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Function
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27 Pathways
- Beta-catenin phosphorylation cascade,
- Disassembly of the destruction complex and recruitment of AXIN to the membrane,
- Disease,
- AMER1 mutants destabilize the destruction complex,
- Hedgehog 'on' state,
- Signal Transduction,
- Signaling by WNT,
- Truncations of AMER1 destabilize the destruction complex,
- Activation of SMO,
- TCF dependent signaling in response to WNT,
- truncated APC mutants destabilize the destruction complex,
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex,
- AXIN missense mutants destabilize the destruction complex,
- Degradation of GLI2 by the proteasome,
- S33 mutants of beta-catenin aren't phosphorylated,
- Signaling by Hedgehog,
- APC truncation mutants have impaired AXIN binding,
- Hedgehog 'off' state,
- Degradation of beta-catenin by the destruction complex,
- Diseases of signal transduction by growth factor receptors and second messengers,
- S37 mutants of beta-catenin aren't phosphorylated,
- T41 mutants of beta-catenin aren't phosphorylated,
- Signaling by WNT in cancer,
- GLI3 is processed to GLI3R by the proteasome,
- S45 mutants of beta-catenin aren't phosphorylated,
- Misspliced GSK3beta mutants stabilize beta-catenin,
- AXIN mutants destabilize the destruction complex, activating WNT signaling
Gene --> GO terms.
Gene -> HPO annotation (Human Phenotype Ontology)
Mouse Gene --> Allele [Phenotype]
Genomics
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Gene --> Chromosomal location.
Gene --> GO terms.
Gene --> Overlapping genes.
Disease
Gene (Hum OR Rat) --> Mouse Allele (Phenotype)
Gene --> Alleles and Disease (clinVar data)
Gene -> HPO annotation (Human Phenotype Ontology)
Mouse Gene --> Allele [Phenotype]
Other
27 Pathways
- Beta-catenin phosphorylation cascade,
- Disassembly of the destruction complex and recruitment of AXIN to the membrane,
- Disease,
- AMER1 mutants destabilize the destruction complex,
- Hedgehog 'on' state,
- Signal Transduction,
- Signaling by WNT,
- Truncations of AMER1 destabilize the destruction complex,
- Activation of SMO,
- TCF dependent signaling in response to WNT,
- truncated APC mutants destabilize the destruction complex,
- phosphorylation site mutants of CTNNB1 are not targeted to the proteasome by the destruction complex,
- AXIN missense mutants destabilize the destruction complex,
- Degradation of GLI2 by the proteasome,
- S33 mutants of beta-catenin aren't phosphorylated,
- Signaling by Hedgehog,
- APC truncation mutants have impaired AXIN binding,
- Hedgehog 'off' state,
- Degradation of beta-catenin by the destruction complex,
- Diseases of signal transduction by growth factor receptors and second messengers,
- S37 mutants of beta-catenin aren't phosphorylated,
- T41 mutants of beta-catenin aren't phosphorylated,
- Signaling by WNT in cancer,
- GLI3 is processed to GLI3R by the proteasome,
- S45 mutants of beta-catenin aren't phosphorylated,
- Misspliced GSK3beta mutants stabilize beta-catenin,
- AXIN mutants destabilize the destruction complex, activating WNT signaling