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Statements

Subject Item
n2:RIV%2F00216208%3A11110%2F14%3A10281055%21RIV15-MSM-11110___
rdf:type
skos:Concept n20:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1371/journal.pone.0107041
dcterms:description
The heart is the first organ required to function during embryonic development and is absolutely necessary for embryo survival. Cardiac activity is dependent on both the sinoatrial node (SAN), which is the pacemaker of heart's electrical activity, and the cardiac conduction system which transduces the electrical signal though the heart tissue, leading to heart muscle contractions. Defects in the development of cardiac electrical function may lead to severe heart disorders. The Erbb2 (Epidermal Growth Factor Receptor 2) gene encodes a member of the EGF receptor family of receptor tyrosine kinases. The Erbb2 receptor lacks ligand-binding activity but forms heterodimers with other EGF receptors, stabilising their ligand binding and enhancing kinase-mediated activation of downstream signalling pathways. Erbb2 is absolutely necessary in normal embryonic development and homozygous mouse knock-out Erbb2 embryos die at embryonic day (E)10.5 due to severe cardiac defects. We have isolated a mouse line, l11Jus8, from a random chemical mutagenesis screen, which carries a hypomorphic missense mutation in the Erbb2 gene. Homozygous mutant embryos exhibit embryonic lethality by E12.5-13. The l11Jus8 mutants display cardiac haemorrhage and a failure of atrial function due to defects in atrial electrical signal propagation, leading to an atrial-specific conduction block, which does not affect ventricular conduction. The l11Jus8 mutant phenotype is distinct from those reported for Erbb2 knockout mouse mutants. Thus, the l11Jus8 mouse reveals a novel function of Erbb2 during atrial conduction system development, which when disrupted causes death at mid-gestation. The heart is the first organ required to function during embryonic development and is absolutely necessary for embryo survival. Cardiac activity is dependent on both the sinoatrial node (SAN), which is the pacemaker of heart's electrical activity, and the cardiac conduction system which transduces the electrical signal though the heart tissue, leading to heart muscle contractions. Defects in the development of cardiac electrical function may lead to severe heart disorders. The Erbb2 (Epidermal Growth Factor Receptor 2) gene encodes a member of the EGF receptor family of receptor tyrosine kinases. The Erbb2 receptor lacks ligand-binding activity but forms heterodimers with other EGF receptors, stabilising their ligand binding and enhancing kinase-mediated activation of downstream signalling pathways. Erbb2 is absolutely necessary in normal embryonic development and homozygous mouse knock-out Erbb2 embryos die at embryonic day (E)10.5 due to severe cardiac defects. We have isolated a mouse line, l11Jus8, from a random chemical mutagenesis screen, which carries a hypomorphic missense mutation in the Erbb2 gene. Homozygous mutant embryos exhibit embryonic lethality by E12.5-13. The l11Jus8 mutants display cardiac haemorrhage and a failure of atrial function due to defects in atrial electrical signal propagation, leading to an atrial-specific conduction block, which does not affect ventricular conduction. The l11Jus8 mutant phenotype is distinct from those reported for Erbb2 knockout mouse mutants. Thus, the l11Jus8 mouse reveals a novel function of Erbb2 during atrial conduction system development, which when disrupted causes death at mid-gestation.
dcterms:title
Erbb2 Is Required for Cardiac Atrial Electrical Activity during Development Erbb2 Is Required for Cardiac Atrial Electrical Activity during Development
skos:prefLabel
Erbb2 Is Required for Cardiac Atrial Electrical Activity during Development Erbb2 Is Required for Cardiac Atrial Electrical Activity during Development
skos:notation
RIV/00216208:11110/14:10281055!RIV15-MSM-11110___
n4:aktivita
n5:P n5:I
n4:aktivity
I, P(GA13-12412S), P(GAP302/11/1308)
n4:cisloPeriodika
9
n4:dodaniDat
n15:2015
n4:domaciTvurceVysledku
n13:5754623 n13:4490010
n4:druhVysledku
n6:J
n4:duvernostUdaju
n16:S
n4:entitaPredkladatele
n17:predkladatel
n4:idSjednocenehoVysledku
14908
n4:idVysledku
RIV/00216208:11110/14:10281055
n4:jazykVysledku
n7:eng
n4:klicovaSlova
embryo; atria; conduction system; mouse; heart
n4:klicoveSlovo
n11:atria n11:embryo n11:heart n11:conduction%20system n11:mouse
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[27F3E9D8B03E]
n4:nazevZdroje
PLoS ONE
n4:obor
n12:FA
n4:pocetDomacichTvurcuVysledku
2
n4:pocetTvurcuVysledku
8
n4:projekt
n10:GA13-12412S n10:GAP302%2F11%2F1308
n4:rokUplatneniVysledku
n15:2014
n4:svazekPeriodika
9
n4:tvurceVysledku
Sedmera, David Cloves, Christopher Wolton, Kathryn Hentges, Kathryn Wright, Jayne A. Tenin, Gennadiy Krejčí, Eliška Lowell, Simon C.
n4:wos
000343671700027
s:issn
1932-6203
s:numberOfPages
13
n3:doi
10.1371/journal.pone.0107041
n19:organizacniJednotka
11110