AKIRIN2 encodes a conserved, predominantly nuclear akirin-family adaptor protein. In vertebrate cells, AKIRIN2 homodimers bind assembled proteasomes and the import receptor IPO9 to promote proteasome import into the nucleus, supporting nuclear protein degradation. Akirin proteins also act as nuclear transcriptional coregulators downstream of NF-kappaB and chromatin-remodeling machinery, linking conserved immune and developmental gene-expression programs to a small, domain-poor adaptor protein.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: AKIRIN2 is well supported as a predominantly nuclear protein by direct human localization data and by the mechanistic proteasome-import study. Reason: Nuclear localization is central to both AKIRIN2 proteasome-import and transcription-coregulator biology. Supporting Evidence: PMID:18066067 Antibody staining of the human cells clearly showed the nuclear localization of HsAkirin1 and HsAkirin2 PMID:34711951 nuclear import of proteasomes in vertebrates |
| GO:0045089 positive regulation of innate immune response | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Akirin2 supports NF-kappaB-dependent innate immune gene expression in model systems, including IL-6 induction downstream of TLR/IL-1R signaling. Reason: The immune-response annotation is biologically supported but represents a regulatory output context rather than the PN core proteostasis role of AKIRIN2. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | ACCEPT | Summary: AKIRIN2 supports NF-kappaB-dependent inducible gene expression and is conserved as a nuclear transcriptional co-regulator. Reason: The process term captures a genuine AKIRIN2 transcriptional role, though it is distinct from the PN proteasome-import function. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators PMID:18066067 Akirin is functionally and evolutionary conserved |
| GO:0000785 chromatin | IBA GO_REF:0000033 | ACCEPT | Summary: The chromatin IBA annotation is consistent with akirin function as a nuclear transcriptional cofactor associated with chromatin/transcription machinery. Reason: AKIRIN2 has a conserved nuclear transcription-coregulator role; chromatin is a reasonable active context for that role. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0003712 transcription coregulator activity | IBA GO_REF:0000033 | ACCEPT | Summary: Akirin proteins act with or downstream of NF-kappaB and are best interpreted as transcriptional cofactors rather than DNA-binding transcription factors, bridging NF-kappaB output to SWI/SNF chromatin remodelers. Reason: This is an appropriate molecular-function annotation for the conserved nuclear gene-expression role; Akirin functions as a coregulator/molecular selector recruiting SWI/SNF rather than binding DNA directly. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0005634 nucleus | IEA GO_REF:0000120 | ACCEPT | Summary: AKIRIN2 is well supported as a predominantly nuclear protein by direct human localization data and by the mechanistic proteasome-import study. Reason: Nuclear localization is central to both AKIRIN2 proteasome-import and transcription-coregulator biology. Supporting Evidence: PMID:18066067 Antibody staining of the human cells clearly showed the nuclear localization of HsAkirin1 and HsAkirin2 PMID:34711951 nuclear import of proteasomes in vertebrates |
| GO:0005737 cytoplasm | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: Cytoplasmic localization is reported by similarity and as a minor compartment in UniProt, but AKIRIN2 is predominantly nuclear. Reason: Retain as peripheral/subordinate localization rather than a primary active site for the gene product. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Present mainly in the nuclear fraction, and at much lower level in the cytoplasmic and membrane fractions. |
| GO:0016020 membrane | IEA GO_REF:0000120 | MARK AS OVER ANNOTATED | Summary: Membrane localization is by similarity and described only as a much lower-level fraction relative to the nucleus. Reason: This is likely an over-specific/peripheral localization for human AKIRIN2; the evidence does not support treating membrane as a core cellular context. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Present mainly in the nuclear fraction, and at much lower level in the cytoplasmic and membrane fractions. |
| GO:0005515 protein binding | IPI PMID:16189514 Towards a proteome-scale map of the human protein-protein in... | MARK AS OVER ANNOTATED | Summary: This PMID:16189514 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005515 protein binding | IPI PMID:28514442 Architecture of the human interactome defines protein commun... | MARK AS OVER ANNOTATED | Summary: This PMID:28514442 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005515 protein binding | IPI PMID:31515488 Extensive disruption of protein interactions by genetic vari... | MARK AS OVER ANNOTATED | Summary: This PMID:31515488 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | MARK AS OVER ANNOTATED | Summary: This PMID:32296183 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | MARK AS OVER ANNOTATED | Summary: This PMID:33961781 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005515 protein binding | IPI PMID:40205054 Multimodal cell maps as a foundation for structural and func... | MARK AS OVER ANNOTATED | Summary: This PMID:40205054 interaction annotation records a generic high-throughput protein interaction rather than a specific AKIRIN2 activity. Reason: Generic protein binding is not informative for AKIRIN2 curation and should not be used as a core function; mechanistic binding is captured separately as proteasome binding/protein-macromolecule adaptor activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0042802 identical protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | ACCEPT | Summary: The binary interactome annotation is generic, but independent mechanistic evidence shows AKIRIN2 forms homodimers. Reason: Identical protein binding is supported as a real AKIRIN2 property, although it is secondary to the proteasome-import adaptor role. Supporting Evidence: PMID:34711951 AKIRIN2 forms homodimers file:human/AKIRIN2/AKIRIN2-uniprot.txt Homodimer (PubMed:34711951) |
