrom
Allele Type: Transgenic
Attribute String: Inserted expressed sequence
Genotype
Symbol: Tbx5/Tbx5 Tg(Kcne1-cre/ERT2)1Imos/?
Background: involves: CD-1
Zygosity: cn
Has Mutant Allele: true
Publication
First Author: Nef P
Year: 1992
Journal: Proc Natl Acad Sci U S A
Title: Spatial pattern of receptor expression in the olfactory epithelium.
Volume: 89
Issue: 19
Pages: 8948-52
Strain
Attribute String: congenic, mutant strain, transgenic
Publication
First Author: Arnolds DE
Year: 2011
Journal: Genesis
Title: Inducible recombination in the cardiac conduction system of minK: CreERT² BAC transgenic mice.
Volume: 49
Issue: 11
Pages: 878-84
Genotype
Symbol: Gt(ROSA)26Sor/Gt(ROSA)26Sor<+> Tg(Kcne1-cre/ERT2)1Imos/?
Background: involves: 129S4/SvJaeSor * CD-1
Zygosity: cn
Has Mutant Allele: true
Publication
First Author: Knollmann BC
Year: 2007
Journal: Biochem Biophys Res Commun
Title: Kcnq1 contributes to an adrenergic-sensitive steady-state K+ current in mouse heart.
Volume: 360
Issue: 1
Pages: 212-8
Publication
First Author: Arnolds DE
Year: 2012
Journal: J Clin Invest
Title: TBX5 drives Scn5a expression to regulate cardiac conduction system function.
Volume: 122
Issue: 7
Pages: 2509-18
Publication
First Author: Burnicka-Turek O
Year: 2020
Journal: Circ Res
Title: Transcriptional Patterning of the Ventricular Cardiac Conduction System.
Volume: 127
Issue: 3
Pages: e94-e106
Genotype
Symbol: Gt(ROSA)26Sor/Gt(ROSA)26Sor<+> Tbx5/Tbx5 Tg(Kcne1-cre/ERT2)1Imos/?
Background: involves: 129S4/SvJaeSor * CD-1
Zygosity: cn
Has Mutant Allele: true
Publication  
First Author: Becchetti A
Year: 2017
Journal: Sci Signal
Title: The conformational state of hERG1 channels determines integrin association, downstream signaling, and cancer progression.
Volume: 10
Issue: 473
Publication  
First Author: Li Y
Year: 2019
Journal: Cells
Title: Regulation of IKs Potassium Current by Isoproterenol in Adult Cardiomyocytes Requires Type 9 Adenylyl Cyclase.
Volume: 8
Issue: 9
Publication  
First Author: Lv J
Year: 2021
Journal: Front Cell Dev Biol
Title: Deletion of Kcnj16 in Mice Does Not Alter Auditory Function.
Volume: 9
Pages: 630361
Publication
First Author: Dai W
Year: 2020
Journal: Circ Res
Title: ZO-1 Regulates Intercalated Disc Composition and Atrioventricular Node Conduction.
Volume: 127
Issue: 2
Pages: e28-e43
Protein
Organism: Mus musculus/domesticus
Length: 143  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 170  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 71  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 64  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 192  
Fragment?: false
Publication
First Author: Abbott GW
Year: 1999
Journal: Cell
Title: MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmia.
Volume: 97
Issue: 2
Pages: 175-87
Publication
First Author: Abbott GW
Year: 2001
Journal: Cell
Title: MiRP2 forms potassium channels in skeletal muscle with Kv3.4 and is associated with periodic paralysis.
Volume: 104
Issue: 2
Pages: 217-31
Publication
First Author: Schroeder BC
Year: 2000
Journal: Nature
Title: A constitutively open potassium channel formed by KCNQ1 and KCNE3.
