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Validated All-in-One™ qPCR Primer for ELK1(NM_005229.3) Search again
Product ID:
HQP004749
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
ETS transcription factor ELK1
Target Gene Accession:
NM_005229.3(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 gene is a member of the Ets family of transcription factors and of the ternary complex factor (TCF) subfamily. Proteins of the TCF subfamily form a ternary complex by binding to the the serum response factor and the serum reponse element in the promoter of the c-fos proto-oncogene. The protein encoded by this gene is a nuclear target for the ras-raf-MAPK signaling cascade.
Gene References into function
- Complexities in Elk-1 transcription factor function and regulation
- The Elk-1 R motif and the p300 CRD1 motif represent a new class of repression domains that are regulated in a context-dependent manner.
- Interaction of serum response factor (SRF) with the Elk-1 B box inhibits RhoA-actin signaling to SRF and potentiates transcriptional activation by Elk-1
- Bombesin-dependent activation of the transcription factor Elk-1 and significant increase of cell proliferation in prostate cancer cell lines
- role in signal cascade in immediate-early gene induction by anisomycin and arsenite
- ERK pathway activation leads to both phosphorylation of Elk-1 and loss of SUMO conjugation. This reciprocal regulation of activation and repression are coupled by MAP kinase modification of Elk-1.
- SUMO conjugation is a novel regulator of Elk-1 function through the control of its nuclear-cytoplasmic shuttling.
- transcriptional activities of ElK-1 and AP-1 are inhibited by TRIM45, a novel human RBCC/TRIM protein
- Deletion analyses of the Egr-1 promoter identify a minimal estradiol-responsive region of the promoter containing a serum response element which binds Elk-1 and serum response factor.
- H. pylori induction of villin in the stomach correlates with activation and cooperative binding of Elk-1 and the SRF to the proximal promoter of villin
- Basal and inducible phosphorylation of Elk-1 is impaired in a patient with premature aging syndrome and insulin resistance.
- Data suggest that residues distal to the binding interface of DNA and Elk-1/SAP-1 may indirectly modulate the binding affinity by stabilizing the protein scaffold required for efficient DNA interaction.
- PKCalpha expression may be modulated by Elk-1 and MZF-1 at the transcriptional level.
- PI3K through p21-activated kinase 1 regulates FRA-1 proto-oncogene induction by cigarette smoke and the subsequent activation of the Elk1 and cAMP-response element-binding protein transcription factors
- JNK1 and JNK2 differentially regulate TBP through Elk-1, controlling c-Jun expression and cell proliferation
- PKC-eta-mediated glioblastoma proliferation involves MEK/mitogen-activated protein (MAP) kinase phosphorylation, activation of ERK and subsequently of Elk-1.
- Increased expression of transcription factor Elk-1 may play an important role in esophageal carcinogenesis.
- Human Rev7 (hRev7)/MAD2B/MAD2L2 is an interaction partner for Elk-1 and hRev7 acts to promote Elk-1 phosphorylation by the c-Jun N-terminal protein kinase (JNK) MAP kinases.
- Elk1 transcription factor targets a binding site in the TBP promoter and its occupancy of this region is reciprocal with that of Mif1.
- The 5' UTR controls ribosomal access to the ELK-1 AUG initiation codon.
- BFGF activates the MAPK and NFkappB pathways that converge on ELK1 to control production of MMP13 by articular chondrocytes.
- Elk-1 exerted opposite effects on hSlu7 transcription:Elk-1 protein represses transcription in a dose-dependent manner
- Elk-1 activated transcription of the HTLV-1 long terminal repeat (LTR), and mutations within either of the TCF sites or the CArG box reduced responsiveness of the LTR to Elk-1.
- Hemin activated Elk-1, SRF, and NF-kappaB and promoted their interaction with the Egr-1 promoter
- MDMX basal promoter activity requires c-Ets-1 and Elk-1. c-Ets-1 and Elk-1 control MDMX transcription and contribute to the suppression of p53 activity.
- These results strongly support that Elk-1 protein is a novel binding-protein partner for FAK, a finding that significantly broadens the potential functioning of FAK and Elk-1.
- ERK and JNK MAPK/Elk-1/Egr-1 signal cascade is required for p53-independent transcriptional activation of p21(Waf1/Cip1) in response to curcumin in U-87MG human glioblastoma cells
- Results suggest that Elk-1 is anchored to neuronal microtubules in resting or unstimulated cells, and upon stimulation is phosphorylated, which relocalizes phospho-Elk-1 to the nucleus in neurons.
- Elk-1 is involved in upregulating HRI expression during stress along with a co-activator p300, while MZF-1 along with HDAC-1 is instrumental in its downregulation during hemin treatment.