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The single nucleotide polymorphisms (SNPs) of NKX2.5, GATA4, and TBX5 are highly associated with congenital heart diseases in the Chinese population, but not significant in the SNPs of FOG2.
NKX2.5 is expressed in most PTC samples analyzed and its presence correlates to better prognosis of PTC. In vitro, NKX2.5 overexpression reduces the expression of thyroid differentiation markers and increases ROS production.
The findings identify HEY2 as a novel component of the NKX2-5 cardiac transcriptional network.
The vast majority of NKX2-5-mutated patients presented with Ostium Secundum or perimembranous/muscular Ventricular Septal defect.
findings suggested that NKX2-5 63A>G polymorphism and 606G>C polymorphism may not be implicated in the pathogenesis of congenital heart disease (Meta-analysis).
73C>T (R25C) and 63A>G (E21E) SNPs are probably related to thyroid hypoplasia
SIRT1 inhibits the transcriptional activity of Nkx2.5.
PDLIM5 isoforms occurred simultaneously to the onset of expression of the early cardiac transcription factor NKX2.5, known to play a key role in cardiac development
There is no difference in NKX2.5 and TBX5 gene mutations between in vitro fertilization and naturally conceived children with congenital heart disease.
This study is the first to associate NKX2-5 loss-of-function mutations with enhanced susceptibility to sporadic DCM, which provides novel insight into the molecular etiology underpinning DCM
Mapping nsSNPs in genes such as NKX 2-5 would provide valuable information about individuals carrying these polymorphisms, where such variations could be used as diagnostic markers
Hence, the variant distribution of NKX2-5, GATA4 and TBX5 are tightly associated with particular Congenital heart disease subtypes. Further structure-modelling analysis revealed that these mutated amino acid residuals maintain their DNA-binding ability and structural stability
The results of the present study expand the spectrum of NKX2.5 mutations linked to congenital atrial septal defect and atrioventricular block, and indicated that NKX2.5 lossoffunction mutations are an uncommon cause of congenital atrial septal defect and atrioventricular block in humans.
I184F-NK2 homeobox 5 homeobox protein is a novel variant associated with congenital heart disease.
NKX2-5 mutations mainly occur in familial congenital heart defects, the signature phenotype is atrial septal defects with conduction disturbances and mutation carriers are at increased risk of sudden cardiac death.
187QNRRYKCKRQR197 was required for exclusive nuclear localization of NKX2.5.
NKX2.5 and GATA4 gene mutations might participate in the development of congenital heart disease and can promote bone marrow derived stroma cell differentiate into cardiomyocytes.
Data indicate that cells cultured on cardiac muscle laminin (LN)-based substrata in combination with stimulation of the canonical Wnt/beta-catenin pathway showed increased gene expression of ISL1, OCT4, KDR and NKX2.5.
There was no evidence of a role for NKX2-5 and GATA4 CNV in fetal CHD; therefore, these CNV may not be common in fetal CHD in China
Overexpression of Nkx2.5 significantly promotes the differentiation of human umbilical cord drived mesenchymal stem cells into cardiomyocytes.
results indicate that during zebrafish cardiogenesis, Foxc1a is active directly upstream of nkx2.5.
Nkx2.5 signaling via activation of Nkx2.5-Calr-p53 signaling pathway results in cardiac dysfunction and hyperglycemia-induced cardiomyopathy.
Nkx2-5 and nkx2.7 genes restrict proliferation of heart field progenitors in the outflow tract, delimit the number of progenitors at the venous pole and pattern the sinoatrial node acting through Isl1 repression.
These findings validate HRV analysis as a useful quantitative tool for assessment of cardiac health in zebrafish and underscore the importance of nkx2.5 in maintaining normal heart rate and HRV during early conduction system development.
Nkx2.5 is required for proper craniofacial development in zebrafish and acts in part by upregulating ece1 expression.
An early requirement for nkx2.5 ensures the first and second heart field ventricular identity and cardiac function into adulthood.
Flanking a transgenic construct by chicken HS4 insulation sequences from beta globin leads to overall increase in the expression of nkx2.5:mRFP.
studies reveal the heart field origin of PAA endothelium and attribute a new vasculogenic function to the cardiac transcription factor Nkx2.5 during great vessel precursor development
findings show that the homeodomain transcription factors Nkx2.5 and Nkx2.7 are necessary to sustain ventricular chamber attributes through repression of atrial chamber identity.
Embryos injected with an nkx2.5 morpholino exhibited SHF phenotypes caused by compromised progenitor cell proliferation. Co-injecting low doses of nkx2.5 and ltbp3 morpholinos revealed a genetic interaction between these factors.
The cardiac connexin Ecx and its downstream signaling are crucial for establishing nkx2.5 expression, which in turn promotes unidirectional, parallel alignment of myofibrils and the subsequent proper heart morphogenesis.[
nkx genes are essential to establish the original dimensions of the linear heart tube.Nkx genes regulate heart tube extension and exert differential effects on ventricular and atrial cell number.
redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but Nkx2.7 plays a more critical function, regulating the expressions of tbx5 and tbx20 through the maturation stage
Nkx2-5 mutations cause heart defects in Xenopus laevis
HIF-1alpha-regulated nkx2.5 expression is required for heart development in Xenopus
we would like to suggest that FGF expressed in anterior neural ectoderm is a major inducer of Nkx2.5 expression in neighboring cells
This gene encodes a homeobox-containing transcription factor. This transcription factor functions in heart formation and development. Mutations in this gene cause atrial septal defect with atrioventricular conduction defect, and also tetralogy of Fallot, which are both heart malformation diseases. Mutations in this gene can also cause congenital hypothyroidism non-goitrous type 5, a non-autoimmune condition. Alternative splicing results in multiple transcript variants.
NK2 transcription factor related, locus 5
, cardiac-specific homeobox 1
, homeobox protein CSX
, homeobox protein NK-2 homolog E
, homeobox protein Nkx-2.5
, tinman paralog
, Drosophila NK2 transcription factor related, locus 5
, cardiac-specific homeobox
, tinman homeobox homolog
, NK2 transcription factor related 5 b
, NK2 transcription factor related, locus 5 (Drosophila)
, transcription factor NKX2.5
, NK2 transcription factor locus 5-like
, Nkx2.5 protein