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Validated All-in-One™ qPCR Primer for TAL1(NM_003189.1) Search again
Product ID:
HQP017895
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SCL, TCL5, bHLHa17, tal-1
Gene Description:
TAL bHLH transcription factor 1, erythroid differentiation factor
Target Gene Accession:
NM_003189.1(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
- role of hypoxia in stimulating phosphorylation, ubiquitination, and proteasomal breakdown in endothelial cells
- SCL locus can rescue knockout scl(-/-) mice
- Ectopic expression of human TAL-1 protein in Ly-6E.1-htal-1 transgenic mice induces defects in B- and T-lymphoid differentiation, but did not cause leukemia.
- regulates c-kit expression in hematopoietic cells through functional interaction with Sp1
- is a survival factor for erythroid cells
- These results indicate that TAL1 can affect both T cell proliferation and differentiation.
- Enforced expression of a TAL1 protein deleted of its DNA-binding domain mimicked most TAL1 effects except for the LTC-IC enhancement, the down-regulation of the CD34 surface marker, and the GPA(+) cell production
- TAL-1 modulates the angiogenic response of endothelial cells by stimulating cell morphogenesis and by influencing their behavior in migration.
- Possible role for SCL in renal vasculogenesis. Undifferentiated mesenchymal cells expressing SCL during early nephrogenesis might represent putative progenitors that can simultaneously give rise to kidney, blood, and endothelium.
- Tal1/SCL binding to pericentromeric DNA represses transcription
- Results show striking coexpression of SCL and its immediate downstream neighbor, MAP17, suggesting that they share regulatory elements.
- TAL1 expression level regulates immature human hematopoietic cell self-renewal and this regulation requires TAL1 DNA-binding activity
- 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
- TAL1 may act as a bifunctional transcriptional regulator (activator and repressor) at the top of a complex regulatory network that disrupts normal T-cell homeostasis and contributes to leukemogenesis.
- Scl acts up-stream of NF-E2 expression to control megakaryocyte development and platelet release in settings of thrombopoietic stress
- TAL1 modulates NFKB1 expression and an NF-kappaB-dependent transcriptional program in a subset of human T-cell leukemia cells.
- Using lentiviral delivery of TAL1-directed shRNA in human hematopoietic cells showed that decreased expression of TAL1 induced major disorders at different levels of adult hematopoietic cell development
- Conditional activation of the SCL transgene under control of ubiquitously expressed SCL interrupting locus (SIL) transgenic regulatory elements impairs normal T-cell development.
- CD3epsilon-mediated signal transduction pathway is essential for this transformation process
- the SCL-LMO2 interaction couples protein stabilization with higher order protein complex assembly, thus providing a powerful means of modulating the stoichiometry and spatiotemporal activity of SCL complexes
- characterize the assembly of a five-component complex containing TAL1, LMO2, Ldb1, E12, and DNA. The bHLH domains of TAL1 and E12 alone primarily formed helical homodimers, but together formed heterodimers, to which LMO2 bound with high affinity
- Operation of cullin-based ubiquitin ligase complexes and potential means by which Notch and Tal1/SCL regulate eukaryotic development.
- LMO2, TAL1, Ttg-1, and SIL support levels of V(D)J recombination above background levels in cell culture and are also cleaved by the RAG proteins, while Hox11 and SCL are nicked but not cleaved efficiently in vitro
- Data definitively delineate the human myeloid progenitors that are regulated by TAL1.
- TAL-1 deletion is associated with T-cell acute lymphoblastic leukemia.
- analysis of cross talk between the human T-cell leukemia virus type 1 Tax transactivator and the oncogenic bHLH transcription factor TAL1
- different mechanisms of SCL's action predominate depending on the developmental/cellular context