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we confirm deleterious de novo mutations in FBXO11 as a cause of Intellectual disability and start the delineation of the associated clinical picture which may also comprise postnatal microcephaly or borderline small head size and behavioural anomalies.
High expression of FBXO11 predicted a poor survival of hepatocellular carcinoma patients.
Understanding of the functions of FBXO11.
FBXO11 is a direct target of miR-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 expression in various cancer cells and HIF-1alpha-driven gene expressions, but the FBXO10 knockdown did not.
Our results identify FBXO11 as a novel miR-21 target gene, and demonstrate that the oncogenic miRNA miR-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, CBFA2T3, AMOTL1, FAT4, FBXO11, PLA2G4D, TRRAP and USH2A.
The PKD1-FBXO11-SNAIL 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(FBXO11)-mediated downregulation of Cdt2 and the consequent stabilization of Set8.
A molecular mechanism controlling BCL6 stability--mutations and deletions in FBXO11 contribute to lymphomagenesis through BCL6 stabilization
these data provide strong evidence for FBXO11 as a susceptibility gene for severe OM.
Results support the notion that FBXO11 plays an important role in regulating proliferation and apoptosis of melanocytes, and functional export of tyrosinase from ER in vitiligo melanocytes.
FBXO11 has a lower expression in skin lesion tissues than in normal tissues from vitiligo patients.
A type II protein arginine methyltransferase that forms asymmetric dimethylarginine modifications in proteins.
The FBXO11 gene is the human homologue of the gene mutated in the novel deaf mouse mutant jeff (Jf), a single gene model of otitis media. FBXO11 gene for association with chronic otitis media with effusion.
FBXO11 promotes the Neddylation (NEDD8) of p53 and inhibits its transcriptional activity
FBXO11 inactivation was associated with the development of lymphoproliferative disorders in mice.
FBXO11 regulates the TGF-beta pathway in the embryonic lung via cross-talk with p53.
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 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
, protein arginine N-methyltransferase 9
, ubiquitin protein ligase E3 component n-recognin 6
, vitiligo-associated protein 1
, vitiligo-associated protein VIT-1
, GENA 104
, F-box protein 11
, F-box only protein 11-like
, f-box only protein 11-like