Gene Ontology annotation through association of InterPro records with GO terms
Gene Ontology annotation based on Enzyme Commission mapping
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 UniPathway vocabulary mapping
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
Mammalian homologs of seven in absentia regulate DCC via the ubiquitin-proteasome pathway.
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SIAH proteins bind the DCC cytoplasmic domain, interact with ubiquitin-conjugating enzymes, localize predominantly to the cytoplasm, and regulate DCC via proteasome-dependent degradation; an N-terminal Ubc-binding-deficient mutant binds but cannot degrade DCC.
Characterization of human homologs of the Drosophila seven in absentia (sina) gene.
Siah-1 mediates a novel beta-catenin degradation pathway linking p53 to the adenomatous polyposis coli protein.
Regulation of BOB.1/OBF.1 stability by SIAH.
An anthropoid-specific locus of orphan C to U RNA-editing enzymes on chromosome 22.
Structural analysis of Siah1-Siah-interacting protein interactions and insights into the assembly of an E3 ligase multiprotein complex.
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Siah1 is the central component of a multiprotein E3 ligase complex (with SIP/CACYBP, SKP1, Ebi) that targets beta-catenin for destruction in response to p53; SIP binds Siah1 via a consensus PXAXVXP motif and provides the scaffold positioning substrate and E2.
Siah1 interacts with the scaffold protein POSH to promote JNK activation and apoptosis.
Synphilin-1A inhibits seven in absentia homolog (SIAH) and modulates alpha-synuclein monoubiquitylation and inclusion formation.
Analysis of the human E2 ubiquitin conjugating enzyme protein interaction network.
Comparison of an expanded ataxia interactome with patient medical records reveals a relationship between macular degeneration and ataxia.
ARTS and Siah collaborate in a pathway for XIAP degradation.
Next-generation sequencing to generate interactome datasets.
E3 ubiquitin ligase Siah-1 facilitates poly-ubiquitylation and proteasomal degradation of the hepatitis B viral X protein.
Toward an understanding of the protein interaction network of the human liver.
Systematic analysis of dimeric E3-RING interactions reveals increased combinatorial complexity in human ubiquitination networks.
Polycystin-1 regulates the stability and ubiquitination of transcription factor Jade-1.
MOR is not enough: identification of novel mu-opioid receptor interacting proteins using traditional and modified membrane yeast two-hybrid screens.
A proteome-scale map of the human interactome network.
The SIAH E3 ubiquitin ligases promote Wnt/β-catenin signaling through mediating Wnt-induced Axin degradation.
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SIAH1/2 are the E3 ligases mediating Wnt-induced ubiquitination and proteasomal degradation of AXIN1 (via a VxP motif), counteracted by GSK3 binding; SIAH1 knockout blocks Wnt-induced Axin ubiquitination and attenuates beta-catenin stabilization, a feed-forward mechanism sustaining Wnt signaling.
De novo variants in SIAH1, encoding an E3 ubiquitin ligase, are associated with developmental delay, hypotonia and dysmorphic features.
DAZAP2 acts as specifier of the p53 response to DNA damage.
DCC interaction with SIAH1
SIAH1:UBE2L6:Ubiquitin binds SNCA
SIAH1:UBE2L6:Ubiquitin ubiquitinates SNCA
Ub-SNCA dissociates from the conjugating enzyme
SIAH1, SIAH2 ubiquitinate SNCAIP
Transfer of Ub from E2 to substrate and release of E2
Release of E3 from polyubiquitinated substrate
Polyubiquitination of substrate
Interaction of E3 with substrate and E2-Ub complex