Use your antibodies-online credentials, if available.
抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Human Polyclonal FBXO11 Primary Antibody for IP, SimWes - ABIN252979
Duan, Cermak, Pagan, Rossi, Martinengo, di Celle, Chapuy, Shipp, Chiarle, Pagano: FBXO11 targets BCL6 for degradation and is inactivated in diffuse large B-cell lymphomas. in Nature 2012
Show all 3 Pubmed References
Human Polyclonal FBXO11 Primary Antibody for IP, WB - ABIN252978
Pagan, Marzio, Jones, Saraf, Jallepalli, Florens, Washburn, Pagano: Degradation of Cep68 and PCNT cleavage mediate Cep215 removal from the PCM to allow centriole separation, disengagement and licensing. in Nature cell biology 2014
Amphibian Polyclonal FBXO11 Primary Antibody for ChIP, WB - ABIN4890506
Lee, Pal, Tasaki, Roy, Jiang, An, Banerjee, Kwon: Synthetic heterovalent inhibitors targeting recognition E3 components of the N-end rule pathway. in Proceedings of the National Academy of Sciences of the United States of America 2008
FBXO11 is a direct target of miR (显示 MLXIP 抗体)-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 (显示 HIF1A 抗体) expression in various cancer cells and HIF-1alpha (显示 HIF1A 抗体)-driven gene expressions, but the FBXO10 (显示 FBXO10 抗体) knockdown did not.
Our results identify FBXO11 as a novel miR (显示 MLXIP 抗体)-21 target gene, and demonstrate that the oncogenic miRNA miR (显示 MLXIP 抗体)-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 (显示 CREBBP 抗体), CBFA2T3 (显示 CBFA2T3 抗体), AMOTL1 (显示 AMOTL1 抗体), FAT4 (显示 FAT4 抗体), FBXO11, PLA2G4D, TRRAP (显示 TRRAP 抗体) and USH2A (显示 USH2A 抗体).
The PKD1 (显示 PKD1 抗体)-FBXO11-SNAIL (显示 SNAI1 抗体) 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 (显示 IL27RA 抗体)(FBXO11)-mediated downregulation of Cdt2 (显示 DTL 抗体) and the consequent stabilization of Set8 (显示 SETD8 抗体).
A molecular mechanism controlling BCL6 (显示 BCL6 抗体) stability--mutations and deletions in FBXO11 contribute to lymphomagenesis through BCL6 (显示 BCL6 抗体) stabilization
FBXO11 inactivation was associated with the development of lymphoproliferative disorders in mice.
FBXO11 regulates the TGF-beta (显示 TGFB1 抗体) pathway in the embryonic lung via cross-talk with p53 (显示 TP53 抗体).
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 (显示 MITF 抗体) 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