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Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7.
FBXW7 is critical for RIG-I stabilization during antiviral responses.
Expression of miR-223 is negatively correlated with F-box and WD repeat domain-containing 7 (FBXW7) expression in cells and tissues.
FBXW7 conduction of tumour suppression was partly through degrading Snai1 directly for ubiquitylating regulation in NSCLC.
Data showed that both chemo and radiation sensitivity increased in TE-8 and KYSE140 cells overexpressing FBXW7 compared with mock cells because of the degradation of the anti-apoptotic protein MCL1.
Fbw7 mutations shifted cellular metabolism toward oxidative phosphorylation and caused context-specific metabolic vulnerabilities.
TINCR suppressed proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer.
Low FBXW7 expression is associated with non-small cell lung cancer.
we identified F-box and WD repeat domain-containing 7 (FBXW7) protein as a direct functional target of miR-25 in esophageal squamous cell carcinoma (ESCC). In conclusion, the present study supports the potential of miR-25 as a prognostic predictor with its high expression in cancer tissues and its association with tumor progression by targeting FBXW7 in ESCC
FBXW7 was significantly downregulated in renal cell carcinoma cell lines. Upregulation of FBXW7 in 786-O and ACHN cell lines significantly inhibited cell migration, invasion and EMT.
FBXW7 missense mutation is associated with metastatic colorectal adenocarcinoma.
miR-92b-3p inhibition prevented colorectal cancer proliferation, invasion, and migration by upregulating FBXW7, which might suggest the potential role of miR-92b-3p in colorectal carcinogenesis and metastasis.
FBXW7 is markedly downregulated in the liver of obese subjects. A functional low-frequency human FBXW7 coding variant (p.Ala204Thr) is associated with elevated blood glucose and T2DM risk in a Chinese population. Mechanistically, FBXW7 directly binds to hepatokine fetuin-A to induce its ubiquitination and subsequent proteasomal degradation, comprising an important mechanism maintaining glucose homeostasis.
Our findings suggest FBW7 mutational status and Mcl-1 stability as key determinants of response to Hsp90 inhibitors, which provides a rationale for using FBW7 genotype for potential patient stratification, and for drug combinations with Hsp90 inhibitors that can effectively overcome Mcl-1-mediated resistance.
a cancer stem cell-specific FBXW7-regulatory mechanism is strongly associated with resistance to chemotherapeutic agents.
FBW7 promoted gemcitabine sensitivity via upregulation of equilibrative nucleoside transporter 1 (ENT1) at the protein level rather than the transcriptional level.
FBW7 overexpression downregulated Aurora B, Mcl1 and Notch1 levels.
FBXW7 was a downstream target of miR-367 and CASC2 prohibited epithelial-to-mesenchymal transition progression and subsequently exerted its anti-metastatic effects via CASC2/miR-367/FBXW7 axis in hepatocellular carcinoma cells.
FBW7 cooperated with gamma-catenin to inhibit G2/M cell cycle transition and cell proliferation.
We also propose a model for the stabilization mechanism in which binding to Aurora-A alters how N-Myc interacts with SCF(FbxW7) to disfavor the generation of Lys48-linked polyubiquitin chains
Loss of Fbxw7 in the presence of BrafV600E mutation is consequential and sufficient to drive melanoma development.
A novel mouse line carrying a conditional knockin allele of a cancer-specific FBXW7 mutation was established for carcinogenesis study.
results thus suggest that Fbxw7 controls the transcription of MyRF target genes in various tissues through regulation of MyRF protein stability in a manner dependent on MyRF phosphorylation by GSK-3.
FBXW7 is markedly downregulated in the liver of obese mice. Mechanistically, FBXW7 directly binds to hepatokine fetuin-A to induce its ubiquitination and subsequent proteasomal degradation, comprising an important mechanism maintaining glucose homeostasis.
the regulatory crosstalk between KLF5, miR-29a, and Fbw7/CDC4 cooperatively promotes atherosclerotic development
found that Fbw7 loss caused activation of NF-kappaB signaling. Thus, FBW7 plays a protective role in acute intestinal inflammation by modulating the inflammatory response of NF-kappaB pathway.
EglN2 might act as an FBW7 ubiquitin ligase substrate contributing to the progression of triple negative breast cancer.
These findings highlight the molecular basis of Hajdu-Cheney syndrome (HCS) pathogenesis and provide clinical insights into potential targeted therapeutic strategies for skeletal disorders associated with the aberrant FBW7/NOTCH2 pathway as observed in patients with HCS.
The findings reveal a PLK1-Fbw7-Myc signaling circuit that underlies tumorigenesis and validate PLK1 inhibitors, alone or with Bcl2 antagonists, as potential effective therapeutics for MYC-overexpressing cancers.
Fbxw7 suppresses KrasG12D-induced pancreatic tumorigenesis via a Yap-dependent mechanism.
Myoblast differentiation potential and muscle regeneration can be regulated by Fbxw7beta.
Study identifies a REV-ERBalpha post-translational regulatory circuit in which cyclin-dependent kinase 1 (CDK1) phosphorylation of REV-ERBalpha is recognized by the F-box protein, FBXW7alpha, to direct REV-ERBalpha degradation via the proteasome. Disruption of this CDK1-FBXW7-mediated REV-ERBalpha degradation pathway in mouse liver alters circadian rhythmicity, in particular amplitude, and whole-body lipid/glucose home...
Gene expression profiling reveals transcriptional regulation by Fbxw7/mTOR pathway in radiation-induced mouse thymic lymphomas.
Prion infection induced the expression of FBXW7 in brain.
FBXW7 facilitates nonhomologous end-joining via K63-linked polyubiquitylation of XRCC4 in tumor cells.
data demonstrate that Fbw7alpha negatively regulates osteogenesis by targeting Runx2 for ubiquitin-mediated degradation in a GSK3beta-dependent manner
In mice, an unusually direct antagonism between an E3 ligase and a deubiquitinase, Fbw7 and Usp28, modulate intestinal homeostasis and cancer.
These data show that cell cycle-dependent mechanisms can control ciliary length through a CDK5-FBW7-NDE1 pathway.
Dual regulation of Fbw7 activity by Usp28 is a safeguard mechanism for maintaining physiological levels of proto-oncogenic Fbw7 substrates, which is equivalently disrupted by loss or overexpression of Usp28.
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. This protein binds directly to cyclin E and probably targets cyclin E for ubiquitin-mediated degradation. Mutations in this gene are detected in ovarian and breast cancer cell lines, implicating the gene's potential role in the pathogenesis of human cancers. Multiple transcript variants encoding different isoforms have been found for this gene.
F-box and WD-40 domain protein 7
, F-box/WD repeat-containing protein 7
, F-box and WD-40 domain protein 7 (archipelago homolog, Drosophila)
, F-box protein FBW7
, F-box protein FBX30
, F-box protein SEL-10
, homolog of C elegans sel-10
, F-box and WD-40 domain protein 7, archipelago homolog
, F-box and WD-40 domain-containing protein 7
, F-box protein Fbxw6
, F-box-WD40 repeat protein 6
, f-box only protein 30