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 through association of InterPro records with GO terms
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
ERdj5, an endoplasmic reticulum (ER)-resident protein containing DnaJ and thioredoxin domains, is expressed in secretory cells or following ER stress.
ERdj4 and ERdj5 are required for endoplasmic reticulum-associated protein degradation of misfolded surfactant protein C.
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ERdj5 shows prolonged specific association with misfolded SP-C and is required for its ERAD; knockdown increases ER retention and inhibits degradation.
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ERdj5 promotes turnover of misfolded SP-C in a manner dependent on its ability to stimulate BiP ATPase activity.
ERdj5 sensitizes neuroblastoma cells to endoplasmic reticulum stress-induced apoptosis.
A luminal flavoprotein in endoplasmic reticulum-associated degradation.
Meckel-Gruber syndrome protein MKS3 is required for endoplasmic reticulum-associated degradation of surfactant protein C.
Defining the membrane proteome of NK cells.
ERdj5 is the ER reductase that catalyzes the removal of non-native disulfides and correct folding of the LDL receptor.
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ERdj5 is the ER reductase that removes non-native disulfides, both preparing misfolded proteins for degradation and catalyzing folding of proteins with obligatory non-native disulfides (e.g. LDLR).
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ERdj5's role in LDLR folding is dependent on its interaction with BiP; the J-domain HPD->QPD (H63Q) mutation prevents BiP binding.
Mechanistic characterization of disulfide bond reduction of an ERAD substrate mediated by cooperation between ERdj5 and BiP.
UniProt entry Q8IXB1 (DJC10_HUMAN), Endoplasmic reticulum disulfide reductase DNAJC10 / ERdj5