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stress-induced homeostatically regulated protein degradation pathway

Term Information

Accession
GO:0120174
Name
stress-induced homeostatically regulated protein degradation pathway
Ontology
biological_process
Synonyms
SHRED pathway
Alternate IDs
None
Definition
A stress-inducible protein catabolic pathway that promotes protein quality control by accelerating the degradation of misfolded ER membrane and cytosolic proteins, as well as native proteins. The pathway starts with the activation, by stress, of the Nma111p/Ynm3p serine protease, which cleaves the stress-induced hydrophilin Roq1p, resulting in the generation of a Roq1p cleavage product that selectively interacts with Ubr1p, an E3 ubiquitin ligase. Interaction with the Ubr1p type-1 substrate binding site reprograms the substrate specificity of this ubiquitin ligase resulting in the selective proteasome-mediated degradation of misfolded and native proteins. The pathway ends with degradation of the protein by the cytoplasmic proteasome. Currently, NMA111, ROQ1, UBR1, RAD6, and CDC48 are considered to be involved in this quality control pathway. Source: GOC:rn, PMID:29861160, GOC:rl
Comment
Note, although the SHRED pathway may contain some components in common with ER-associated protein degradation (ERAD) pathways (GO:0036503), such as UBR1, RAD6 and CDC48, other ERAD components, such as HRD1 and DOA10 do not appear to be involved, and as such these pathways are currently considered to be distinct. ERAD pathways target misfolded ER lumenal proteins (ERAD-L), ER membrane proteins (ERAD-M) and ER proteins with misfolded cytosolic domains (ERAD-C) by recognizing aberrant proteins, retrotranslocating these substrates to the cytosol, followed by subsequent substrate ubiquitination and proteosome-mediated degradation. In contrast the SHRED pathway, although inducible by stress, targets diverse ER membrane and cytosolic proteins as well as numerous other native proteins in the absence of stress. In the SHRED pathway an Nma111p serine protease-mediated cleavage results in the generation of a Roq1p fragment that then binds to the type-1 active site of Ubr1p, altering its substrate specificity, and leading to the proteasome-mediated degradation of both misfolded and native proteins. SHRED is also considered to be distinct from the endoplasmic reticulum unfolded protein response (GO:0030968), a process by which ER stress activates the ER membrane protein Ire1p, resulting in splicing of the HAC1 mRNA, followed by Hac1p-mediated up-regulation of UPR genes. Induction of SHRED does not require IRE1 or HAC1, and as such is currently considered to be distinct.
History
See term history for GO:0120174 at QuickGO
Subset
None
Feedback
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Parents of stress-induced homeostatically regulated protein degradation pathway (GO:0120174)
subject[Reorder by subject] relation[Reorder by relation] object[Reorder by object]
stress-induced homeostatically regulated protein degradation pathway [is_a relation] is_a  proteasome-mediated ubiquitin-dependent protein catabolic process (GO:0043161)
stress-induced homeostatically regulated protein degradation pathway [is_a relation] is_a  response to organonitrogen compound (GO:0010243)
stress-induced homeostatically regulated protein degradation pathway [is_a relation] is_a  cellular response to stress (GO:0033554)

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