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Family with sequence similarity 123B

The protein encoded by this gene upregulates trancriptional activation by the Wilms tumor protein and interacts with many other proteins, including CTNNB1, APC, AXIN1, and AXIN2. Defects in this gene are a cause of osteopathia striata with cranial sclerosis (OSCS). [provided by RefSeq, May 2010] (from NCBI)
Top mentioned proteins: beta Catenin, CAN, p53, HAD, ACID
Papers on WTX
Clinical, pathologic, and genetic features of Wilms tumors with WTX gene mutation.
Vargas et al., Boston, United States. In Pediatr Dev Pathol, Feb 2016
UNASSIGNED: Clinical and pathologic features of patients with WTX-mutated Wilms tumor (WT) have not been studied in detail.
Adenoma development in familial adenomatous polyposis and MUTYH-associated polyposis: somatic landscape and driver genes.
Adams et al., Cardiff, United Kingdom. In J Pathol, Jan 2016
With these data we examined the profile of mutated genes, the mutational signatures and the somatic mutation rates, observing significant diversity in the constellations of mutated driver genes in different adenomas, and loss-of-function mutations in WTX (9%; p < 9.99e-06), a gene implicated in regulation of the WNT pathway and p53 acetylation.
Exome Sequencing Reveals AMER1 as a Frequently Mutated Gene in Colorectal Cancer.
Moreno et al., Barcelona, Spain. In Clin Cancer Res, Nov 2015
Among this mutational heterogeneity, variants resulting in early stop codons in the AMER1 (also known as FAM123B or WTX) gene emerged as recurrent mutations in colorectal cancer.
Structural Insight into Specificity of Interactions between Nonconventional Three-finger Weak Toxin from Naja kaouthia (WTX) and Muscarinic Acetylcholine Receptors.
Kirpichnikov et al., Moscow, Russia. In J Biol Chem, Oct 2015
Weak toxin from Naja kaouthia (WTX) belongs to the group of nonconventional "three-finger" snake neurotoxins.
Neurotoxins from snake venoms and α-conotoxin ImI inhibit functionally active ionotropic γ-aminobutyric acid (GABA) receptors.
Utkin et al., Moscow, Russia. In J Biol Chem, Oct 2015
The α1β3γ2 receptor was also inhibited by some other three-finger toxins, long α-neurotoxin Ls III and nonconventional toxin WTX.
[Establishment of a colorectal cancer SW620 cell line stably over-expressing Wilm's tumor on X chromosome using a recombinant lentivirus vector].
Ding et al., Guangzhou, China. In Nan Fang Yi Ke Da Xue Xue Bao, Aug 2015
OBJECTIVE: To construct a recombinant lentivirus vector for Wilm's tumor on X chromosome (WTX) gene and establish a colorectal cancer SW620 cell line with stable WTX over-expression.
The development of Wilms tumor: from WT1 and microRNA to animal models.
Yang et al., Zhengzhou, China. In Biochim Biophys Acta, 2014
This has been illustrated by the findings that mutations of Wnt/β-catenin pathway-related WT1, β-catenin, and WTX together account for about one-third of Wilms tumor cases.
Genetics of pediatric renal tumors.
Royer-Pokora, Düsseldorf, Germany. In Pediatr Nephrol, 2013
Other genes frequently altered somatically in subsets of WT are CTNNB1 and WTX; both genes influence the Wnt signalling pathway.
Comprehensive molecular characterization of human colon and rectal cancer.
Cancer Genome Atlas Network, In Nature, 2012
Twenty-four genes were significantly mutated, and in addition to the expected APC, TP53, SMAD4, PIK3CA and KRAS mutations, we found frequent mutations in ARID1A, SOX9 and FAM123B.
The WTX tumor suppressor enhances p53 acetylation by CBP/p300.
Haber et al., United States. In Mol Cell, 2012
WTX modulates p53 function, in part through regulation of its activator CBP/p300.
Wilms tumor gene on X chromosome (WTX) inhibits degradation of NRF2 protein through competitive binding to KEAP1 protein.
Moon et al., Seattle, United States. In J Biol Chem, 2012
WTX and NRF2 compete for binding to KEAP1, and thus loss of WTX leads to rapid ubiquitination and degradation of NRF2 and a reduced response to cytotoxic insult.
WTX R353X mutation in a family with osteopathia striata and cranial sclerosis (OS-CS): case report and literature review of the disease clinical, genetic and radiological features.
Duse et al., Roma, Italy. In Ital J Pediatr, 2011
WTX gene (Xq11) has been recently identified as the disease causing gene.
Two novel WTX mutations underscore the unpredictability of male survival in osteopathia striata with cranial sclerosis.
Van Hul et al., Edegem, Belgium. In Clin Genet, 2011
Recently, the disease-causing gene was identified as the WTX gene (FAM123B).
Structural and functional characterization of the Wnt inhibitor APC membrane recruitment 1 (Amer1).
Behrens et al., Erlangen, Germany. In J Biol Chem, 2011
Amer1 exerts its negative regulatory role in Wnt signaling by acting as a scaffold protein for the beta-catenin destruction complex and promoting stabilization of Axin at the plasma membrane.
The WTX tumor suppressor regulates mesenchymal progenitor cell fate specification.
Bardeesy et al., Boston, United States. In Dev Cell, 2011
The constellation of anomalies in Wtx null mice suggests that this tumor suppressor broadly regulates mesenchymal progenitor cells in multiple tissues.
WT1 mutation and 11P15 loss of heterozygosity predict relapse in very low-risk wilms tumors treated with surgery alone: a children's oncology group study.
Huff et al., Chicago, United States. In J Clin Oncol, 2011
PATIENTS AND METHODS: Fifty-six VLRWTs (10 relapses) were analyzed for mutation of WT1, CTNNB1, and WTX; for 11p15 LOH using microsatellite analysis; and for H19DMR and KvDMR1 methylation.
Functional characterization of Wilms tumor-suppressor WTX and tumor-associated mutants.
Licht et al., Chicago, United States. In Oncogene, 2011
When gene expression changes mediated by wild-type WTX were compared with those affected by mutant WTX, WTX565 had a 55% overlap in differentially regulated genes, whereas WTX358 regulated only two genes affected by wild-type WTX.
Wilms' tumours: about tumour suppressor genes, an oncogene and a chameleon gene.
Huff, Houston, United States. In Nat Rev Cancer, 2011
Genes identified as being mutated in Wilms' tumour include TP53, a classic tumour suppressor gene (TSG); CTNNB1 (encoding β-catenin), a classic oncogene; WTX, which accumulating data indicate is a TSG; and WT1, which is inactivated in some Wilms' tumours, similar to a TSG.
Germline mutations in WTX cause a sclerosing skeletal dysplasia but do not predispose to tumorigenesis.
Robertson et al., Dunedin, New Zealand. In Nat Genet, 2009
The observed phenotypic discordance dependent upon whether a mutation is germline or occurs somatically suggests the existence of temporal or spatial constraints on the action of WTX during tumorigenesis.
Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling.
Moon et al., Seattle, United States. In Science, 2007
findings show that WTX, a protein encoded by a gene mutated in Wilms tumors, forms a complex with beta-catenin, AXIN1, beta-TrCP2 and APC; data provide a possible mechanistic explanation for the tumor suppressor activity of WTX
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