Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Select your species
Data show that GATA4 or 6 regulate both cardiogenic potential and subsequent cardiomyocyte differentiation but that GATA5 is involved in regulating cardiomyocyte differentiation.
Results describe the expression of GATA4 and 6 during gastrulation and their function in migratory behaviour.
The data demonstrate that KLF13 (Montrer KLF13 Kits ELISA) is an important component of the transcription network required for heart development and suggest that KLF13 (Montrer KLF13 Kits ELISA) is a GATA-4 modifier
Data show that GATA4 knockdown only affects cardiac marker expression in the absence of either GATA5 or GATA6, suggesting redundancy in this family during myocardial development.
These results indicate a higher capacity of adipose-derived than bone marrow-derived mesenchymal stem cells to express GATA4.
GATA4 is a regulator of osteoblastic differentiation via the p38 (Montrer CRK Kits ELISA) signaling pathways.
miR (Montrer MLXIP Kits ELISA)-126 inhibits the migration and invasion of glioma cells, which may be linked to GATA4 as a target gene.
Study identified effects of GATA4 variant [(SNP) rs13273672] on regional gray matter (GM) volume in alcohol dependence: higher GM volume in the hypothalamus and caudate in the AA genotype group compared to the AG/GG group. GM volume specific to GATA4 variant predicted heavy relapse risk within 60 d following discharge for both caudate and amygdala and within 90 d for the amygdala only.
The role of GATA4 was elucidated in alcohol dependence susceptibility by identifying rare genetic variants.
disruption of GATA4-mediated transactivation in hepatocellular carcinoma suppresses hepatocyte epithelial differentiation to sustain replicative precursor phenotype
This study attempts to correlate the pattern of intronic variants of GATA4 gene which might provide new insights to unravel the possible molecular etiology of congenital heart disease.
GATA4 induces autocrine BMP2 (Montrer BMP2 Kits ELISA) signaling in endothelial cells
study identified a novel mutation in GATA4 that likely contributed to the Congenital Heart Disease in this family. This finding expanded the spectrum of GATA4 mutations and underscored the pathogenic correlation between GATA4 mutations and Congenital Heart Disease.
Hence, the variant distribution of NKX2-5 (Montrer NKX2-5 Kits ELISA), GATA4 and TBX5 (Montrer TBX5 Kits ELISA) 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
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4, cand TBX5 (Montrer TBX5 Kits ELISA))genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.
investigation of genes regulated by GATA4, GATA6 (Montrer GATA6 Kits ELISA), and both in combination: studies in granulosa cells primed for luteinization
GATA-4 and C/EBPbeta (Montrer CEBPB Kits ELISA) are both required for FSH (Montrer BRD2 Kits ELISA) +/- IGF-I (Montrer IGF1 Kits ELISA) stimulation of the porcine steroidogenic acute regulatory protein (Montrer STAR Kits ELISA) gene promoter in homologous granulosa cell cultures.
The altered ratio of GATA4 to GATA6 (Montrer GATA6 Kits ELISA) after ovulation may allow GATA6 (Montrer GATA6 Kits ELISA) to enhance STAR mRNA accumulation.
Mechanistically, decreased GATA4 levels caused the downregulation of several pro-regenerative genes (among them interleukin-13 (Montrer IL13 Kits ELISA), Il13 (Montrer IL13 Kits ELISA)) in the myocardium.
GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence, which are indispensable for liver development.
study provides novel insights into the role of WT1 (Montrer WT1 Kits ELISA) and GATA4 during the sex differentiation phase and represents an approach that can be applied to assess other proteins with as yet unknown functions during gonadal development
we have identified a distinct lineage of adult HSCs characterized by its derivation of progenitors where Gata4 expression is activated by a specific enhancer. Most adult HSCs belonging to this lineage probably originate in the placenta.
Histone acetylation/methylation and DNA methylation (Montrer HELLS Kits ELISA) were both involved in regulating GATA4 expression, but Nkx2.5 (Montrer NKX2-5 Kits ELISA) expression was not regulated by DNA methylation (Montrer HELLS Kits ELISA). These three modifications had high correlation with each other during regulation of GATA4 and produced a regulation loop at the GATA4 promoter.
GATA4 acts as a negative regulator of Bsp (Montrer KLK6 Kits ELISA) expression in osteoblasts.
Detailed analysis of specific lineage markers expression showed selective downregulation of endoderm markers in REST-null cells, thus contributing to a loss of cardiogenic signals. REST regulates cardiac differentiation of ESCs (Montrer NR2E3 Kits ELISA) by negatively regulating the Wnt (Montrer WNT2 Kits ELISA)/beta-catenin (Montrer CTNNB1 Kits ELISA) signaling pathway and positively regulating the cardiogenic TF Gata4
GATA4 and GATA6 (Montrer GATA6 Kits ELISA) are essential for female fertility, whereas targeting either factor alone causes subfertility. GATA4 and GATA6 (Montrer GATA6 Kits ELISA) are also required for the expression of the receptors for prolactin (Montrer PRL Kits ELISA) and luteinizing hormone.
Loss of Gata4 in Sertoli cells impairs the spermatogonial stem cell niche and causes germ cell exhaustion by attenuating chemokine (Montrer CCL1 Kits ELISA) signaling.
The activity of Gata4 cardiac enhancer in transgenic embryos and in cultured aortic endothelial cells is dependent on four ETS (Montrer ETS1 Kits ELISA) sites.
Study finds that emergent juvenile cortical cardiomyocytes induce expression of gata4 in a manner similar to during regeneration.
ATOH8, GATA4, and FOG2 (Montrer ZFPM2 Kits ELISA) associate in a single complex
gata4 gene regulates sdf1a (Montrer CXCL12 Kits ELISA) levels during early embryogenesis
mga (Montrer MGA Kits ELISA) restricts the normal levels of Gata4 required for heart tube looping.
Through the use of a transgenic reporter strain, we found that cardiomyocytes throughout the subepicardial ventricular layer trigger expression of the embryonic cardiogenesis gene gata4 within a week of trauma
Gata4 and Gata6 (Montrer GATA6 Kits ELISA) have distinct non-redundant functions in cardiac morphogenesis (Montrer XIRP1 Kits ELISA), but are redundant for an early step of liver development; and Gata4 and Gata6 (Montrer GATA6 Kits ELISA) are essential and non-redundant for liver growth following initial budding
Data show that GATA4 knockdown only affects cardiac marker expression in the absence of either GATA5 (Montrer GATA6 Kits ELISA) or GATA6 (Montrer GATA6 Kits ELISA), suggesting redundancy in this family during myocardial development.
Results suggest that GATA4 and -6 play a key role in the regulation of ventricular myosin heavy chain gene expression in the ventricle.
This gene encodes a member of the GATA family of zinc-finger transcription factors. Members of this family recognize the GATA motif which is present in the promoters of many genes. This protein is thought to regulate genes involved in embryogenesis and in myocardial differentiation and function. Mutations in this gene have been associated with cardiac septal defects.
GATA binding protein 4
, glutamyl-tRNA(Gln) amidotransferase subunit A
, GATA-4 zinc-finger transcription factor
, gata4 transcription factor
, GATA-4 transcription factor
, GATA-binding factor 4
, transcription factor GATA-4
, GATA-binding protein 4
, DNA-binding protein GATA-GT2
, transcription factor GATA4
, transcription factor xGATA-4