|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for ETV6(NM_001987.4) Search again
Product ID:
HQP005022
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
TEL, TEL/ABL, THC5
Gene Description:
ETS variant transcription factor 6
Target Gene Accession:
NM_001987.4(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:
|
|
| A | B |
|
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. |
|
Summary
This gene encodes an ETS family transcription factor. The product of this gene contains two functional domains: a N-terminal pointed (PNT) domain that is involved in protein-protein interactions with itself and other proteins, and a C-terminal DNA-binding domain. Gene knockout studies in mice suggest that it is required for hematopoiesis and maintenance of the developing vascular network. This gene is known to be involved in a large number of chromosomal rearrangements associated with leukemia and congenital fibrosarcoma. [provided by RefSeq].
Gene References into function
- We identified a novel ETV6 partner gene, fibroblast growth factor receptor 3 (FGFR3), in a patient with peripheral T-cell lymphoma (PTCL) with a t(4;12)(p16;p13) translocation.
- activates phosphatidylinositol 3 (PI3) kinase and requires PI3 kinase to regulate the cell cycle [TEL/platelet-derived growth factor receptor beta]
- a variant ETV6-mediated leukemogenic mechanism in myeloid leukemias with a t(4;12)(q11-q12;p13) or t(5;12)(q31;p13)
- ETV6 functions with ARG as oncofusion protein and triggers the same signaling pathways associated with ABL oncogenes
- the chromosomal translocation leads o formation of TEL/AML1 fusion oncogene and is most common genetic aberration in childhood B-cell precursor ALL.
- TEL-negative PBC-ALL cells expressing a transfected TEL at high levels showed a decreased expression of endogenous TCL1.
- The product of the ETV6-MDS2 fusion transcript in a patient with myelodysplastic syndrome predicts a short ETV6 protein containing the first 54 amino acids of ETV6 plus four novel amino acids, lacking both the PTN and the DNA-binding domains.
- mutational inactivation of ETV6 may occur in prostate carcinoma
- Different clones of t(1;12)/t(12;12) involving the ETV6 gene in a case of acute myeloid leukemia.
- TEL's functions are potentially regulated by p38 which is activated by various kinds of stresses
- Expression of the ETV6-NTRK3 gene fusion is a primary event in human secretory breast carcinoma.
- Chronic myelocytic leukemia with eosinophilia, t(9;12)(q34;p13), and ETV6-ABL gene rearrangement: case report and review of the literature.
- Breakpoints in TEL intron 5 and AML1 intron 1 leading to TEL-AML1 fusion is shown to be the initiating step, preceding differentiation to pre-B cells, in childhood acute lymphoblastic leukemia.
- The ability of TEL to repress TEL-responsive promoters is enhanced by the presence of H-L(3)MBT, an effect dependent on the H-L(3)MBT and the TEL interacting domains, which are mapped to their respective SPM/SAM domains.
- the ability of TEL to repress transcription and suppress growth is regulated by sumoylation and nuclear export
- nucleo-cytoplasmic delocalization of the major isoform of TEL-ETV6 is regulated by V-src
- ETV6-NTRK3.IRS-1 complex formation through the NTRK3 C terminus is essential for ETV6-NTRK3 transformation
- TEL-AML1 dramatically alters differentiation of HPCs in vitro, preferentially promoting B-lymphocyte development, enhancing self-renewal of B-cell precursors, and leading to the establishment of long-term growth factor-dependent pre-B-cell lines
- the WW-like domain in the context of TELPDGFbetaR may have both positive and negative regulatory roles in kinase activation.
- we found an incidence of 8.6% of TEL/AML1 translocation in ALL patients (12% of B-lineage ALL)
- TEL-AML1 ALL has significantly lower de novo purine synthesis and differential expression of genes involved in purine metabolism.
- Data show that the repressor activity of TEL/RUNX1 differs from that of TEL, even though both TEL and TEL/RUNX1 interact with the nuclear hormone co-repressor (N-CoR) and histone deacetylase (mSin3A) in vivo.
- Inhibition of Stat3 activity by TEL represents a novel mechanism regulating the Stat3 signaling pathway
- Independent Tel deletion demonstrates a comprehensive analysis of the relationship between diagnostic and relapse clones in childhood ALL.
- Fusion with RUNX1 may provide circumstantial evidence of an increased risk of relapse in leukemia.
- several critical domains within TEL/ARG necessary for function
- Onr third of acute myeloid leukemiea patients have deficient ETV6 protein expression.
- ETV6 rearrangements in invasive breast cancer using fluorescence in situ hybridization (FISH)
- TEL may decide the fate of human erythrocyte/megakaryocyte common progenitors to differentiate towards the erythroid lineage and against the megakaryocytic lineage
- the mechanisms of drug sensitivity and resistance differs between TELAML1-positive ALL and other precursor B-lineage ALL patients.
