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Validated All-in-One™ qPCR Primer for GATA3(NM_001002295.1) Search again
Product ID:
HQP007165
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HDR, HDRS
Gene Description:
GATA binding protein 3
Target Gene Accession:
NM_001002295.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Strong GATA-3 binding to an oligonucleotide containing two GATA-3 motifs has been mapped at a DNase hypersensitivity site in cluster IV of the CD8 gene complex.
- Identification of an alternative GATA-3 promoter directing tissue-specific gene expression
- A marked reduction in both GATA-3 mRNA and protein expression in HPV-immortalized cell lines was confirmed in cervical carcinoma cell lines.
- GATA-3 transcriptional imprinting in Th2 lymphocytes: a mathematical model. GATA-3 autoactivation creates a bistable system that can memorize a transient inductive signal.
- VZV virus and mite antigens induce expression of this transcription factor in cord blood mononuclear cells, differenetially affecting Th1 and Th2 cells
- GATA-3 is an important transcription factor in regulating human Th2 cell differentiation in vivo.
- GATA3 mutations may have a role in the hypoparathyroidism, deafness, and renal dysplasia (HDR) syndrome
- GATA3 plays important roles in the maintenance of the Th2 phenotype and continuous chromatin remodeling of the specific Th2 cytokine gene locus through cell division.
- GATA-3 suppresses IFN-gamma promoter activity independently of binding to cis-regulatory elements
- Erythropoietin (Epo) gene expression is under the control of hypoxia-inducible factor 1 (HIF-1), and is negatively regulated by GATA3.
- GATA3 is involved in growth control and the maintenance of the differentiated state in epithelial cells and may contribute to tumorigenesis in breast cancer.
- Expressed in Hodgkin disesase Reed Sternberg cells.
- GATA-3 binds and transactivates the NKG2A promoter; coexpression of human GATA-3 with an NKG2A promoter construct in K562 cells leads to enhanced promoter activity.
- interleukin-5 transcription repression by the glucocorticoid receptor targets GATA3 signaling and involves histone deacetylase recruitment
- GATA3 is crucially involved in IL-5 gene transcription in human peripheral CD4-positive t cells.
- strong specific upregulation of Gata-3 impaired nuclear translocation and its cooperative action with the TGF-beta pathway, suggesting that Gata-3 plays a central role in human pancreatic cancer
- DL1-induced activation of the Notch1 pathway controls the lineage commitment of early thymic precursors by altering the levels between Spi-B and GATA-3.
- Low expression of GATA3 is associated with invasive breast carcinomas
- Segmental allergen challenge in asthmatics leads to increased GATA-3, c-maf and T-bet expression in BAL cells but not in bronchial biopsies
- Direct sequencing after PCR amplification of genomic DNA revealed a novel insertional mutation (405insC) in the GATA3 gene of two patients with HDR syndrome (Hypoparathyroidism, sensorineural Deafness and Renal anomaly syndrome).
- Three novel mutations in the GATA3 gene responsible for familial hypoparathyroidism and deafness.
- the GATA-3/T-bet transcription factor complex regulates the cell-lineage-specific expression of the lymphocyte homing receptors
- GATA3 is probably a mediator for the transcriptional upregulation of MUC1 expression in some breast cancers.
- Overexpression of GATA3 rescues T-helper type 2 (Th2) cytokine expression in protein kinase C theta-deficient transgenic Th2 cells.
- A novel heterozygous deletion frameshift mutation of GATA3 in a Japanese kindred with the hypoparathyroidism, deafness and renal dysplasia syndrome.
- There is an association between expression of Th1/Th2 transcription factors and cytokines (T-bet, GATA-3, IFN-gamma, IL-4,IL-18) in systemic lupus erythematosus.
- No mutations were identified in patients with isolated hypoparathyroidism, thereby indicating that GATA3 abnormalities are more likely to result in two or more of the phenotypic features of the HDR syndrome.
- The human GATA-3 gene is not regulated in response to polarizing signals that are sufficient to direct Th2-specific expression in mouse cells.
- E2A proteins prevent lymphoma cell expansion, at least in part through regulation of Gfi1b and modulation of Gata3 expression.
- GATA-3 nuclear translocation is dependent on its phosphorylation on serine residues by p38 MAPK
- GATA3 establishes a positive feedback loop that increases transgenic T-cell receptor surface expression in developing CD4 lineage cells.
- Gata-3 has a role in specifying and maintaining mammary cell fate
- WNT8B expression in hepatocyte progenitors derived from human ES cells is due to POU5F1 (OCT3/OCT4) and GATA3, and WNT8B expression in diffuse-type gastric cancer is due to POU5F1 and GATA6
- GATA-3 is a critical component of the master cell-type-specific transcriptional network including ER alpha and FoxA1 that dictates the phenotype of hormone-dependent breast cancer
- GATA-3 expression in bone marrow stromal cells from chronic aplastic anemia was significantly higher than controls. Expression levels of GATA genes may influence hematopoiesis in BM microenvironment & relate to the pathogenesis/development of AA.
- Gata3 is a critical element determining inductive T helper (Th) type 2 cell differentiation and limiting Th1 differentiation by Notch.
- Transactivation by GATA-3 increased luciferase expression 100-fold, in the absence of stimulation. Synergistic interactions were demonstrated between Ets1, GATA-3 and AP-1.
- Gene-gene interaction between GATA3 and IL13 polymorphisms can influence the risk of childhood rhinitis.
- Direct interactions between NKX2-5 and GATA3 as indicated by co-immunoprecipitation data may contribute to MEF2C regulation.
- Role in the proliferaative and regenerative capacity of mammary stem and progenitor cells.
- The expression patterns of T-Bet and GATA-3 oppose progesterone receptor, suggesting antagonistic function and/or regulation between PR and T-Bet/GATA-3
- GATA-3 is a breast cancer marker almost exclusively expresses among ER-positive tumors.
- A SNP in GATA3 is associated with atopic eczema. This finding highlights the importance of GATA3 as an immune-modulating gene in atopic eczema.
- GATA3 is hypothesized to be integral to the ERalpha pathway
- the T cell receptor-mediated induction of Gfi1 controls Th2 cell differentiation through the regulation of GATA3 protein stability
- cyclic AMP signals enhance histone H3 acetylation at the IL-5 promoter and the concerted binding of GATA-3 and NFATc to the promoter.
- GlcNAc6ST-1 transcription is coordinated with the NF-kappaB/GATA-3 axis, which is known to figure heavily in Th2 cell differentiation
- expression of S100P, GATA3, and p63 by a majority of ovarian Brenner tumors underscores the similarity between these neoplasms and urothelial proliferations of bladder origin.