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
Additional sex comb-like 1 (ASXL1), in cooperation with SRC-1, acts as a ligand-dependent coactivator for retinoic acid receptor.
Protein interaction data set highlighted with human Ras-MAPK/PI3K signaling pathways.
Defining the human deubiquitinating enzyme interaction landscape.
Histone H2A deubiquitinase activity of the Polycomb repressive complex PR-DUB.
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Reconstituted human and fly PR-DUB complexes act on nucleosomal H2A; the catalytic subunit is BAP1/Calypso.
"Reconstituted recombinant Drosophila and human PR-DUB complexes remove
monoubiquitin from H2A but not from H2B in nucleosomes."
ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression.
A High-Density Map for Navigating the Human Polycomb Complexome.
A reference map of the human binary protein interactome.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
BAP1 binds BAP1-interacting complex
Histone H2A is dubiquitinated by the PR-DUB complex
Additional sex comb-like (ASXL) proteins 1 and 2 play opposite roles in adipogenesis via reciprocal regulation of peroxisome proliferator-activated receptor {gamma}.
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ASXL1 and ASXL2 were assayed for PPAR association; the original Methods distinguish their expression constructs.
"ASXL1 and its paralog, ASXL2, interacted with PPARĪ± and PPARĪ³."
BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.
An Adversarial DNA N(6)-Methyladenine-Sensor Network Preserves Polycomb Silencing.
MBD5 and MBD6 stabilize the BAP1 complex and promote BAP1-dependent cancer.
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ASXL PHD domains can connect MBD proteins to BAP1; endogenous deletion experiments specifically involve ASXL1 and ASXL2.
"the removal of the PHD fingers completely blocked the interaction between endogenous MBD6 and ASXL1/ASXL2 proteins"
Structural basis of histone H2A lysine 119 deubiquitination by Polycomb repressive deubiquitinase BAP1/ASXL1.
ASXL1 manual source and evidence notes