Volume: 403
Issue: 6766
Pages: 196-9
Protein Domain
Type: Family
Description: Two types of beta subunit (KCNE and KCNAB) are presently known to associate with voltage-gated alpha subunits (Kv, KCNQ and eag-like). However, not all combinations of alpha and beta subunits are possible. The KCNE family of K+ channel subunits are membrane glycoproteins that possess a single transmembrane (TM) domain. They share no structural relationship with the alpha subunit proteins, which possess pore forming domains. The subunits appear to have a regulatory function, modulating the kinetics and voltage dependence of the alpha subunits of voltage-dependent K+ channels. KCNE subunits are formed from short polypeptides of ~130 amino acids, and are divided into five subfamilies: KCNE1 (MinK/IsK), KCNE2 (MiRP1), KCNE3 (MiRP2), KCNE4 (MiRP3) and KCNE1L (AMMECR2). Potassium channels are the most diverse group of the ion channel family [, ]. They are important in shaping the action potential, and in neuronal excitability and plasticity []. The potassium channel family is composed of several functionally distinct isoforms, which can be broadly separated into 2 groups []: the practically non-inactivating 'delayed' group and the rapidly inactivating 'transient' group.These are all highly similar proteins, with only small amino acid changes causing the diversity of the voltage-dependent gating mechanism, channel conductance and toxin binding properties. Each type of K+channel is activated by different signals and conditions depending on their type of regulation: some open in response to depolarisation of the plasma membrane; others in response to hyperpolarisation or an increase in intracellular calcium concentration; some can be regulated by binding of a transmitter, together with intracellular kinases; while others are regulated by GTP-binding proteins or other second messengers []. In eukaryotic cells, K+channels are involved in neural signalling and generation of the cardiac rhythm, act as effectors in signal transduction pathways involving G protein-coupled receptors (GPCRs) and may have a role in target cell lysis by cytotoxic T-lymphocytes []. In prokaryotic cells, they play a role in the maintenance of ionic homeostasis [].All K+channels discovered so far possess a core of alpha subunits, each comprising either one or two copies of a highly conserved pore loop domain (P-domain). The P-domain contains the sequence (T/SxxTxGxG), which has been termed the K+selectivity sequence. In families that contain one P-domain, four subunits assemble to form a selective pathway for K+across the membrane. However, it remains unclear how the 2 P-domain subunits assemble to form a selective pore. The functional diversity of these families can arise through homo- or hetero-associations of alpha subunits or association with auxiliary cytoplasmic beta subunits. K+channel subunits containing one pore domain can be assigned into one of two superfamilies: those that possess six transmembrane (TM) domains and those that possess only two TM domains. The six TM domain superfamily can be further subdivided into conserved gene families: the voltage-gated (Kv) channels; the KCNQ channels (originally known as KvLQT channels); the EAG-like K+channels; and three types of calcium (Ca)-activated K+channels (BK, IK and SK) []. The 2TM domain family comprises inward-rectifying K+channels. In addition, there are K+channel alpha-subunits that possess two P-domains. These are usually highly regulated K+selective leak channels.
Protein Domain
Type: Family
Description: Potassium channels are the most diverse group of the ion channel family [, ]. They are important in shaping the action potential, and in neuronal excitability and plasticity []. The potassium channel family is composed of several functionally distinct isoforms, which can be broadly separated into 2 groups []: the practically non-inactivating 'delayed' group and the rapidly inactivating 'transient' group.These are all highly similar proteins, with only small amino acid changes causing the diversity of the voltage-dependent gating mechanism, channel conductance and toxin binding properties. Each type of K+channel is activated by different signals and conditions depending on their type of regulation: some open in response to depolarisation of the plasma membrane; others in response to hyperpolarisation or an increase in intracellular calcium concentration; some can be regulated by binding of a transmitter, together with intracellular kinases; while others are regulated by GTP-binding proteins or other second messengers []. In eukaryotic cells, K+channels are involved in neural signalling and generation of the cardiac rhythm, act as effectors in signal transduction pathways involving G protein-coupled receptors (GPCRs) and may have a role in target cell lysis by cytotoxic T-lymphocytes []. In prokaryotic cells, they play a role in the maintenance of ionic homeostasis [].All K+channels discovered so far possess a core of alpha subunits, each comprising either one or two copies of a highly conserved pore loop domain (P-domain). The P-domain contains the sequence (T/SxxTxGxG), which has been termed the K+selectivity sequence. In families that contain one P-domain, four subunits assemble to form a selective pathway for K+across the membrane. However, it remains unclear how the 2 P-domain subunits assemble to form a selective pore. The functional diversity of these families can arise through homo- or hetero-associations of alpha subunits or association with auxiliary cytoplasmic beta subunits. K+channel subunits containing one pore domain can be assigned into one of two superfamilies: those that possess six transmembrane (TM) domains and those that possess only two TM domains. The six TM domain superfamily can be further subdivided into conserved gene families: the voltage-gated (Kv) channels; the KCNQ channels (originally known as KvLQT channels); the EAG-like K+channels; and three types of calcium (Ca)-activated K+channels (BK, IK and SK) []. The 2TM domain family comprises inward-rectifying K+channels. In addition, there are K+channel alpha-subunits that possess two P-domains. These are usually highly regulated K+selective leak channels.Two types of beta subunit (KCNE and KCNAB) are presently known to associate with voltage-gated alpha subunits (Kv, KCNQ and eag-like). However, not all combinations of alpha and beta subunits are possible. The KCNE family of K+ channel subunits are membrane glycoproteins that possess a single transmembrane (TM) domain. They share no structural relationship with the alpha subunit proteins, which possess pore forming domains. The subunits appear to have a regulatory function, modulating the kinetics and voltage dependence of the alpha subunits of voltage-dependent K+ channels. KCNE subunits are formed from short polypeptides of ~130 amino acids, and are divided into five subfamilies: KCNE1 (MinK/IsK), KCNE2 (MiRP1), KCNE3 (MiRP2), KCNE4 (MiRP3) and KCNE1L (AMMECR2). KCNE2 subunits associate with the eag-like HERG alpha subunits, which arethe pore-forming subunits of cardiac IKr channels. Channels formed solelyfrom HERG subunits display similar properties to native IKr channels;however, they differ in their gating and single channel conductance. Channels formed from both KCNE2 and HERG exhibit properties that are identical to those seen in native IKr channels. Three mutations in the KCNE2gene are associated with long QT syndrome and ventricular fibrillation. These mutations result in channels that open slower and close more rapidly,the net effect being a reduced K+ current [].
