GATA Binding Protein 5 (GATA5) ELISA Kits

Human GATA Binding Protein 5 (GATA5) Interaktionspartner

1. findings show that GATA5 mutations, in addition to heart diseases, can result in congenital abnormalities of the female genitourinary tract in humans

2. 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

3. These results suggest that the induction of GATA-6 dysfunction may be more effective for chemotherapy for colorectal cancer, although the mechanism underlying the synergistic effect of 5-FU and anisomycin remains unknown.

4. 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).

5. we identified gene promoter methylation signatures (WT1, MSH6, GATA5 and PAX5) that are strongly correlated to, and can have a predictive value for the clinical outcome of oral squamous cell carcinoma patients

6. 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.

7. Transcriptomic analysis of human microvascular endothelial cells with GATA5 knockdown reveals that GATA5 affects several genes and pathways critical for endothelial function.

8. 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.

9. Promoter hypermethylation is an important mechanism of the transcriptional inactivation of GATA5 in invasive ductal breast carcinoma.

10. A combination of GATA5 and SFRP2 methylation could be promising as a marker for the detection and diagnosis of colorectal cancers and adenomas.

11. A new potentially pathogenic variant in GATA5 contributes to the development of bicuspid aortic valve syndrome.

12. DSVs in the GATA5 gene promoter may increase the susceptibility to the development of VSD as a risk factor.

13. Rare sequence variants, p.Gln3Arg and p.Leu233Pro, in GATA5 are associated with human bicuspid aortic valve.

14. study provides genetic evidence on the association of GATA5 loss-of-function mutations with enhanced susceptibility to bicuspid aortic valve (BAV), providing novel insight into the molecular mechanism involved in human BAV

15. Results of this study showed an association of somatic GATA5 mutations with TOF, providing further insight into the underlying molecular mechanism of TOF.

16. Epigenetic alterations in GATA family members may be associated with aggressive tumor phenotypes in renal cell cancer

17. Reduced GATA5 mRNA levels are associated with a poor clinical outcome, indicating a possible role of GATA5 for the development of aggressive clear cell renal cell carcinoma.

18. GATA5, possibly through upregulation of eNOS, plays a role in the development of aortic dilatation in patients with unicuspid and bicuspid aortic valves.

19. GATA5 mutations were associated with congenital heart disease.

20. The findings expand the spectrum of GATA5 mutations linked to atrial fibrillation and provide novel insights into the molecular mechanism involved in the pathogenesis of atrial fibrillation

Mouse (Murine) GATA Binding Protein 5 (GATA5) Interaktionspartner

1. GATA5 is expressed in microvascular endothelial cells and its inactivation in mice leads to vascular endothelial dysfunction and hypertension.

2. GATA transcription factors are repressors of hedgehog signaling, and NKX3.2 maintains the ability of sclerotomal cells to express SHH transcriptional targets in the presence of BMP signals by repressing the induction of Gata4/5/6

3. Gata5 deficiency induces airway hyperresponsiveness, at least in part, by blunting apoE and increasing IL-13 expression.

4. Expression of Gata5 very efficiently promotes cardiomyocyte fate from murine embryonic stem cells.

5. USF1 transactivates GATA5 expression by binding to the E-box in its promoter

6. compound Gata4/Gata5 and Gata5/Gata6 mutants die embryonically or perinatally due to severe congenital heart defects

7. 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.

8. These results demonstrate functional redundancy between Gata4 and Gata5 during cardiac development and implicate Gata5 as a candidate modifier gene for congenital heart disease.

9. data reveal that transcription factor GATA5 is required for differentiation of cardiogenic precursors into endothelial endocardial cells

10. collaboration between GATA-6 and GATA-4, or GATA-6 and GATA-5 which can substitute for GATA-4, is involved in the perception of differentiation cues by embryonic stem cells in their determination of endoderm lineage

11. GATA5 is not expressed in Sertoli cells. Transfected GATA5 & GATA4 work together with human AR to activate human PSA transcription.

12. Report alternative promoter and GATA5 transcripts in mouse.

Xenopus laevis GATA Binding Protein 5 (GATA5) Interaktionspartner

1. Data show that GATA4 or 6 regulate both cardiogenic potential and subsequent cardiomyocyte differentiation but that GATA5 is involved in regulating cardiomyocyte differentiation.

Zebrafish GATA Binding Protein 5 (GATA5) Interaktionspartner

1. identified GATA5 as a SUMO substrate, and lysine 324 (K324) and lysine 360 (K360) as two major modification sites

2. specification of cardiac fate downstream of gata5/6 involves activation of the tmem88a gene to constrain WNT signaling and expand the number of cardiac progenitors.

3. 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.

4. First evidence for a regulatory function for gata5 in the formation of Kupffer's vesicle and left-right patterning.

5. Grl forms a complex with Gata5 through the carboxyl region and can repress Gata5-mediated transcription.

6. 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.

7. the gata5 genes are redundant for specification of cardiomyocytes.