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Validated All-in-One™ qPCR Primer for BTRC(NM_033637.3) Search again
Product ID:
HQP021753
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BETA-TRCP, FBW1A, FBXW1, FBXW1A, FWD1, bTrCP, bTrCP1, betaTrCP
Gene Description:
beta-transducin repeat containing E3 ubiquitin protein ligase
Target Gene Accession:
NM_033637.3(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 member of the F-box protein family which is characterized by an approximately 40 amino acid motif, the F-box. The F-box proteins constitute one of the four subunits of ubiquitin protein ligase complex called SCFs (SKP1-cullin-F-box), which function in phosphorylation-dependent ubiquitination. The F-box proteins are divided into 3 classes: Fbws containing WD-40 domains, Fbls containing leucine-rich repeats, and Fbxs containing either different protein-protein interaction modules or no recognizable motifs. The protein encoded by this gene belongs to the Fbws class; in addition to an F-box, this protein contains multiple WD-40 repeats. This protein is homologous to Xenopus bTrCP1, yeast Met30, Neurospora Scon2 and Drosophila Slimb proteins. It interacts with HIV-1 Vpu and connects CD4 to the proteolytic machinery. It also associates specifically with phosphorylated IkappaBalpha and beta-catenin destruction motifs, probably functioning in multiple transcriptional programs by activating the NF-kappaB pathway and inhibiting the beta-catenin pathway. [provided by RefSeq].
Gene References into function
- Genetic evidence for the essential role of beta-transducin repeat-containing protein in the inducible processing of NF-kappa B2/p100
- Protein kinase CK2 dependent phosphorylation of the E2 ubiquitin conjugating enzyme UBC3B induces its interaction with beta-TRCp and enhances beta-catenin degradation
- Molecular genetic analysis of malignant melanomas for aberrations of the WNT signaling pathway genes CTNNB1, APC, ICAT and BTRC.
- HOS plays a role in inhibiting cell differentiation and cell transformation
- Prophase destruction of emi1 by the betaTrCP ubiquitin ligase activates the anaphase promoting complex to allow progression beyond prometaphase.
- BTRC complexes with Skp1 and beta-catenin. The destruction motif binding and lysine specificity of the SCF (beta-TrCP1) ubiquitin ligase were studied.
- Upon hyperphosphorylation, hDlg interacts with the beta-TrCP ubiquitin ligase receptor through a DSGLPS motif, and consequently, overexpression of beta-TrCP enhances ubiquitination of Dlg protein and decreases its stability.
- alternative splicing and role implicated in interaction with HIV-1
- Vpu is a strong competitive inhibitor of betaTrCP that impairs the degradation of SCFbetaTrCP substrates as long as Vpu has an intact phosphorylation motif and can bind to betaTrCP.
- beta-TrCP has a crucial role in mediating the response to DNA damage through Cdc25A degradation
- An analysis of the NEDD8 modification on beta-TrCP ubiquitin ligase was made.
- SCF(beta-TrCP1) abrogates TGF-beta function in vivo by decreasing Smad4 stability
- beta-TrCP-dependent degradation of Wee1A is important for the normal onset of M-phase in vivo.
- to investigate the role of betaTrcp1 in mammary gland development, we generated transgenic mice expressing human betaTrcp1 targeted to epithelial cells
- Overexpression of Delta F beta TrCP1 or beta TrCP1 in vivo induce tumors through beta-catenin activation.
- beta-TRCP1 and beta-TRCP2 were identified as F-box proteins that would associate with Per1 in a CK1epsilon-dependent manner
- analysis of conformation of the oncogenic protein beta-catenin containing the phosphorylated motif DpSGXXpS bound to the beta-TrCP protein
- Two Vpu analog phosphopeptides are characterized efficiently by nuclear magnetic resonance to bind to human F-box protein beta-transducin repeat containing (BTRC) protein WD domain.
- These data suggest that p100 processing involves its phosphorylation at specific terminal serines, which form a binding site for beta-TrCP thereby regulating p100 ubiquitination.
- betaTrCP, the vertebrate homolog of Slimb, is required for Gli3 processing, and can bind phosphorylated Gli3 both in vitro and in vivo.
- beta-TrCP2 is a pivotal regulator of Gli2 expression and there may be an important role for posttranslational modulation of GLI2 protein levels in Hh pathway-associated human prostate cancer
- Overexpression of BTRC is associated with Split-hand/split-foot malformation 3
- Multisite glycogen synthase kinase 3beta (GSK3beta) phosphorylation and ubiquitination by SCFbetaTrCP are required for Gli3 processing.
- constitutive FN degradation, as well as UV-induced degradation, is ubiquitination dependent and controlled by beta-TrCP
- in response to mitogens, PDCD4 was rapidly phosphorylated by protein kinase S6K1 & then degraded by ubiquitin ligase SCF(betaTRCP); it is proposed that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis & cell growt
- beta-TRCP1 expression significantly shortens the protein half-life of pro-caspase 3.
- Somatic mutations of the beta-TrCP gene may contribute to the development of gastric cancer through beta-catenin stabilization.
- The bound structure of 24P-IkappaBalpha peptide suggests that these domains are crucial for the interaction of the peptide with its receptor showing the protons identified by STD NMR as exposed in close proximity to the beta-TrCP surface.
- Results indicate that the turnover of Mcl-1 by beta-TrCP is an essential mechanism for GSK-3beta-induced apoptosis and contributes to GSK-3beta-mediated tumor suppression and chemosensitization.
- ESE-1 functions are coordinately regulated by Pak1 phosphorylation and beta-TrCP-dependent ubiquitin-proteasome pathways.
- Study reveals that SCF(betaTrCP1) is an E3 ligase that activates p63 through ubiquitylation.
- NMR allowed the study of competition for binding to beta-TrCP, between the phosphorylation motifs of ATF4 and beta-catenin and identifies the residues of the beta-TrCP receptor involved in ligand recognition.
- GSK3 beta is a bona fide PRLr kinase that phosphorylates PRLr on Ser(349) and is required for the recognition of PRLr by beta Trcp, as well as for PRLr ubiquitination and degradation
- REST is degraded by means of the ubiquitin ligase SCF(beta-TrCP) during the G2 phase of the cell cycle to allow transcriptional derepression of Mad2, an essential component of the spindle assembly checkpoint
- REST is a key target in beta-TRCP-driven transformation and the beta-TRCP-REST axis is a new regulatory pathway controlling neurogenesis
- a high level of p53 downregulates the beta-catenin expression, but this effect is attenuated by non-functional AXIN2 or betaTrCP in lung cancer.
- Proteolysis of Bora requires the Plk1 kinase activity and is mediated by SCF-beta-TrCP; Plk1 phosphorylates a conserved DSGxxT degron in Bora and promotes its interaction with beta-TrCP.
- We conclude that SCF(betaTrCP) is the E3 ubiquitin ligase responsible for securin degradation after UV irradiation, and that it is involved in securin turnover in nonstressed cells.
- beta-TrCP-dependent degradation takes part in controlling cyclin D1 turnover when cancer cells undergo glucose starvation, which endows physiological relevance to this novel mechanism.
- The SCF(beta-TrCP) binding site created by phosphorylation of beta-catenin is highly vulnerable to protein phosphatase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protein.
- betaTrCP promotes cell survival in cooperation with the ERK-RSK pathway by targeting BimEL for degradation.