Protein Domain
Type: Family
Description: Potassium channels are the most diverse group of the ion channel family [, ]. They are important in shaping the action potential, and in neuronal excitability and plasticity []. The potassium channel family is composed of several functionally distinct isoforms, which can be broadly separated into 2 groups []: the practically non-inactivating 'delayed' group and the rapidly inactivating 'transient' group.These are all highly similar proteins, with only small amino acid changes causing the diversity of the voltage-dependent gating mechanism, channel conductance and toxin binding properties. Each type of K+channel is activated by different signals and conditions depending on their type of regulation: some open in response to depolarisation of the plasma membrane; others in response to hyperpolarisation or an increase in intracellular calcium concentration; some can be regulated by binding of a transmitter, together with intracellular kinases; while others are regulated by GTP-binding proteins or other second messengers []. In eukaryotic cells, K+channels are involved in neural signalling and generation of the cardiac rhythm, act as effectors in signal transduction pathways involving G protein-coupled receptors (GPCRs) and may have a role in target cell lysis by cytotoxic T-lymphocytes []. In prokaryotic cells, they play a role in the maintenance of ionic homeostasis [].All K+channels discovered so far possess a core of alpha subunits, each comprising either one or two copies of a highly conserved pore loop domain (P-domain). The P-domain contains the sequence (T/SxxTxGxG), which has been termed the K+selectivity sequence. In families that contain one P-domain, four subunits assemble to form a selective pathway for K+across the membrane. However, it remains unclear how the 2 P-domain subunits assemble to form a selective pore. The functional diversity of these families can arise through homo- or hetero-associations of alpha subunits or association with auxiliary cytoplasmic beta subunits. K+channel subunits containing one pore domain can be assigned into one of two superfamilies: those that possess six transmembrane (TM) domains and those that possess only two TM domains. The six TM domain superfamily can be further subdivided into conserved gene families: the voltage-gated (Kv) channels; the KCNQ channels (originally known as KvLQT channels); the EAG-like K+channels; and three types of calcium (Ca)-activated K+channels (BK, IK and SK) []. The 2TM domain family comprises inward-rectifying K+channels. In addition, there are K+channel alpha-subunits that possess two P-domains. These are usually highly regulated K+selective leak channels.Two types of beta subunit (KCNE and KCNAB) are presently known to associate with voltage-gated alpha subunits (Kv, KCNQ and eag-like). However, not all combinations of alpha and beta subunits are possible. The KCNE family of K+ channel subunits are membrane glycoproteins that possess a single transmembrane (TM) domain. They share no structural relationship with the alpha subunit proteins, which possess pore forming domains. The subunits appear to have a regulatory function, modulating the kinetics and voltage dependence of the alpha subunits of voltage-dependent K+ channels. KCNE subunits are formed from short polypeptides of ~130 amino acids, and are divided into five subfamilies: KCNE1 (MinK/IsK), KCNE2 (MiRP1), KCNE3 (MiRP2), KCNE4 (MiRP3) and KCNE1L (AMMECR2). KCNE3 is known to associate with the pore forming subunits KCNQ1, KCNQ4,HERG and Kv3.4. KCNE3 forms complexes with Kv3.4 in skeletal muscle -KCNE3 mutations have been identified in families with skeletal muscledisorders []. In the intestine, KCNE3 associates with KCNQ1 to formchannels that are stimulated by cAMP and are thought to be involved insecretory diarrhoea and cystic fibrosis [].
Protein
Organism: Mus musculus/domesticus
Length: 103  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 123  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 103  
Fragment?: false
Protein
Organism: Mus musculus/domesticus
Length: 123  
Fragment?: false