Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling.
AMER1 regulates the distribution of the tumor suppressor APC between microtubules and the plasma membrane.
Amer1/WTX couples Wnt-induced formation of PtdIns(4,5)P2 to LRP6 phosphorylation.
Structural and functional characterization of the Wnt inhibitor APC membrane recruitment 1 (Amer1).
Wnt signaling through inhibition of β-catenin degradation in an intact Axin1 complex.
Adenomatous polyposis coli (APC) membrane recruitment 3, a member of the APC membrane recruitment family of APC-binding proteins, is a positive regulator of Wnt-β-catenin signalling.
A human interactome in three quantitative dimensions organized by stoichiometries and abundances.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Assembly of the destruction complex
Phosphorylation of APC component of the destruction complex
Dissociation of beta-catenin from Axin and association of beta catenin with phospho-(20 aa) APC in the detruction complex
Phosphorylation of phospho- (Ser45, Thr41) beta-catenin at Ser37 by GSK-3
Phosphorylation of phospho-(Ser45 ) at Thr 41 by GSK-3
Phosphorylation of phospho-(Ser45,Thr41,Ser37) at Ser33 by GSK-3
Association of beta-catenin with the destruction complex
Phosphorylation of beta-catenin at Ser45 by CK1 alpha
Beta-catenin is released from the destruction complex
Association of beta-catenin with the RBX1:SCF(beta-TrCP1) ubiquitin ligase complex
Degradation of ubiquitinated beta catenin by the proteasome
Multi-ubiquitination of phospho-beta-catenin by RBX1:SCF(beta-TrCP1)
APC truncation mutants have impaired AXIN binding
CTNNB1 S45 mutants aren't phosphorylated by CK1alpha
CTNNB1 S33 mutants aren't phosphorylated by GSK3beta
CTNNB1 S37 mutants aren't phosphorylated by GSK3beta
CTNNB1 T41 mutants aren't phosphorylated by GSK3beta
AXIN mutants destabilize the destruction complex
AXIN is phosphorylated in the destruction complex
Misspliced GSK3beta mutants stabilize beta-catenin levels
An X chromosome gene, WTX, is commonly inactivated in Wilms tumor.
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WTX is recurrently inactivated in the assayed Wilms tumors; this supports tumor-associated biology, not a direct molecular activity.
"This gene,
which we call WTX, is inactivated in approximately one-third of Wilms tumors (15
of 51 tumors)."
Germline mutations in WTX cause a sclerosing skeletal dysplasia but do not predispose to tumorigenesis.
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Human germline WTX variants are associated with OSCS; construct-specific molecular effects remain outside this abstract.
"Here we demonstrate that germline mutations
in WTX (FAM123B), a gene that encodes a repressor of canonical WNT signaling,
cause an X-linked sclerosing bone dysplasia, osteopathia striata congenita with
cranial sclerosis (OSCS; MIM300373)."
The tumor suppressor WTX shuttles to the nucleus and modulates WT1 activity.
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WTX shuttles to a nuclear pool and co-localizes with a paraspeckle marker; the abstract does not map this to every current isoform.
"WTX is present in distinct subnuclear structures and
co-localizes with the paraspeckle marker p54NRB/NONO, suggesting a role in
transcriptional regulation."
The WTX/AMER1 gene family: evolution, signature and function.
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In the reported HEK293T reporter comparison, mouse Amer1 suppresses beta-catenin output whereas Amer2 and Amer3 do not; this does not resolve PAINT node placement.
"As previously reported, WTX/AMER1 acts as a negative regulator of β-catenin activity. In contrast, AMER2 and AMER3 do not interfere with β-catenin dependent activation of the TOP-flash reporter gene."
Wilms tumor gene on X chromosome (WTX) inhibits degradation of NRF2 protein through competitive binding to KEAP1 protein.
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A historical human 804-residue WTX construct directly binds KEAP1; motif-dependent competition with NRF2 reduces its ubiquitination without making WTX a ubiquitin ligase.
"Using this method, we determined that WTX directly interacts with KEAP1 but not with the KEAP1-associated CUL3 protein"