- meningioma 1-translocation-ETS-leukemia exerts its nonlineage-specific leukemogenic effects by promoting the growth of primitive progenitors and blocking their differentiation
- leukemogenic effect of meningioma 1-TEL in our knock-in mice is pleiotropic, and the type of secondary mutation determines disease outcome
- TEL-AML1 may have a role in T-cell receptor gene rearrangements in pediatric acute lymphoblastic leukemia
- The expression of TEL was found in in 20.3% of children with B-lineage ALL.
- The TCR gene rearrangements in childhood B-lineage acute lymphoblastic leukemia was associated with expression of TEL chimeric oncogene.
- The t(5;12)(q23-31;p13)translocation with ETV6-ACSL6 genomic alteration rearrangement in polycythemia vera patients was reported.
- novel TEL-AML1 fusion in precursor B acute lymphoblastic leukemia
- A nuclear localization signal exists in the C-terminal region of ETV6 within residues 332-452.
- These results suggest that methylation profile may be a potential new biomarker of risk prediction in ETV6/RUNX1-positive acute lymphoblastic leukemias.
- TEL-AML1 fusion in transgenic zebrafish induces a B cell differentiation arrest and demonstrates leukemia development associated with loss of TEL expression and elevated Bcl2/Bax ratio.
- expression of TEL-JAK2, a constitutively active variant of the JAK2 kinase, in lineage-depleted umbilical cord blood cells results in erythropoietin-independent erythroid differentiation in vitro and induces the rapid development of myelofibrosis
- functional relationship between TEL/AML1, HSP90, and survivin provides the rational for targeted therapy.
- One of the chromosome bands most often involved in structural rearrangements in B-cell precursor acute lymphoblastic leukemia.
- conclude that our patient represents another case of the rare hematological entity characterized by an ETV6-ABL translocation
- c-MET is associated with FAS and when activated enhances drug-induced apoptosis in pediatric B acute lymphoblastic leukemia with TEL-AML1 translocation
- ETV6/RUNX1-positive acute lymphoblastic leukemias have a high incidence of cryptic Xq duplications
- ETV6/RUNX1 rearrangement is associated with acute lymphoblastic leukemia
- analysis of the prevalence of the ETV6-RUNX1 fusion gene in children with acute lymphoblastic leukemia in China
- Gene expression analyses of leukemia cells from children with TEL/AML1-positive and -negative B-lineage ALL led to the identification of five biological processes.
- Disruption of ETV6 in intron 2 results in upregulatory and insertional events in childhood acute lymphoblastic leukemia
- ETV6 interacts with TIP60 through a 63 amino acids region located in the central domain of ETV6 between the pointed and the ets domain.
- The PAX5/TEL protein has a dominant effect on wild-type PAX5, interferes with the process of B-cell differentiation and migration, and induces resistance to apoptosis.
- analysis of TEL-AML1-transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties
- PIAS3 binds to Tel and stimulates sumoylation of K11 in the nucleus. sumoylation impedes Tel association with DNA. A Tel isoform lacking K11 (TelM43) is strongly repressive.
- ETV6-NCOA2 fusion may define a novel subgroup of acute leukemia with T-lymphoid and myeloid features, which is associated with a high prevalence of NOTCH1 mutations.
- the number and variety of ETV6 translocations together with loss of ETV6 by deletion makes a mutually supportive and compelling case for loss and haplo-insufficiency of ETV6 as a leukemogenic step in acute myeloid leukemia
- Fbl6 regulates Tel/Yan protein stability and allows appropriate spatiotemporal control of gene expression by these repressors.
- Conclude that acute lymphoblastic leukemia TEL-AML1 gene status should be incorporated into risk classification schemes.
- study excludes occurrence and persistence of ETV6-RUNX1 transcript in most pregnancies between 6th and 10th week of development at levels of >/=10-4
- No acinar cell carcinoma of the breast showed any definite evidence of ETV6 gene rearrangement.
- Low frequency of the ETV6/RUNX1 fusion observed in Hispanics.
- TEL/AML1 fusion gene may have a role in childhood acute lymphoblastic leukemia
- genomic profile of ETV6-RUNX1 positive acute lymphoblastic leukemia highlights a recurrent deletion of TBL1XR1.
- MNX1-ETV6 fusion gene in an acute megakaryoblastic leukemia.
- Expression of ETV6 rearrangement in a subject with acute myeloid leukemia-M4Eo.
- ETV6/RUNX1 fusion lacking prognostic effect in pediatric patients with acute lymphoblastic leukemia.