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Validated All-in-One™ qPCR Primer for GATA1(NM_002049.3) Search again
Product ID:
HQP098354
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ERYF1, GATA-1, GF-1, GF1, HAEADA, NF-E1, NFE1, XLANP, XLTDA, XLTT
Gene Description:
GATA binding protein 1
Target Gene Accession:
NM_002049.3(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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Summary
This gene encodes a protein which belongs to the GATA family of transcription factors. The protein plays an important role in erythroid development by regulating the switch of fetal hemoglobin to adult hemoglobin. Mutations in this gene have been associated with X-linked dyserythropoietic anemia and thrombocytopenia. [provided by RefSeq].
Gene References into function
- The nature of the amino acid substitution at position 218 of the Nf of GATA1 is of crucial importance in determining the severity of the phenotype in X-linked macrothrombocytopenia patients and possibly also in inducing skewed X inactivation.
- Essential and instructive roles of GATA factors in eosinophil development.
- GATA-1 and GATA-2 gene expression is related to the severity of dysplasia in myelodysplastic syndrome.
- findings indicate that loss of wildtype GATA1 constitutes one step in the pathogenesis of acute megakaryoblastic leukemia in Down syndrome
- with NF-E2, mediates expression of alpha-spectrin gene promoter in erythroid cells in vitro
- X-linked thrombocytopenia with thalassemia from a mutation in the amino finger of GATA-1 affects DNA binding rather than FOG-1 interaction.
- Interacts with other transcription factors to regulate transcription of the gene encoding eosinophil granule major basic protein.
- role in regulating megakaryocyte-specific glycoprotein VI promoter
- REVIEW: Roles of hematopoietic transcription factors GATA-1 and GATA-2 in the development of red blood cell lineage
- Erythroid and megakaryocytic lineage differentiation and maturation are regulated via cooperation between transcription factor GATA1 and its essential cofactor FOG1. It depends on the binding of FOG1 to the N-terminal zinc finger of GATA1.
- anthracyclines can induce the erythroid differentiation of neoplastic cells by activating the transcription factor GATA-1, probably via its clustering into nuclear foci.
- levels of GATA-1 and gamma-globin mRNA were increased in cells treated with progesterone; data suggest interactions of steroid receptors with basal transcriptional machinery and with transcription factors might mediate their transcriptional effects
- GATA1 is likely to play a critical role in the etiology of transient myeloproliferative disorder, and mutagenesis of GATA1 represents a very early event in DS myeloid leukemogenesis.
- how RUNX1 might program divergence from the erythroid pathway to the megakaryocytic lineage commitment through functional and physical interactions with GATA-1
- Findings suggest a model of malignant transformation in Down syndrome AMKL in which GATA1 mutations are an early event and AMKL arises from latent TL clones following initial apparent remission.
- EDRF1 regulated alpha- and gamma-globin gene synthesis by modulating DNA-binding activity of GATA-1 transcription factor.
- findings suggest that acquired intrauterine inactivating mutations in GATA1 and generation of GATA1s cooperate frequently with trisomy 21 in initiating megakaryoblastic proliferation, but are insufficient for progression to AMKL.
- Fli-1 and GATA-1 work together to activate the expression of genes associated with the terminal differentiation of megakaryocytes
- expression of GATA-1 with a defective N-terminal activation domain contributes to the expansion of transient myeloproliferative disorder blast cells and other genetic changes contribute to the development of acute megakaryocytic leukemia in Down syndrome
- GATA-1 instigates GATA-2 repression by means of disruption of positive autoregulation, followed by establishment of a domain-wide repressive chromatin structure.
- GATA1 mutations in Down syndrome and its altered role in DS and myeloid leukemia may lead to an increased understanding of why children with DS are markedly predisposed to leukemia. (review)
- Altogether, these results demonstrate for the first time the implication of GATA-1 in differentiation-specific variations of GSTP1-1 expression
- GATA1 is likely to play a critical role in the etiology of myeloproliferative disorder and Down syndrome acute megakaryoblastic leukemia, and mutagenesis of GATA1 represents a very early event in DS myeloid leukemogenesis
- Mutations in GATA1 occur in Down syndrome, acute Megakaryoblastic Leukemia amd myeloproliferative disorders.
- GATA-1 has a role in erythropoiesis and megakaryocytopoiesis
- Presence of several GATA1 binding sites in the CDAsf promoter and the uniform detection of GATA1 mutations in DS megakaryocytic leukemia suggested the potential role of GATA1 in regulating CDA transcription.
- IL-1beta up-regulates expression in megakaryocytic cells
- mode of vascular regulation in which GATA-1 controls NK-B synthesis in erythroid cells
- Results suggest that the GATA-1 transcription factor represents a cell type-restricted mediator of interferon-gamma induction of the HLA-E gene.
- some cis-elements regulating human and mouse GATA1 genes differ.
- These results define a novel regulatory pathway linking the transcription factors c-Jun, HERP2, and GATA-1.
