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F-box protein 11

Jeff, FBXO11, VIT1, J-F
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. [provided by RefSeq, Jun 2010] (from NCBI)
Top mentioned proteins: Ubiquitin, SCF, CAN, Cullin, V1a
Papers on Jeff
Interactions between the otitis media gene, Fbxo11, and p53 in the mouse embryonic lung.
Brown et al., London, United Kingdom. In Dis Model Mech, Jan 2016
The Jeff mouse mutant carries a mutation in the Fbxo11 gene, a member of the F-box family, and develops deafness due to a chronic proliferative OM.
F-box proteins: Keeping the epithelial-to-mesenchymal transition (EMT) in check.
de Herreros et al., Barcelona, Spain. In Semin Cancer Biol, Dec 2015
Here we summarize the role that these F-box proteins (Fbxw1, Fbxw7, Fbxl14, Fbxl5, Fbxo11 and Fbxo45) play in controlling EMT during development and cancer progression, a process dependent on post-translational modifications that govern their interaction with target proteins.
Overexpression of Arabidopsis VIT1 increases accumulation of iron in cassava roots and stems.
Anderson et al., Saint Louis, United States. In Plant Sci, Nov 2015
Iron is extremely abundant in the soil, but its uptake in plants is limited due to low solubility in neutral or alkaline soils.
FBXO11 represses cellular response to hypoxia by destabilizing hypoxia-inducible factor-1α mRNA.
Chun et al., Seoul, South Korea. In Biochem Biophys Res Commun, Oct 2015
PRMT9 (alternatively named FBXO11) and PRMT11 (FBXO10) are expected to have the E3 ubiquitin ligase activity through their F-box domains as well as the methyltrasferase activity.
FBXO11 promotes ubiquitination of the Snail family of transcription factors in cancer progression and epidermal development.
Lu et al., Gainesville, United States. In Cancer Lett, Jul 2015
Here we show that the F-box protein FBXO11 recognizes and promotes ubiquitin-mediated degradation of multiple Snail family members including Scratch.
MiRNA-621 sensitizes breast cancer to chemotherapy by suppressing FBXO11 and enhancing p53 activity.
Wu et al., Shanghai, China. In Oncogene, May 2015
We further show that FBXO11 is a direct functional target of miR-621 and miR-621 level is negatively correlated with FBXO11 expression in breast cancer patients.
The oncogenic microRNA-21 inhibits the tumor suppressive activity of FBXO11 to promote tumorigenesis.
Pfeffer et al., Memphis, United States. In J Biol Chem, Apr 2015
By microarray analysis and quantitative PCR we identified and validated FBXO11 (a member of the F-box subfamily lacking a distinct unifying domain) as a miR-21 target gene.
MiR-21: an environmental driver of malignant melanoma?
Melnik, Osnabrück, Germany. In J Transl Med, 2014
MiR-21 is an oncomiR that affects critical target genes of malignant melanoma, resulting in sustained proliferation (PTEN, PI3K, Sprouty, PDCD4, FOXO1, TIPE2, p53, cyclin D1), evasion from apoptosis (FOXO1, FBXO11, APAF1, TIMP3, TIPE2), genetic instability (MSH2, FBXO11, hTERT), increased oxidative stress (FOXO1), angiogenesis (PTEN, HIF1α, TIMP3), invasion and metastasis (APAF1, PTEN, PDCD4, TIMP3).
Erratum to: Ethosuximide ameliorates neurodegenerative disease phenotypes by modulating DAF-16/FOXO target gene expression.
Morgan et al., Grand Rapids, United States. In Mol Neurodegener, 2014
The corrected author list is given below:Xi Chen, Hannah V. McCue, Shi Quan Wong, Sudhanva S. Kashyap, Brian C. Kraemer, Jeff W. Barclay, Robert D. Burgoyne and Alan Morgan
PKD1 phosphorylation-dependent degradation of SNAIL by SCF-FBXO11 regulates epithelial-mesenchymal transition and metastasis.
Kang et al., Princeton, United States. In Cancer Cell, 2014
To better understand the posttranslational regulation of SNAIL, we performed a luciferase-based, genome-wide E3 ligase siRNA library screen and identified SCF-FBXO11 as an important E3 that targets SNAIL for ubiquitylation and degradation.
NMDA receptors and memory encoding.
Morris, Edinburgh, United Kingdom. In Neuropharmacology, 2013
It is humbling to think that 30 years have passed since the paper by Collingridge, Kehl and McLennan showing that one of Jeff Watkins most interesting compounds, R-2-amino-5-phosphonopentanoate (d-AP5), blocked the induction of long-term potentiation in vitro at synapses from area CA3 of the hippocampus to CA1 without apparent effect on baseline synaptic transmission (Collingridge et al., 1983).
Genetic susceptibility to otitis media in childhood.
Jamieson et al., Australia. In Laryngoscope, 2012
Reviewed in this article, these studies have identified positive association at 21 genes, including FBXO11, TLR4, and TNF, with association at five of these replicated in independent populations.
FBXO11 targets BCL6 for degradation and is inactivated in diffuse large B-cell lymphomas.
Pagano et al., New York City, United States. In Nature, 2012
A molecular mechanism controlling BCL6 stability--mutations and deletions in FBXO11 contribute to lymphomagenesis through BCL6 stabilization
FBXO11, a regulator of the TGFβ pathway, is associated with severe otitis media in Western Australian children.
Jamieson et al., Australia. In Genes Immun, 2011
these data provide strong evidence for FBXO11 as a susceptibility gene for severe OM.
The role of VIT1/FBXO11 in the regulation of apoptosis and tyrosinase export from endoplasmic reticulum in cultured melanocytes.
Xu et al., Hangzhou, China. In Int J Mol Med, 2010
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.
[Expression of InnVit/FBXO11 in vitiligo and its role in tyrosinase export from endoplasmic reticulum].
Xu et al., Hangzhou, China. In Zhonghua Yi Xue Za Zhi, 2010
FBXO11 has a lower expression in skin lesion tissues than in normal tissues from vitiligo patients.
VIT1/FBXO11 knockdown induces morphological alterations and apoptosis in B10BR mouse melanocytes.
Xu et al., Hangzhou, China. In Int J Mol Med, 2009
Relationship between dilation of endoplasmic reticulum and decreased levels of the FBXO11 gene in vitiligo melanocytes.
Localization of iron in Arabidopsis seed requires the vacuolar membrane transporter VIT1.
Guerinot et al., United States. In Science, 2006
This localization is completely abolished when the vacuolar iron uptake transporter VIT1 is disrupted.
Pharmacology of NMDA Receptors
Jane et al., Boca Raton, United States. In Unknown Journal, 0001
The discovery of NMDA receptors (NMDARs) was made possible by the synthesis and study of NMDA (Figure 12.1) and various NMDAR antagonists by Jeff Watkins and colleagues [1].
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