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Validated All-in-One™ qPCR Primer for SRF(NM_003131.3) Search again
Product ID:
HQP017706
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MCM1
Gene Description:
serum response factor
Target Gene Accession:
NM_003131.3(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 encodes a ubiquitous nuclear protein that stimulates both cell proliferation and differentiation. It is a member of the MADS (MCM1, Agamous, Deficiens, and SRF) box superfamily of transcription factors. This protein binds to the serum response element (SRE) in the promoter region of target genes. This protein regulates the activity of many immediate-early genes, for example c-fos, and thereby participates in cell cycle regulation, apoptosis, cell growth, and cell differentiation. This gene is the downstream target of many pathways; for example, the mitogen-activated protein kinase pathway (MAPK) that acts through the ternary complex factors (TCFs). [provided by RefSeq].
Gene References into function
- Crystal structure of a ternary SAP-1/SRF/c-fos SRE DNA complex
- mechanisms by which Vav1 can regulate c-fos serum response element transcriptional activity.
- activation by muscarinic receptors via RhoA
- 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
- Results show that alpha-catulin co-expression leads to increased Lbc-induced serum response factor activation and may modulate Rho pathway signaling in vivo by providing a scaffold for the Lbc Rho guanine nucleotide exchange factor.
- Tissue inhibitor of metalloproteinase-3 is downregulated in lymphangioleiomyomatosis as a consequence of abnormal SRF expression.
- role in signal cascade in immediate-early gene induction by anisomycin and arsenite
- SRF is modified by SUMO-1 chiefly at lysine(147) within the DNA-binding domain.
- serum response factor plays a role in facilitating a program of smooth muscle cell-restricted gene expression [review]
- Genistein down-regulated mRNA of SRF.
- SRF was reduced and processed into 55- and 32-kDa subfragments in failing hearts; SRF-N the N-terminal fragment inhibited transcription of alpha-actin gene promoters in myogenic cells suggesting function as a dominant-negative transcription factor
- SRF is a downstream mediator of VEGF signaling in endothelial cells and a critical requirement for VEGF-induced angiogenesis.
- Results identify protein kinase C delta as the kinase responsible for inactivation of serum response factor both in vitro and endogenously in senescent cells.
- Galphaz signals may attenuate Rho-induced stimulation of serum response factor-mediated transcription.
- TCF-SRF-regulated gene activity has a role in regulating proliferation and in protecting cells from apoptotic cell death
- 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
- NFAT and SRF may interact to cooperatively regulate smooth muscle cell-specific gene expression and NFAT may have a role in the phenotypic maintenance of smooth muscle
- HERP1 may play a role in promoting the phenotypic modulation of vascular smooth muscle cells during vascular injury and atherosclerotic process by interfering with SRF binding to CArG-box through physical association between HERP1 and SRF
- preventing the age-associated increase in serum response factor is associated with better preserved intracellular calcium handling and functional response to stress
- identified 216 putative SRF binding sites in the genome
- SRF-myocardin overexpression in small cerebral arteries appears to initiate independently of amyloid beta-peptide a pathogenic pathway mediating arterial hypercontractility
- In the presence of Tax, SRF selects more divergent consensus (CArG) box sequences than in the absence of Tax, revealing a novel mechanism for regulating SRF-responsive gene expression.
- Our data indicate that the SRF isoforms were differentially expressed in the human versus mouse cardiac muscle.
- These results suggest a novel indirect mechanism of androgen action on FHL2 expression and provide evidence that SRF is an important determinant of AR action in prostate cancer cells.
- These results suggest induction of SRF-mediated transcription by alpha(E)-catenin either downstream of RhoA or via a parallel pathway.
- identified novel protein-protein interacting domains within Nkx3.1 and SRF
- Mosaic inactivation of the SRF gene in the myocardium induces focal lesions and heart failure.
- Serum induction initially stimulates MKL1 nuclear localization due to a decrease in G-actin levels, but MKL1 is then downregulated by nuclear export due to ERK1/2 phosphorylation.
- growth factors and serum induce expression of Egr-1 and SRF, respectively, which in turn induces E2-EPF UCP expression that positively regulates cancer cell growth
- An important age associated decrease in SRF expression in mice and human muscles, is reported.
- We suggest that SRF and MYOCD function as a transcriptional switch, controlling Abeta cerebrovascular clearance and progression of AD.