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Validated All-in-One™ qPCR Primer for SPI1(NM_001080547.1) Search again
Product ID:
HQP017662
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AGM10, OF, PU.1, SFPI1, SPI-1, SPI-A
Gene Description:
Spi-1 proto-oncogene
Target Gene Accession:
NM_001080547.1(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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Summary
This gene encodes an ETS-domain transcription factor that activates gene expression during myeloid and B-lymphoid cell development. The nuclear protein binds to a purine-rich sequence known as the PU-box found near the promoters of target genes, and regulates their expression in coordination with other transcription factors and cofactors. The protein can also regulate alternative splicing of target genes. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- PU.1 trans activation of gp91(phox) promoter
- Loss of PU.1 expression is associated with defective immunoglobulin transcription in Hodgkin and Reed-Sternberg cells of classical Hodgkin disease.
- Multiple PU.1 sites cooperate in the regulation of p40(phox) transcription during granulocytic differentiation of myeloid cells.
- C/EBPalpha and PU.1 interact physically and colocalize in myeloid cells, and C/EBPalpha blocks the function of PU.1.
- Heterozygous PU.1 mutations are associated with acute myeloid leukemia, causing disruption of PU.1 function, contributing to the block in cell differentiation found in AML patients.
- Distinct functions for STAT1 and PU.1 in transcriptional activation of Fc gamma receptor I promoter.
- Interacts with other transcription factors to regulate transcription of the gene encoding eosinophil granule major basic protein
- PU.1 transcriptional activity is down-regulated by AML1-ETO in t(8;21) myeloid leukemia by physical binding.
- Transactivation & DNA-binding domains of PU.1 were required for induction of Stat6-mediated transcription. The co-operation of PU.1 & Stat6 in Igepsilon gene transactivation fine-tunes cell-type-restricted expression of IL-4-induced gene responses.
- PU.1 directly regulated the expression of only the glutathione peroxidase gene through binding sites in the promoter and a 3' regulatory region.
- PU.1 is critical in the terminal differentiation of human alveolar macrophages.
- In conclusion, we provide evidence for AML-1, PU.1, and Sp3 cooperatively and directly mediating BPI-expression during myeloid differentiation.
- MeCP2 acts as a corepressor of PU.1 probably due to facilitating complex formation with mSin3A and HDACs.
- downregulated by Ehrlichia chaffeensis infection in monocytes
- in B cells, E47 and PU.1/IRF-4 interact with the E-box motifs and the EICE, respectively, and act synergistically in the activation of CIITA-PIII
- RANKL-induced cathepsin K gene expression is cooperatively regulated by the combination of the transcription factors and p38 MAP kinase in a gradual manner.
- Antibodies to LSP1 and PU.1 may represent useful reagents for the differential diagnosis between T-cell-rich B-cell lymphoma and lymphocyte-predominant Hodgkin's disease.
- high PU.1 activity favors dendritic cells at the expense of macrophage fate by inhibiting expression and activity of the macrophage factor MafB.
- The expression of PU.1 is a critical event for osteoclastogenesis.
- nuclear import of the transcription factor PU.1 occurs via RanGTP-stimulated binding to Nup153
- Alteration of the PU.1 locus does not correlate with its suppressed expression in Hodgkin lymphoma.
- PU.1 regulates the tissue-specific expression of dendritic cell-specific (ICAM)-3-grabbing nonintegrin.
- PU.1 regulates RANK gene transcription; this may represent one of the key roles of PU.1 in osteoclast differentiation
- Our results indicate that the NMTS region of Runx1 is required for functional interactions with PU.1.
- PU.1 and Id2 modulate lineage options of langerhans cell precursors, downstream of TGF-beta1.
- c-Myb and c-Ets family members (Ets-1/2, PU.1, and Spi-B) control hGR 1A promoter regulation in T- and B-lymphoblast cells
- PU.1, in addition to its positive role in TAL-1 expression in early hematopoietic progenitors, may also act as a mediator of TAL-1 silencing in some hematopoietic lineages
- The c.-292 T allele in the ALOX15 promoter generates a novel binding site for the transcription factor SPI1 that results in higher transcription of the gene in macrophages.
- PU.1 is suppressed in acute promyelocytic leukemia, and that all-trans retinoic acid restores PU.1 expression in cells harboring t(15;17).
- hydroquinone induces a dysregulation in the external signals modulating PU.1 protein phosphorylation and this dysregulation may be an early event in the generation of benzene-induced AML
- Spi-1 affects splicing decisions in a promoter binding-dependent manner
- 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.
- The mechanism of action of VIP on monocyte differentiation may be via inhibition of the transcription factor PU.1.
- IRF8 cooperates with PU.1 and IRF-2 to activate a composite ets/IRF-cis element in the NF1 promoter. The conserved IRF domain tyrosine in ICSBP/IRF8 is required for interaction with the DNA-bound PU.1-IRF2 heterodimer.
- findings provide an insight into the structure of the hematopoietic cell-specific P2 promoter of the SHP-1 gene and identify PU.1 as the transcriptional activator of the P2 promoter
- IRF8 is involved in a cooperative interaction with transcription factors Spi-1/PU.1 and non-tyrosine phosphorylated Stat1 in the formation of a pre-associated, poised complex for interleukin 1-beta gene induction.
- data strongly indicate that germline mutations in SPI1 and MADD genes do not confer a high risk of chronic lymphocytic leukaemia and do not make a major contribution to the familial risk of the disease
- PU.1 was down-regulated in the majority of human myeloma cell lines and a subset of freshly isolated myeloma cells, in contrast to relatively high expression of PU.1 in normal plasma cells.
- The type IV isoform of PML interacted with PU.1, promoted its association with p300, and then enhanced PU.1-induced transcription and granulocytic differentiation and PU.1 directly activates the transcription of the C/EBPepsilon gene.
- Ski-mediated repression of PU.1 is due to Ski's ability to recruit histone deacetylase 3 to PU.1 bound to DNA.
- Transcription factor PU.1 controls transcription start site positioning and alternative TLR4 promoter usage.
- C/EBPalpha binds and activates the PU.1 distal enhancer to induce monocyte lineage.
- identify a single nucleotide polymorphism within this element in humans that is more frequent in acute myeloid leukemia with a complex karyotype, leads to decreased enhancer activity, and reduces PU.1 expression in myeloid progenitors
- PU.1 activates the transcription of miR-424, and this up-regulation is involved in stimulating monocyte differentiation through miR-424-dependent translational repression of NFI-A
- These data provide evidence that NFATc1, in concert with PU.1, are involved in regulation of beta(3) integrin expression during osteoclast differentiation.
- Low PU.1 levels were observed in monoblastic leukemias
- Arginine-methylated RUNX1 regulates PU.1 gene expression.
- PU.1 is severely impaired in patients with chronic myeloid leukemia but is restored upon treatment.
- PU.1 is involved in the regulation of human innate epithelial defences
- PU.1 expression is modulated by the balance of functional sense and antisense RNAs regulated by a shared cis-regulatory element.
- LSECtin is expressed by liver myeloid cells, and its expression is dependent on the PU.1 transcription factor.
- These data provide critical insights into the transcriptional regulation of the IP gene in human megakaryocytic and endothelial cells, identifying Sp1, PU.1 and Oct-1 as the critical factors involved in its basal regulation in humans.
- EVI1 point mutant, unable to bind PU.1, restores the activation of PU.1-regulated genes and allows a normal differentiation of bone marrow progenitors in vitro.