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FBXO11 is a direct target of miR (show MLXIP ELISA Kits)-621 in breast cancer cells.
UBR3/6 regulate cardiomyocyte Nav 1.5 channel protein levels via the ubiquitin-proteasome pathway.
siRNA-mediated knockdown of FBXO11 facilitated HIF-1alpha (show HIF1A ELISA Kits) expression in various cancer cells and HIF-1alpha (show HIF1A ELISA Kits)-driven gene expressions, but the FBXO10 (show FBXO10 ELISA Kits) knockdown did not.
Our results identify FBXO11 as a novel miR (show MLXIP ELISA Kits)-21 target gene, and demonstrate that the oncogenic miRNA miR (show MLXIP ELISA Kits)-21 decreases the expression of FBXO11, which normally acts as a tumor suppressor, and thereby promotes tumorigenesis.
study defined eight additional recurrently mutated genes in SMZL; these genes are CREBBP (show CREBBP ELISA Kits), CBFA2T3 (show CBFA2T3 ELISA Kits), AMOTL1 (show AMOTL1 ELISA Kits), FAT4, FBXO11, PLA2G4D (show PLA2G4D ELISA Kits), TRRAP (show TRRAP ELISA Kits) and USH2A (show USH2A ELISA Kits).
The PKD1 (show PKD1 ELISA Kits)-FBXO11-SNAIL (show SNAI1 ELISA Kits) axis is a mechanism of posttranslational regulation of epithelial-mesenchymal transition and cancer metastasis.
TGF-beta signaling promotes exit from the cell cycle and cellular migration through cullin cross-regulation: SCF-FBXO11 turns off CRL4-Cdt2.
The functional interaction between FBXO11 and CDT2 is evolutionary conserved from worms to humans and plays an important role in regulating the timing of cell-cycle exit.
Migration of epithelial cells is stimulated by CRL1 (show IL27RA ELISA Kits)(FBXO11)-mediated downregulation of Cdt2 (show DTL ELISA Kits) and the consequent stabilization of Set8 (show SETD8 ELISA Kits).
A molecular mechanism controlling BCL6 (show BCL6 ELISA Kits) stability--mutations and deletions in FBXO11 contribute to lymphomagenesis through BCL6 (show BCL6 ELISA Kits) stabilization
FBXO11 inactivation was associated with the development of lymphoproliferative disorders in mice.
FBXO11 regulates the TGF-beta (show TGFB1 ELISA Kits) pathway in the embryonic lung via cross-talk with p53 (show TP53 ELISA Kits).
FBXO11 is one of the first molecules to be identified, contributing to the genetic aetiology of otitis media
Relationship between dilation of endoplasmic reticulum and decreased levels of the FBXO11 gene in vitiligo (show MITF ELISA Kits) melanocytes.
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 Fbxs class. It can function as an arginine methyltransferase that symmetrically dimethylates arginine residues, and it acts as an adaptor protein to mediate the neddylation of p53, which leads to the suppression of p53 function. This gene is known to be down-regulated in melanocytes from patients with vitiligo, a skin disorder that results in depigmentation. Polymorphisms in this gene are associated with chronic otitis media with effusion and recurrent otitis media (COME/ROM), a hearing loss disorder, and the knockout of the homologous mouse gene results in the deaf mouse mutant Jeff (Jf), a single gene model of otitis media. Alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene.
F-box only protein 11
, F-box protein 11
, F-box only protein 11-like
, f-box only protein 11-like
, protein arginine N-methyltransferase 9
, ubiquitin protein ligase E3 component n-recognin 6
, vitiligo-associated protein 1
, vitiligo-associated protein VIT-1
, GENA 104