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Validated All-in-One™ qPCR Primer for CTCF(NM_006565.3) Search again
Product ID:
HQP000809
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CFAP108, FAP108, MRD21
Gene Description:
CCCTC-binding factor
Target Gene Accession:
NM_006565.3(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 BORIS + CTCF gene family and encodes a transcriptional regulator protein with 11 highly conserved zinc finger (ZF) domains. This nuclear protein is able to use different combinations of the ZF domains to bind different DNA target sequences and proteins. Depending upon the context of the site, the protein can bind a histone acetyltransferase (HAT)-containing complex and function as a transcriptional activator or bind a histone deacetylase (HDAC)-containing complex and function as a transcriptional repressor. If the protein is bound to a transcriptional insulator element, it can block communication between enhancers and upstream promoters, thereby regulating imprinted expression. Mutations in this gene have been associated with invasive breast cancers, prostate cancers, and Wilms' tumors. [provided by RefSeq].
Gene References into function
- It's proposed that Tsix and CTCF together establish a regulatable epigenetic switch for X-inactivation.
- observations suggest that CTCF may represent a novel tumor suppressor gene that displays tumor-specific "change of function" rather than complete "loss of function"
- Insertional mutagenesis identified nucleosome positioning sequences (NPSs) allow the remarkably precise distribution of target sites for the chromatin insulator protein CTCF to nucleosome linker sequences in the H19 ICR.
- Conserved CTCF insulator elements flank the mouse and human beta-globin loci.
- Transforming growth factor-beta-induced transcription of the Alzheimer beta-amyloid precursor protein gene involves interaction between the CTCF-complex and Smads
- Loss of CTCF mRNA or protein in Wilms tumors does not predispose to de novo methylation of the maternal allele of H19 but leaves open the possibility that post-transcriptional loss of CTCF protein may account for some instances of loss of imprinting.
- CTCF is a common determinant to different pathways of death signaling in immature B cells.
- the insulator activity of CTCF apparently involves an HDAC-independent association with the nuclear matrix
- CTCF binding at the human IGF2/H19 imprinting control region(ICR). CTCF binding at the IGF2/H19 ICR is insufficient to regulate expression of IGF2/H19 in many human tissues.
- CTCF can be inactivated by somatic mutation and genetic or epigenetic silencing of the wild-type allele in individual cases of invasivene ductal breast cancer; loss of CTCF protein function may contribute to tumor heterogeneity
- beta-globin locus control region HS5 contains enhancer-blocking (insulator) activity that is both CTCF and developmental stage dependent
- CTCF has a role in tethering an insulator to subnuclear sites
- CTCF regulates Pax6 transcription by binding to its repressor element, which in turn blocks the effect of the ectoderm enhancer resulting in the inhibition of P0 promoter activity.
- The terminal domain is active in HeLa, HEK293 and COS-7 cell lines where it is both sufficient and necessary for silencing an SV40 core promoter.
- novel mechanism for IGF2 imprinting regulation, that is, the reduction of CTCF expression in the control of IGF2 imprinting
- CTCF plays a major role in IRAK2 transcription; EMSA revealed a CTCF-binding site within the mouse Irak2 promoter
- point mutations in the XIST promoter reveal a correlation between CTCF binding and pre-emptive choices of X chromosome inactivation
- CTCF is involved in the control of myeloid cell growth and differentiation
- CTCF overexpression may have evolved as a compensatory mechanism to protect breast cancer cells from apoptosis, thus providing selective survival advantages to these cells.
- chromatin loop organized by the CTCF-bound, differentially methylated region at the Igf2/H19 locus can be detected in mitosis
- Data indicate that reciprocal binding of CTCF and BORIS to the NY-ESO-1 promoter mediates epigenetic regulation of this CT gene in lung cancer cells.
- the Kaiso-CTCF interaction negatively regulates CTCF insulator activity
- increased CTCF can repress EBNA2 transcription
- CTCF is a multifunctional epigenetic regulator with a role in carcinogenesis (review)
- this study reports the identification and characterization of an insulator from the herpes simplex virus-1 LAT intron region that functions via CTCF
- Study describes 13,804 CTCF-binding sites in potential insulators of the human genome in primary human fibroblasts; most of these sequences are located far from the transcriptional start sites, with their distribution strongly correlated with genes
- Results reveal that CTCF is a down stream target of stress-induced signaling cascades and it plays a significant anti-apoptotic role in regulation of stress-induced cellular responses in HCE and hematopoietic myeloid cells.
- a small number of zinc fingers mediate strong binding of CTCF to DNA, and a single finger-DNA interaction controls binding at imprinted loci
- CTCF is indeed a protein with multifunctional activity that plays a significant role in modulating signalling pathways to mediate insulin-induced ML-1 cell proliferation.
- Band-shift analysis upon the nuclear fractions from HIV-1 resistant cells showed that CTCF protein bound to HIV-1 promoter and this binding prevented the formation of NF-kappaB/LTR complex.
- description of cohesin-binding sites in the human genome; most of these are associated with the CCCTC-binding factor (CTCF), a zinc-finger protein required for transcriptional insulation
- Study shows that the distribution of cohesins on mammalian chromosome arms is not driven by transcriptional activity, instead, cohesins are found at most CTCF sites and CTCF is required for cohesin localization to these sites.
- The results suggest a model whereby both HLA-DRB1 and HLA-DQA1 loci can interact simultaneously with XL9, and describe a regulatory mechanism involving the alteration of the general chromatin conformation and their regulation by CTCF.
- STAG1 (Scc3/SA1) subunit of cohesin interacts with the CCTC-binding factor CTCF bound to the c-myc insulator element.
- Results decribethe loss IGF2/H19 imprinting,loss of heterozygosity of IGF2R and CTCF, and incidental H. pylori infections in laryngeal squamous cell carcinoma.
- CTCF positions 20 nucleosomes around its binding sites across the human genome.
- CTCF is required in a dose-dependent manner and is involved in cell cycle progression of alphabeta T cells in the thymus.
- CTCF binding-site mutation promotes triplet repeat instability both in the germ line and in somatic tissues.
- mapped the genome-wide binding sites of CTCF in three cell types and identified significant binding of CTCF to the boundaries of repressive chromatin domains marked by H3K27me3
- intrinsic looping activity of CTCF sites can nullify locus control region function.
- These data argue that the regulation of the IL-3 and the GM-CSF promoters depends on the positions of their enhancers relative to the conserved CTCF/cohesin-binding sites.
- Regulation of the D4Z4 array depends on both the number of repeats and the presence of CTCF and A-type Lamins in facio-scapulo-humeral dystrophy.