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anti-Human GATA4 Antikörper:
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Human Monoclonal GATA4 Primary Antibody für BI, WB - ABIN967667
Oka, Xu, Molkentin: Re-employment of developmental transcription factors in adult heart disease. in Seminars in cell & developmental biology 2007
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Human Polyclonal GATA4 Primary Antibody für ICC, IF - ABIN446790
Virgone, Cecchetto, Ferrari, Bisogno, Donofrio, Boldrini, Collini, DallIgna, Alaggio: GATA-4 and FOG-2 expression in pediatric ovarian sex cord-stromal tumors replicates embryonal gonadal phenotype: results from the TREP project. in PLoS ONE 2012
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Human Monoclonal GATA4 Primary Antibody für ELISA, WB - ABIN969169
Rajagopal, Ma, Obler, Shen, Manichaikul, Tomita-Mitchell, Boardman, Briggs, Garg, Srivastava, Goldmuntz, Broman, Benson, Smoot, Pu: Spectrum of heart disease associated with murine and human GATA4 mutation. in Journal of molecular and cellular cardiology 2007
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Human Monoclonal GATA4 Primary Antibody für ELISA, WB - ABIN4313655
Sato, Okumura, Ariga, Hatakeyama: TRIM6 interacts with Myc and maintains the pluripotency of mouse embryonic stem cells. in Journal of cell science 2012
Human Monoclonal GATA4 Primary Antibody für WB - ABIN2452241
Huang, Chen, Hwang, Yu, Su, Mai, Wang, Cheng, Schuyler, Ma, Lu, Lu: miR-200c and GATA binding protein 4 regulate human embryonic stem cell renewal and differentiation. in Stem cell research 2014
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 (zeige KLF13 Antikörper) is an important component of the transcription network required for heart development and suggest that KLF13 (zeige KLF13 Antikörper) 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.
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 (zeige BMP2 Antikörper) 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 (zeige NKX2-5 Antikörper), GATA4 and TBX5 (zeige TBX5 Antikörper) 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 (zeige TBX5 Antikörper))genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.
Meta-analysis suggested that GATA4 99 G>T and 487 C>T mutations may not be related to the incidence of congenital heart disease (CHD (zeige CHDH Antikörper)). However, GATA4 354 A>C mutation was significantly associated with CHD (zeige CHDH Antikörper) risk.
common variants in 3'UTR (zeige UTS2R Antikörper) of the GATA4 gene jointly interact, affecting the congenital heart disease susceptibility, probably by altering microRNA posttranscriptional regulation
Our studies suggest that GATA5 (zeige GATA5 Antikörper) but especially GATA4 are main contributors to SCN5A (zeige SCN5A Antikörper) gene expression, thus providing a new paradigm of SCN5A (zeige SCN5A Antikörper) expression regulation that may shed new light into the understanding of cardiac disease.
GATA4-G296S mutation led to failure of GATA4 and TBX5 (zeige TBX5 Antikörper)-mediated repression at non-cardiac genes and enhanced open chromatin states at endothelial/endocardial promoters. These results reveal how disease-causing missense mutations can disrupt transcriptional cooperativity, leading to aberrant chromatin states and cellular dysfunction, including those related to morphogenetic defects.
investigation of genes regulated by GATA4, GATA6 (zeige GATA6 Antikörper), and both in combination: studies in granulosa cells primed for luteinization
GATA-4 and C/EBPbeta (zeige CEBPB Antikörper) are both required for FSH (zeige BRD2 Antikörper) +/- IGF-I (zeige IGF1 Antikörper) stimulation of the porcine steroidogenic acute regulatory protein (zeige STAR Antikörper) gene promoter in homologous granulosa cell cultures.
The altered ratio of GATA4 to GATA6 (zeige GATA6 Antikörper) after ovulation may allow GATA6 (zeige GATA6 Antikörper) to enhance STAR mRNA accumulation.
Mechanistically, decreased GATA4 levels caused the downregulation of several pro-regenerative genes (among them interleukin-13 (zeige IL13 Antikörper), Il13 (zeige IL13 Antikörper)) 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 (zeige WT1 Antikörper) 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 (zeige HELLS Antikörper) were both involved in regulating GATA4 expression, but Nkx2.5 (zeige NKX2-5 Antikörper) expression was not regulated by DNA methylation (zeige HELLS Antikörper). 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 (zeige KLK6 Antikörper) 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 (zeige NR2E3 Antikörper) by negatively regulating the Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) signaling pathway and positively regulating the cardiogenic TF Gata4
GATA4 and GATA6 (zeige GATA6 Antikörper) are essential for female fertility, whereas targeting either factor alone causes subfertility. GATA4 and GATA6 (zeige GATA6 Antikörper) are also required for the expression of the receptors for prolactin (zeige PRL Antikörper) and luteinizing hormone.
Loss of Gata4 in Sertoli cells impairs the spermatogonial stem cell niche and causes germ cell exhaustion by attenuating chemokine (zeige CCL1 Antikörper) signaling.
The activity of Gata4 cardiac enhancer in transgenic embryos and in cultured aortic endothelial cells is dependent on four ETS (zeige ETS1 Antikörper) sites.
Study finds that emergent juvenile cortical cardiomyocytes induce expression of gata4 in a manner similar to during regeneration.
ATOH8 (zeige ATOH8 Antikörper), GATA4, and FOG2 (zeige ZFPM2 Antikörper) associate in a single complex
gata4 gene regulates sdf1a (zeige CXCL12 Antikörper) levels during early embryogenesis
mga (zeige MGA Antikörper) 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 (zeige GATA6 Antikörper) have distinct non-redundant functions in cardiac morphogenesis (zeige XIRP1 Antikörper), but are redundant for an early step of liver development; and Gata4 and Gata6 (zeige GATA6 Antikörper) 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 (zeige GATA6 Antikörper) or GATA6 (zeige GATA6 Antikörper), 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