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Validated All-in-One™ qPCR Primer for HES1(NM_005524.3) Search again
Product ID:
HQP100411
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HES-1, HHL, HRY, bHLHb39
Gene Description:
hes family bHLH transcription factor 1
Target Gene Accession:
NM_005524.3(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 protein belongs to the basic helix-loop-helix family of transcription factors. It is a transcriptional repressor of genes that require a bHLH protein for their transcription. The protein has a particular type of basic domain that contains a helix interrupting protein that binds to the N-box rather than the canonical E-box. [provided by RefSeq].
Gene References into function
- HES-1 preserves the long-term reconstituting hematopoietic activity of 34-KSL stem cells ex vivo.
- These results indicate that the molecular association between HES1-, HEY2- and SIRT1-related proteins is conserved among metazoans, from Drosophila to human, and suggest that the Sir2-bHLH interaction also plays important roles in human cells.
- Hes1 transcription repression activity is inhibited by Hes6.
- the estrogen receptor and AhR signaling pathways regulate HES-1, but with opposing effects, suggests the existence of a new pathway by which AhR represses E2-signaling.
- IkappaBalpha is recruited to the promoter regions of the Notch-target gene, hes1
- Notch1 inhibits the development of erythroid/megakaryocytic cells by suppressing GATA-1 activity through HES1
- For marking and purifying neural stem cells to ascertain whether differences exist, we generated transgenic mice using promoters from Hes genes (pHes1 or pHes5) to drive expression of destabilized enhanced green fluorescent protein.
- HES-1 is an upstream negative regulator of REST expression.
- HES-1 alone is not able to substitute for Notch-1 signaling to induce T-cell differentiation of human CD34+ hematopoietic stem cells.
- Notch protein binding to Hes5-GFP is extinguished fast and recovered slowly, whereas Hes1-GFP is inhibited late and recovered quickly
- Expression of HES1 increased significantly during chondrogenesis in chondrocytes while expression in mesenchymal stem cells was maintained at a low level.
- Increased expression of Notch3, Jagged1, Hes1, and Hes6 gene transcripts were observed during differentiation of cultured human skeletal muscle cells.
- expression significantly higher in squamous cervical carcinoma than in CIN as well as higher in CIN than normal cervical epithelia
- Overexpression of hes1 is associated with breast cancer
- Notch-mediated Hes1 expression contributes to the maintenance of the proliferative crypt compartment of the small intestine by transcriptionally repressing two CDK inhibitors.
- lack of nuclear expression of HES1 may contribute to the abundance of ASCL1 and to tumorigenesis in the endocrine pancreas.
- regulates brain development process.[review]
- HES1 interaction with Fanconi anemia (FA) core complex members is dependent on a functional FA pathway. Cells depleted of HES1 exhibit an FA-like phenotype.
- Inhibition of HES-1 expression using shRNA resulted in significantly reduced pancreatic beta-cell replication and dedifferentiation
- it is concluded that HES1 safeguards against irreversible cell cycle exit both during normal cellular quiescence and pathologically in the setting of tumorigenesis
- ChIP-on-chip data reveal 3 oncogenic transcription factors, NOTCH1, MYC, and HES1, bind to several thousand target gene promoters