Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
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
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
GSK-3beta-dependent phosphorylation of adenomatous polyposis coli gene product can be modulated by beta-catenin and protein phosphatase 2A complexed with Axin.
Mutations in AXIN2 cause colorectal cancer with defective mismatch repair by activating beta-catenin/TCF signalling.
Activation of AXIN2 expression by beta-catenin-T cell factor. A feedback repressor pathway regulating Wnt signaling.
Subcellular distribution of Wnt pathway proteins in normal and neoplastic colon.
Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer.
Epigenetic silencing of AXIN2 in colorectal carcinoma with microsatellite instability.
Axis inhibition protein 2 (AXIN2) polymorphisms may be a risk factor for selective tooth agenesis.
Aberrant Wnt/beta-catenin signaling can induce chromosomal instability in colon cancer.
A Wnt-Axin2-GSK3beta cascade regulates Snail1 activity in breast cancer cells.
Wilms tumor suppressor WTX negatively regulates WNT/beta-catenin signaling.
Frameshift mutations of Wnt pathway genes AXIN2 and TCF7L2 in gastric carcinomas with high microsatellite instability.
Tankyrase inhibition stabilizes axin and antagonizes Wnt signalling.
Conductin/axin2 and Wnt signalling regulates centrosome cohesion.
The ubiquitin-specific protease USP34 regulates axin stability and Wnt/β-catenin signaling.
RNF146 is a poly(ADP-ribose)-directed E3 ligase that regulates axin degradation and Wnt signalling.
Nuclear PKM2 regulates β-catenin transactivation upon EGFR activation.
Interlaboratory reproducibility of large-scale human protein-complex analysis by standardized AP-MS.
The protein interaction landscape of the human CMGC kinase group.
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.
TGIF governs a feed-forward network that empowers Wnt signaling to drive mammary tumorigenesis.
An AP-MS- and BioID-compatible MAC-tag enables comprehensive mapping of protein interactions and subcellular localizations.
Isoform-specific GSK3A activity is negatively correlated with human sperm motility.
A reference map of the human binary protein interactome.
Kinase Interaction Network Expands Functional and Disease Roles of Human Kinases.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
Downregulation of beta-catenin by human Axin and its association with the APC tumor suppressor, beta-catenin and GSK3 beta.
RNF146 binds RibC-AXIN:TNKS complex
Tankyrase ADP-ribosylates AXIN
RNF146 ubiquitinates ADP-ribosylated AXIN
USP34 deubiquitinates AXIN1,AXIN2
Ub-RibC-AXIN is degraded by the proteasome
TCF/LEF:CTNNB1 promote transcription of AXIN2
AXIN is ubiquitinated by SMURF2
Ubiquitinated AXIN is degraded by the proteasome
CHD8:CTNNB1 represses AXIN2 expression
Up-regulation of Axin2 by dexamethasone promotes adipocyte differentiation in ROB-C26 mesenchymal progenitor cells.
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In rat ROB-C26 progenitor cells, dexamethasone induces Axin2 through glucocorticoid-receptor signaling. Axin2 knockdown alters beta-catenin-associated osteoblastic and adipogenic responses. This supports the existing ortholog-inferred response and differentiation annotations without implying steroid binding or a direct human experiment.
Loss of Axin2 results in impaired heart valve maturation and subsequent myxomatous valve disease.
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Axin2-deficient mice have increased Wnt signaling, abnormal postnatal valve maturation and progressive valve extracellular-matrix changes. These mouse perturbation results support existing transferred developmental annotations; they do not establish a separate extracellular-matrix structural activity or a human valve assay.