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Validated All-in-One™ qPCR Primer for FLI1(NM_002017.4) Search again
Product ID:
HQP005792
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BDPLT21, EWSR2, FLI-1, SIC-1
Gene Description:
Fli-1 proto-oncogene, ETS transcription factor
Target Gene Accession:
NM_002017.4(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
- role in regulating megakaryocyte-specific glycoprotein VI promoter
- Fli-1 and GATA-1 work together to activate the expression of genes associated with the terminal differentiation of megakaryocytes
- overexpression of this protein affects cell growth and differentiation of K562 cells
- This study supports the role of Fli1 as a suppressor of collagen transcription in human skin in vivo.
- FLI1 interacts with EWS and their oncogenic fusion protein.
- oncogenic rearrangement of EWS to produce EWS/Fli-1 may enhance the antiapoptotic effect of Brn-3a and inhibit its ability to promote neuronal differentiation.
- Overoverexpression of FLI1 in patient CD34(+) cells restores the megakaryopoiesis in vitro, indicating that FLI1 hemizygous deletion contributes to Paris-Troudeau syndrome hematopoietic defects.
- Ability of Ewing Sarcoma-Fli-1/Fli-1 to target transcriptional cofactor(s) and modulate apoptotic pathways may be responsible for its antiapoptotic and tumorigenic activities.
- These findings identify the repression of insulin-like growth factor binding protein 3 gene by EWS/FLI-1 as a key event in the development of Ewing's sarcoma.
- Two functional NLSs were shown to exist in Fli-1; each NLS is sufficient to target Fli-1 to the nucleus for activation of megakaryocyte-specific promoters.
- Protein phosphatase 2A controls FLI-1 phosphorylation. Newly synthesized FLI-1 decreased during human T cell activation. Although the FLI-1 & ERG genes are highly homologous, their distinct properties may contribute to different roles in gene regulation
- EWS-Fli1 may play a role in the regulation of PDGF-induced tumor proliferation-signaling enzymes via PLD2 expression in Ewing sarcoma cells
- the repressive properties of PIASxalpha/ARIP3 require its physical interaction with FLI-1, identifying PIASxalpha as a novel corepressor of FLI-1
- The signal transduction leading to the systemic sclerosis (SSc) fibrotic phenotype appears to converge on DNA methylation and histone deacetylation at the FLI1 gene.
- Fli1 and Ets1 have roles in the pathological extracellular matrix regulation during fibrosis and cancer
- Fli-1 is rather constitutively expressed by bone marrow cells in Ph(-) CMPD independent of the underlying JAK2 status
- EWS/Fli-1 and Fli-1 increase PLD2 gene expression by binding to an erythroblast transformation-specific domain of PLD2 promoter
- variation in overall gene expression patterns downstream of EWS-FLIl was observed, but also differential regulation of directly EWS-FLI1-bound genes
- PCAF-dependent acetylation of lysine 380 abrogates repressor function of Fli1 with respect to collagen expression; TGFb-dependent acetylation of Fli1 may represent the principal mechanism for TGFb-induced dissociation of Fli1 from the collagen promoter
- EWS/FLI mediates transcriptional repression via NKX2.2 during oncogenic transformation in Ewing's sarcoma
- IGF1 is a common target gene of Ewing's sarcoma fusion proteins EWS-FLI-1, EWS-ERG and FUS-ERG in mesenchymal progenitor cells
- Expression of Fli-1 in malignant melanoma appears to be associated with biologically more aggressive tumors.
- The phosphorylation-acetylation cascade triggered by PKC delta represents the primary mechanism whereby TGF-beta regulates the transcriptional activity of Fli1 in the context of the collagen promoter.