Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB Subcellular Location vocabulary mapping
Gene Ontology annotation based on curation of immunofluorescence data
Gene Ontology annotation based on inference from GO term-to-term logical definitions
Combined Automated Annotation using Multiple IEA Methods
Huntingtin interacting proteins are genetic modifiers of neurodegeneration.
HYPK, a Huntingtin interacting protein, reduces aggregates and apoptosis induced by N-terminal Huntingtin with 40 glutamines in Neuro2a cells and exhibits chaperone-like activity.
Huntingtin interacting protein HYPK is intrinsically unstructured.
The chaperone-like protein HYPK acts together with NatA in cotranslational N-terminal acetylation and prevention of Huntingtin aggregation.
Human-chromatin-related protein interactions identify a demethylase complex required for chromosome segregation.
A proteome-scale map of the human interactome network.
Architecture of the human interactome defines protein communities and disease networks.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
Multimodal cell maps as a foundation for structural and functional genomics.
Falcon deep research report for HYPK
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HYPK is a non-catalytic regulator of the NatA (NAA10-NAA15) complex that stabilizes the complex and allosterically inhibits NAA10; it is ribosome/polysome-associated near the exit tunnel together with NatA, NAC and MAP1/MAP2.
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HYPK additionally functions as a selective autophagy receptor that bridges polyneddylated protein cargo (via its C-terminal UBA domain binding NEDD8) to LC3/GABARAP autophagosomal proteins (via an atypical N-terminal LIR), per Ghosh & Ranjan 2022.