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Validated All-in-One™ qPCR Primer for REST(NM_005612.4) Search again
Product ID:
HQP054425
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DFNA27, GINGF5, HGF5, NRSF, WT6, XBR
Gene Description:
RE1 silencing transcription factor
Target Gene Accession:
NM_005612.4(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:
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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 transcriptional repressor which represses neuronal genes in non-neuronal tissues. It is a member of the Kruppel-type zinc finger transcription factor family. It represses transcription by binding a DNA sequence element called the neuron-restrictive silencer element. The protein is also found in undifferentiated neuronal progenitor cells, and it is thought that this repressor may act as a master negative regular of neurogenesis. Alternatively spliced transcript variants have been described; however, their full length nature has not been determined. [provided by RefSeq].
Gene References into function
- role in blocking the expression of neuronal phenotypic traits in non-neuronal cells
- we have identified a functional binding site for REST in the first intron of the human synaptophysin gene indicating that REST blocks human synaptophysin gene transcription through an intronic neuron-specific silencer element
- Role in the regulation of cholinergic gene expression
- Regulates the expression of Pax4 protein.
- the transcriptional repressor NRSF/REST regulates connexin36
- NRSF, a transcriptional repressor, selectively regulates expression of multiple fetal cardiac genes, including those for atrial natriuretic peptide, brain natriuretic peptide and alpha-skeletal actin
- REST-dependent proteins are comparably expressed in fetal Down syndrome (DS) and control brains by studies in the 18/19th week of gestation at the protein level; therefore, the REST-hypothesis in DS is not confirmed.
- individual RE1/NRSE sites interact differentially with REST/NRSF within a particular cell type.
- NRSF can function as a repressor of MOR transcription in specific cells, via a mechanism dependent on the mu opioid receptor gene neuron-restrictive silencer element
- interplay between REST and Sp1 determines the cell-specific expression of REST target genes
- results show that REST/NRSF recruits SCPs to neuronal genes that contain RE-1 elements, leading to neuronal gene silencing in non-neuronal cells
- REST is overexpressed in human medulloblastoma tumors
- derepression of NRSF-regulated genes including these neuron-specific genes could contribute to enhance tumorigenicity and also would provide selective markers for Brm/BRG1-deficient tumors
- HES-1 is an upstream negative regulator of REST expression.
- Down-regulation of NRP1 by NRSF overexpression reduced Sema3A activity. It was concluded that NRSF is a transcription factor that silences NRP1 expression and thereby diminishes the Sema3A mediated inhibition of HaCaT keratinocyte migration
- REST/NRSF-interacting LIM domain protein (RILP) is required for REST/NRSF nuclear targeting and function.
- Data suggest that REST/NRSF contains a NLS around ZFD-5, while the putative NLS at residues 512-522 is non-functional.
- abnormal expression of REST/NRSF and MYC in undifferentiated neural stem/progenitor cells causes cerebellum-specific tumors. Furthermore, these results suggest that such a mechanism plays a role in the formation of human medulloblastoma.
- BRG1 facilitates REST repression by increasing the interaction between REST and chromatin
- loss of SMCX activity impairs REST-mediated neuronal gene regulation, thereby contributing to SMCX-associated X-linked mental retardation
- sequence census method was used to map in vivo binding of the neuron-restrictive silencer factor to 1946 locations in the human genome
- these results suggest that REST/NRSF may have an important role in the establishment and/or maintenance of HSV-1 gene silencing during latency by targeting ICP4 expression.
- These findings show abnormal regulation of NRSF/REST as a mechanism associated with the aberrant expression of selected neuron-related proteins, which in turn accumulate in abnormal protein aggregates, in myotilinopathy.
- in undifferentiated human neural stem cells, neuronal genes encoding synaptic vesicle proteins are accessible for the REST mutant and are sensitive to enhanced histone acetylation
- The high levels of REST or its truncated variants found in certain human tumours may contribute to cellular transformation by promoting genomic instability.
- REST is a key target in beta-TRCP-driven transformation and the beta-TRCP-REST axis is a new regulatory pathway controlling neurogenesis
- critical role of REST target genes in pancreatic beta cells; evidence that the downregulation is detrimental for the exocytosis of large dense core vesicles.
- Results demonstrate that NRSF silencing can activate some neuronal genes and induce neuronal differentiation of mesenchymal stem cells.
- DYRK1A-mediated deregulation of REST is a very early pathological consequence of trisomy 21 with potential to disturb the development of all embryonic lineages.
- REST/NRSF, dynactin p150(Glued), huntingtin, HAP1, and RILP form a complex involved in the translocation of REST/NRSF into the nucleus and HAP1 controls REST/NRSF cellular localization in neurons
- REST is a transcriptional repressor of neuronal genes.
- The change in expression of sNRSF and TAC1 mRNA following mechanical stimulation in osteoarthritic (OA) but not normal chondrocytes suggests that sNRSF may be involved in the regulation of substance P production in OA cartilage.
- Chromodomain on Y-like (CDYL) is identified as a REST corepressor that physically bridges REST and the histone methylase G9a to repress transcription.