GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 19 Dec 2016.
Chibby homolog 1
cBy
Beta-catenin is a transcriptional activator and oncoprotein involved in the development of several cancers. The protein encoded by this gene interacts directly with the C-terminal region of beta-catenin, inhibiting oncogenic beta-catenin-mediated transcriptional activation by competing with transcription factors for binding to beta-catenin. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from
NCBI)
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HAD, ACID, CAN, AGE, TCF
Papers on
cBy
Chibby functions to preserve normal ciliary morphology through the regulation of intraflagellar transport in airway ciliated cells.
New
Stony Brook, United States. In Cell Cycle, Nov 2015
We have previously reported that loss of the basal body protein Chibby (Cby) results in chronic upper airway infection in mice due to a significant reduction in the number of airway cilia.
Maintenance of Clonogenic KIT(+) Human Colon Tumor Cells Requires Secretion of Stem Cell Factor by Differentiated Tumor Cells.
New
Utrecht, Netherlands. In Gastroenterology, Sep 2015
Expression of KIT in human tumors was analyzed with gene expression arrays and by immunohistochemistry. Colonospheres were injected into the livers of CBy.Cg-Foxn1nu/J mice.
Immune-mediated bone marrow failure in C57BL/6 mice.
New
Bethesda, United States. In Exp Hematol, Apr 2015
Lowering the total-body irradiation dose to 5 G or altering the LN source from FVB to BALB/cBy donors failed to produce BM destruction.
Expression of CBY and methylation of CBY at promoter region in human laryngeal squamous cell carcinoma.
New
Huzhou, China. In Tumori, Mar 2015
AIMS AND BACKGROUND: Chibby (CBY), a β-catenin binding partner, inhibits Wnt/β-catenin-mediated transcriptional activation by competing with Tcf/Lef factors for β-catenin binding and promoting the export of β-catenin from nucleus to cytoplasm.
Structural Analysis of the 14-3-3ζ/Chibby Interaction Involved in Wnt/β-Catenin Signaling.
London, Canada. In Plos One, 2014
The partially disordered Chibby (Cby) is a conserved nuclear protein that antagonizes the Wnt/β-catenin signaling pathway.
Chibby functions in Xenopus ciliary assembly, embryonic development, and the regulation of gene expression.
Boulder, United States. In Dev Biol, 2014
Chibby (Cby), a basal-body associated protein, regulates β-catenin-mediated Wnt signaling in the mouse but not Drosophila.
Downregulated Chibby in laryngeal squamous cell carcinoma with increased expression in laryngeal carcinoma Hep-2 cells.
Huzhou, China. In Oncol Rep, 2014
Chibby (Cby) inhibits Wnt/β-catenin-mediated transcriptional activation by competing with Lef-1 (the transcription factor and target of β-catenin) to bind to β-catenin.
Chibby promotes ciliary vesicle formation and basal body docking during airway cell differentiation.
Stony Brook, United States. In J Cell Biol, 2014
Mice lacking the basal body component Chibby (Cby) exhibit impaired mucociliary transport caused by defective ciliogenesis, resulting in chronic airway infection.
Chibby drives β catenin cytoplasmic accumulation leading to activation of the unfolded protein response in BCR-ABL1+ cells.
Bologna, Italy. In Cell Signal, 2013
Here we studied the impact of β catenin antagonist Chibby (CBY) on β catenin signaling in BCR-ABL1+ cells.
Inflammatory dilated cardiomyopathy in Abcg5-deficient mice.
Davis, United States. In Toxicol Pathol, 2013
B- and T-cell-deficient BALB/cBy-Rag1(null) trac/trac mice fed normal diets did not develop inflammatory infiltrates or DCM.
No important role for genetic variation in the Chibby gene in monogenic and complex obesity.
Antwerp, Belgium. In Mol Biol Rep, 2013
Chibby (CBY) has been identified as a potent proadipogenic factor required for adipocyte differentiation.
Reduced supraspinal nociceptive responses and distinct gene expression profile in CXBH recombinant inbred mice.
Tokyo, Japan. In J Pain, 2013
UNLABELLED: CXBH mice, known as an "opioid receptor-rich" strain, are a recombinant inbred mouse strain established by crossing the C57BL/6By and BALB/cBy strains.
MSH3 polymorphisms and protein levels affect CAG repeat instability in Huntington's disease mice.
Toronto, Canada. In Plos Genet, 2012
We show that in liver and striatum the R6/1 Huntington's disease (HD) (CAG)∼100 transgene, when present in a congenic C57BL/6J (B6) background, incurred expansion-biased repeat mutations, whereas the repeat was stable in a congenic BALB/cByJ (CBy) background.
Sex bias in experimental immune-mediated, drug-induced liver injury in BALB/c mice: suggested roles for Tregs, estrogen, and IL-6.
Baltimore, United States. In Plos One, 2012
METHODS: To model DILI, we immunized BALB/c, BALB/cBy, IL-6-deficient, and castrated BALB/c mice with trifluoroacetyl chloride-haptenated liver proteins.
Structural characterization of partially disordered human Chibby: insights into its function in the Wnt-signaling pathway.
GeneRIF
London, Canada. In Biochemistry, 2011
The N-terminal portion of the CBY1 is unstructured in solution, but the C-terminal half forms a coiled-coil structure.
Chibby interacts with NBPF1 and clusterin, two candidate tumor suppressors linked to neuroblastoma.
GeneRIF
Gent, Belgium. In Exp Cell Res, 2010
Chibby and clusterin were co-immunoprecipitated with NBPF1.
Nuclear-cytoplasmic shuttling of Chibby controls beta-catenin signaling.
GeneRIF
Stony Brook, United States. In Mol Biol Cell, 2010
These findings unravel the molecular basis through which a combinatorial action of Cby and 14-3-3 proteins controls the dynamic nuclear-cytoplasmic trafficking of beta-catenin.
Fine-tuning of nuclear-catenin by Chibby and 14-3-3.
Review
Stony Brook, United States. In Cell Cycle, 2009
Chibby (Cby) is an evolutionarily conserved antagonist of beta-catenin, a central player of the canonical Wnt signaling pathway, which acts as a transcriptional coactivator.
Chibby forms a homodimer through a heptad repeat of leucine residues in its C-terminal coiled-coil motif.
GeneRIF
Stony Brook, United States. In Bmc Mol Biol, 2008
Alanine substitutions of two or more of four critical leucine residues within the C-terminal heptad repeats eliminate the Cby-Cby interaction.
Real-time quantitative PCR analysis of pediatric ependymomas identifies novel candidate genes including TPR at 1q25 and CHIBBY at 22q12-q13.
GeneRIF
London, United Kingdom. In Genes Chromosomes Cancer, 2008
genes including CHIBBY involved in pediatric ependymomas.