- Ski cooperates in the process of transformation in erythroid cells by interfering with GATA1 function
- Notch1 inhibits the development of erythroid/megakaryocytic cells by suppressing GATA-1 activity through HES1
- a multiprotein complex containing GATA-1, Oct-1, and other protein factors may contribute to the formation of a repressive chromatin structure that silences gamma-globin gene expression
- 3D structure of a complex comprising the interaction domains of FOG1 and GATA1 reveals how zinc fingers can act as protein recognition motifs and provides a molecular explanation for how GATA-1 mutations contribute to distinct, related genetic diseases.
- GATA1 protein reveals specific functions of a particular posttranscriptional modification[Review].
- results are consistent with GATA1 regulating some but not all pathways of platelet activation
- We show that the dominant action of GATA1s leads to hyperproliferation of a unique, previously unrecognized yolk sac and fetal liver progenitor, which we propose accounts for the transient nature of TMD and the restriction of DS-AMKL to infants.
- Mutated in acute myelocytic leukemia combined with acute lymphocytic leukemia in a case report.
- identified an AHSP gene erythroid promoter with functionally important binding sites for GATA-1- and Oct-1-related proteins
- GATA1 increased endogenous hRFC-A1/A2 transcripts. Altogether, our results demonstrate a transcriptionally important region in the hRFC-A1/A2 promoter including E-box and GATA elements.
- Acute megakaryocytic leukemia in Down syndrome may be identified by microarray analysis and that differential gene expression and reflect relative transactivation capacities of the GATA1s and full-length GATA1 proteins.
- data suggest that GATA-1 is a critical transcription factor to fix erythroid progenitors to the erythroid lineage
- The patient-specific GATA1 mutants interacted efficiently with RUNX1 and retained their ability to act synergistically with RUNX1 on the megakaryocytic GP1balpha promoter, whereas the levels of transcriptional activities were diverse among the mutants.
- The effects of the EBV nuclear antigen 3C on the activities of Nm23-H1 via GATA-1 and Sp1 are reported.
- The functiuonal interaction of CP2 with GATA1 in the regulation of erythroid promoters was studied.
- GATA-1 may have a role in Down syndrome leukemogenesis [review]
- PU.1-Ets domain and the GATA-1 C-terminal zinc finger (CF) form a low affinity interaction in which specific regions of each protein are implicated.
- Hb F level of 59.5% suggests a role for GATA-1 in globin switching
- in erythroid precursors undergoing terminal differentiation, Hsp70 prevents active caspase-3 from cleaving GATA-1 and inducing apoptosis
- These results imply that GATA-1 is sufficient to direct chromatin structure reorganization within the beta-globin locus control region and an erythroid pattern of gene expression in the absence of other hematopoietic transcription factors.
- GATA-1 plays an essential role in the induction of ERCC1 through the mitogen-activated protein kinase (MAPK) pathway.
- findings suggest that GATA1 mutations are not frequent occurrences in the evolution of blast crisis from chronic myeloid leukaemia chronic phase
- GATA1 and GFI1B interplay to regulate bcl-X protein transcription.
- present study has carried out detailed ultrastructural studies of abnormal platelet morphology in one, previously described family with a GATA-1 G208S mutation
- GATA1 mutation is associated with Down syndrome related acute megakaryoblastic leukemia
- There was no difference in the expression level of GATA-1 gene in the bone marrow stromal cells between normal controls and chronic aplastic anemia group.
- study describes the second family with a GATA1G208R allele causing congenital dyserythropoietic anemia and thrombocytopenia
- findings support the concept that GATA-1 platelets are macrothrombocytes because they are not able to detach normally from each other during separation from megakaryocyte proplatelets
- disorder derived from GATA1 Arg216Gln mutation is X-linked thrombocytopenia with thalassemia
- Myeloid leukemia in children 4 years or older with Down syndrome often lacks GATA1 mutation and cytogenetics and risk of relapse are more akin to sporadic AML.
- GATA-1 binding sites in exon 1 constitute key regulatory elements in differential expression of PPOX in erythroid and non-erythroid cells.
- Altered SDF-1/CXCR4 axis in patients with primary myelofibrosis and in the Gata1 low mouse model of the disease
- These results suggest that the GATA motif under study has a functional role in silencing gamma-globin gene expression in adults.
- Results support the idea that GATA-1 interaction in DNase I hypersensitive site 2 has a prominent and direct role in co-activator and RNA polymerase II recruitment.
- The inhibition of the EDAG gene by PMA is mediated through down-regulation of transcription factor GATA-1.
- Abnormalities in the myeloid progenitor compartment in Down syndrome fetal liver precede acquisition of GATA1 mutations.
- D6 expression is GATA1 dependent
- functional and physical interaction of GATA-1 with components of the positive transcriptional elongation factor P-TEFb
- analysis of human phenotypes associated with GATA-1 mutations
- TALIN WAS UNDETECTABLE IN THE CYTOSKELETAL PROTEINS OF THE GATA-1,G208S MACROTHROMBOCYTES OF 2 MALE PATIENTS
- Gata-1 overexpression in AML was related to advanced age and a low percentage of bone marrow blasts and was associated with the expression of CD34 antigen and lymphoid T markers.
- The unique pathology of the megathrombocytes from a patient with the GATA-1, R216Q mutation was the near absence of dense bodies in his giant cells.