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The protein encoded by GATA5 is a transcription factor that contains two GATA-type zinc fingers. Zusätzlich bieten wir Ihnen GATA5 Antikörper (73) und GATA5 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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findings show that GATA5 mutations, in addition to heart diseases, can result in congenital abnormalities of the female genitourinary tract in humans
A multivariate regression model revealed that the effects of both the promoter methylation and the exonic SNPs in GATA5 were independent.This interaction between GATA5 variants and GATA5 promoter methylation indicates that the association of either factor with gastric disease progression is modified by the other
These results suggest that the induction of GATA-6 (zeige GATA6 ELISA Kits) dysfunction may be more effective for chemotherapy for colorectal cancer, although the mechanism underlying the synergistic effect of 5-FU and anisomycin remains unknown.
The Correlation between GATA5, WT1 and PAX5 methylation and clinical/histological parameters is suggestive of applicability of these markers in non-invasive (epi)genetic testing in hepatocellular carcinoma (HCC).
we identified gene promoter methylation signatures (WT1 (zeige WT1 ELISA Kits), MSH6, GATA5 and PAX5 (zeige PAX5 ELISA Kits)) that are strongly correlated to, and can have a predictive value for the clinical outcome of oral squamous cell carcinoma patients
Evidence supporting a genetic basis includes the autosomal dominance of Bicuspid aortic valve inheritance patterns, and the identification of mutations in GATA binding protein 5 transcription factor.
Transcriptomic analysis of human microvascular endothelial cells with GATA5 knockdown reveals that GATA5 affects several genes and pathways critical for endothelial function.
This study firstly links GATA5 mutation to DCM, which provides novel insight into the molecular mechanisms of DCM, suggesting a potential molecular target for the prenatal prophylaxis and allele-specific treatment of DCM.
Promoter hypermethylation is an important mechanism of the transcriptional inactivation of GATA5 in invasive ductal breast carcinoma.
A combination of GATA5 and SFRP2 (zeige SFRP2 ELISA Kits) methylation could be promising as a marker for the detection and diagnosis of colorectal cancers and adenomas.
GATA5 is expressed in microvascular endothelial cells and its inactivation in mice leads to vascular endothelial dysfunction and hypertension.
GATA (zeige QRSL1 ELISA Kits) transcription factors are repressors of hedgehog (zeige SHH ELISA Kits) signaling, and NKX3.2 maintains the ability of sclerotomal cells to express SHH (zeige SHH ELISA Kits) transcriptional targets in the presence of BMP signals by repressing the induction of Gata4 (zeige GATA4 ELISA Kits)/5/6
Gata5 deficiency induces airway hyperresponsiveness, at least in part, by blunting apoE (zeige APOE ELISA Kits) and increasing IL-13 (zeige IL13 ELISA Kits) expression.
Expression of Gata5 very efficiently promotes cardiomyocyte fate from murine embryonic stem cells.
USF1 transactivates GATA5 expression by binding to the E-box in its promoter
compound Gata4 (zeige GATA4 ELISA Kits)/Gata5 and Gata5/Gata6 (zeige GATA6 ELISA Kits) mutants die embryonically or perinatally due to severe congenital heart defects
Results unravel a critical cell-autonomous role for endocardial Gata5 in aortic valve formation and identify GATA5 as a potential gene responsible for congenital heart disease in humans.
These results demonstrate functional redundancy between Gata4 and Gata5 during cardiac development and implicate Gata5 as a candidate modifier gene for congenital heart disease.
data reveal that transcription factor GATA5 is required for differentiation of cardiogenic precursors into endothelial endocardial cells
collaboration between GATA-6 (zeige GATA6 ELISA Kits) and GATA-4 (zeige GATA4 ELISA Kits), or GATA-6 (zeige GATA6 ELISA Kits) and GATA-5 which can substitute for GATA-4 (zeige GATA4 ELISA Kits), is involved in the perception of differentiation cues by embryonic stem cells in their determination of endoderm lineage
Data show that GATA4 or 6 regulate both cardiogenic potential and subsequent cardiomyocyte differentiation but that GATA5 is involved in regulating cardiomyocyte differentiation.
identified GATA5 as a SUMO substrate, and lysine 324 (K324) and lysine 360 (K360) as two major modification sites
specification of cardiac fate downstream of gata5 (zeige GATA6 ELISA Kits)/6 involves activation of the tmem88a gene to constrain WNT (zeige WNT2 ELISA Kits) signaling and expand the number of cardiac progenitors.
Overexpression of smarcd3b and gata5 in zebrafish results in an enlarged heart, whereas combinatorial loss of cBAF components inhibits cardiac differentiation, demonstrating that Smarcd3b and Gata5 can induce a primitive, progenitor cell-like state.
First evidence for a regulatory function for gata5 in the formation of Kupffer's vesicle and left-right patterning.
Grl forms a complex with Gata5 through the carboxyl region and can repress Gata5-mediated transcription.
Data show that GATA4 (zeige GATA4 ELISA Kits) knockdown only affects cardiac marker expression in the absence of either GATA5 (zeige GATA6 ELISA Kits) or GATA6 (zeige GATA6 ELISA Kits), suggesting redundancy in this family during myocardial development.
the gata5 genes are redundant for specification of cardiomyocytes.
The protein encoded by this gene is a transcription factor that contains two GATA-type zinc fingers. The encoded protein is known to bind to hepatocyte nuclear factor-1alpha (HNF-1alpha), and this interaction is essential for cooperative activation of the intestinal lactase-phlorizin hydrolase promoter. In other organisms, similar proteins may be involved in the establishment of cardiac smooth muscle cell diversity.
GATA binding factor-5
, GATA-binding factor 5
, GATA-binding protein 5
, transcription factor GATA-5
, Transcription factor GATA-5 (GATA binding factor-5)
, GATA-5 transcription factor
, GATA binding protein 5
, GATA-binding factor 5-A
, transcription factor xGATA-5a