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Validated All-in-One™ qPCR Primer for FBXW7(NM_033632.3) Search again
Product ID:
HQP106116
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AGO, CDC4, DEDHIL, FBW6, FBW7, FBX30, FBXO30, FBXW6, SEL-10, SEL10, hAgo, hCdc4
Gene Description:
F-box and WD repeat domain containing 7
Target Gene Accession:
NM_033632.3(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.
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 was previously referred to as FBX30, and belongs to the Fbws class; in addition to an F-box, this protein contains 7 tandem WD40 repeats.
Gene References into function
- associates specifically with phosphorylated cyclin E, and SCFFbw7 catalyzes cyclin E ubiquitination in vitro
- Both BRAF and FBXW7 mutations functionally activate kinase effectors important in pancreatic cancer and extend the potential options for therapeutic targeting of kinases in the treatment of phenotypically distinct pancreatic adenocarcinoma subsets.
- antagonizes the apoptotic c-Jun-dependent effector arm of JNK signaling, allowing neurons to tolerate potentially neurotoxic JNK activity
- hCdc4 function is a prerequisite for cell cycle regulation of cyclin E levels, and loss of hCdc4 function is sufficient to deregulate cyclin E in cancer.
- genetic inactivation of hCDC4, by means of targeted disruption of the gene in karyotypically stable colorectal cancer cells, results in a striking phenotype associated with micronuclei and chromosomal instability
- Results show that the F-box protein Fbw7 interacts with and destabilizes c-Myc in a manner dependent on phosphorylation of its MB1 domain.
- Because Fbw7 mediates the degradation of cyclin E, Notch, and c-Jun, as well as c-Myc, the loss of Fbw7 is likely to elicit profound effects on cell proliferation during tumorigenesis.
- The observed cyclin E deregulation is attributed to the downregulation of Fbxw7, which encodes the Fbw7 receptor subunit of the SCF(FBW7) ubiquitin ligase (E3) responsible for targeting cyclin E for proteolysis.
- Fbw7gamma regulates c-Myc's growth-promoting function in the nucleolus.
- SV40 large T antigen competes with cellular proteins for Fbw7 binding in a substrate-like fashion
- The SV40 large T antigen contains a decoy phosphodegron that mediates its interactions with Fbw7/hCdc4
- Fbw7 may be a major regulator of lipid metabolism through control of the phosphorylation-dependent degradation of the sterol regulatory element binding protein family of transcription factors.
- These results identify glycogen synthase kinase 3beta and FBW7 as potential cancer therapeutic targets and MYC as a critical substrate in the GSK3beta survival-signaling pathway.
- Fbxw7 seems to regulate the levels of multiple targets to suppress cancer development.
- We conclude that somatic hCDC4 mutations are infrequent in osteosarcoma, and are unlikely to play an important role in aneuploidy of this tumor.
- highly suppressed mRNA expression of the FBXW7 beta-form was found in all the human glioma cell lines analyzed; enhanced expressions of CCNE1, MYC, and AURKA were observed in these cells.
- mutations were present in only five (11.4%) of cases of primary ovarian cancer; low frequency of these mutations suggests that they are unlikely to play an important role in human ovarian tumorigenesis
- FBXW7 deficiency is unlikely to contribute to the extensive copy number aberrations associated with breast and possibly other tumor types
- FBW7 is a novel tumor suppressor in T cell leukemia, and its loss may be a potential mechanism of drug resistance in T-ALL
- FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to gamma-secretase inhibitors
- Usp28 dissociates from Fbw7alpha in response to UV irradiation, providing a mechanism how Fbw7-mediated degradation of Myc is enhanced upon DNA damage.
- FBXW7 is inactivated by mutation in diverse human cancer types with an overall mutation frequency of approximately 6%.
- There were no mutations in exons 8 or 9 in 160 acute leukemia samples from Korea, in contrast to earlier reports suggesting a role in T-ALL.
- FBW7 has a role in the development of cancer
- Fbw7 regulates the activity of endoreduplication mediators and the p53 pathway to prevent drug-induced polyploidy.
- Both SCF(Cdc4alpha) and SCF(Cdc4gamma) are required for cyclin E turnover in cell lines that do not overexpress cyclin E.
- could not confirm that hCDC4 is frequently mutated in colon cancers.
- FBXW7 mutation is associated with adult T-cell and B-cell acute lymphocytic leukemias
- summarize what is known about Fbxw7/hCdc4-mediated degradation in the regulation of cellular proliferation and discuss how alteration of its function contributes to human tumorigenesis
- These data suggest that oscillations in cyclin E-CDK2-specific activity during the cell cycle regulate the timing of cyclin E degradation.
- Fbxw7, the F-box protein of an SCF complex, targets c-Myb for degradation in a Wnt-1- and NLK-dependent manner.
- p18-Cyclin E by the Skp1-Cul1-Fbw7 (SCF) complex and its interaction with the Fbw7 protein isoforms can take place independently of phosphorylation of p18-Cyclin E at a C-terminal phosphodegron.
- findings show mTOR is targeted for ubiquitination & degradation by binding to FBXW7; breast cancer cell lines & primary tumors showed a reciprocal relation between loss of FBXW7 & deletion or mutation of PTEN, which also activates mTOR
- The inactivation of the FBXW7 beta-form plays an important role in the pathogenesis of gliomas;an unknown mechanism(s) other than mutation and methylation is the major cause of the suppression of the FBXW7 beta-form in gliomas.
- A significantly high frequency of methylation in the FBXW7 beta-form promoter was observed in types B1 or higher human thymomas.