| GO:0002821 positive regulation of adaptive immune response | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of adaptive immune response is supported only indirectly/by orthology as an immune-system output of AKIRIN2 transcriptional regulation. Reason: Keep as a contextual immune/developmental annotation, not as a core AKIRIN2 molecular function or PN proteostasis projection. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0009792 embryo development ending in birth or egg hatching | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: embryo development ending in birth or egg hatching is inferred from vertebrate/model-organism developmental phenotypes and is plausible for AKIRIN2 but broad. Reason: Developmental annotations should be retained as pleiotropic outcome/context terms rather than core PN function assignments. Supporting Evidence: PMID:18066067 MmAkirin2-/- mice were embryonic lethal |
| GO:0021987 cerebral cortex development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cerebral cortex development is inferred by orthology/by similarity; UniProt specifically describes a role in survival and proliferation of cerebral cortical progenitor cells. Reason: Retain as a contextual developmental annotation, not as a core PN proteostasis function assignment. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Involved in brain development: required for the survival and proliferation of cerebral cortical progenitor cells |
| GO:0030674 protein-macromolecule adaptor activity | IEA GO_REF:0000107 | ACCEPT | Summary: AKIRIN2 bridges assembled proteasomes and IPO9 during proteasome nuclear import, matching a protein-macromolecule adaptor role. Reason: This is an appropriate core molecular-function annotation and a better functional descriptor than generic protein binding. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes file:human/AKIRIN2/AKIRIN2-uniprot.txt directly binds to fully assembled 20S proteasomes at one end and to nuclear import receptor IPO9 at the other end |
| GO:0032755 positive regulation of interleukin-6 production | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse Akirin2 loss impairs IL-6 production downstream of TLR/IL-1R stimulation. Reason: The annotation is valid as an immune transcriptional-output context, but it is not a core PN proteostasis function. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation |
| GO:0042742 defense response to bacterium | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: defense response to bacterium is supported only indirectly/by orthology as an immune-system output of AKIRIN2 transcriptional regulation. Reason: Keep as a contextual immune/developmental annotation, not as a core AKIRIN2 molecular function or PN proteostasis projection. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0045089 positive regulation of innate immune response | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Akirin2 supports NF-kappaB-dependent innate immune gene expression in model systems, including IL-6 induction downstream of TLR/IL-1R signaling. Reason: The immune-response annotation is biologically supported but represents a regulatory output context rather than the PN core proteostasis role of AKIRIN2. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IEA GO_REF:0000107 | ACCEPT | Summary: AKIRIN2 supports NF-kappaB-dependent inducible gene expression and is conserved as a nuclear transcriptional co-regulator. Reason: The process term captures a genuine AKIRIN2 transcriptional role, though it is distinct from the PN proteasome-import function. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators PMID:18066067 Akirin is functionally and evolutionary conserved |
| GO:0050871 positive regulation of B cell activation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of B cell activation is directly supported by a B-cell-specific Akirin2 knockout study showing impaired BRG1 recruitment to Myc/Ccnd2 promoters and defective B-cell proliferation and humoral responses. Reason: Keep as a contextual immune/developmental annotation, not as a core AKIRIN2 molecular function or PN proteostasis projection; primary experimental support exists but it is a downstream transcriptional output. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0051147 regulation of muscle cell differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of muscle cell differentiation is inferred by orthology/by similarity; UniProt specifically describes a myogenesis role for AKIRIN2. Reason: Retain as a contextual developmental annotation, not as a core PN proteostasis function assignment. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Involved in myogenesis: required for skeletal muscle formation and skeletal development, possibly by regulating expression of muscle differentiation factors |
| GO:0005654 nucleoplasm | IDA GO_REF:0000052 | ACCEPT | Summary: The HPA nucleoplasm annotation is consistent with the direct nuclear localization literature and AKIRIN2 function in nuclear proteasome import. Reason: Nucleoplasmic/nuclear localization is compatible with the core nuclear functions of AKIRIN2. Supporting Evidence: PMID:18066067 Antibody staining of the human cells clearly showed the nuclear localization of HsAkirin1 and HsAkirin2 PMID:34711951 nuclear import of proteasomes in vertebrates |
| GO:0005737 cytoplasm | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Cytoplasmic localization is reported by similarity and as a minor compartment in UniProt, but AKIRIN2 is predominantly nuclear. Reason: Retain as peripheral/subordinate localization rather than a primary active site for the gene product. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Present mainly in the nuclear fraction, and at much lower level in the cytoplasmic and membrane fractions. |
| GO:0016020 membrane | ISS GO_REF:0000024 | MARK AS OVER ANNOTATED | Summary: Membrane localization is by similarity and described only as a much lower-level fraction relative to the nucleus. Reason: This is likely an over-specific/peripheral localization for human AKIRIN2; the evidence does not support treating membrane as a core cellular context. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Present mainly in the nuclear fraction, and at much lower level in the cytoplasmic and membrane fractions. |
| GO:0002821 positive regulation of adaptive immune response | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: positive regulation of adaptive immune response is supported only indirectly/by orthology as an immune-system output of AKIRIN2 transcriptional regulation. Reason: Keep as a contextual immune/developmental annotation, not as a core AKIRIN2 molecular function or PN proteostasis projection. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0005515 protein binding | IPI PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | MODIFY | Summary: The 2021 AKIRIN2 paper supports specific proteasome and IPO9 adaptor interactions, so generic protein binding is too uninformative. Reason: Replace the broad binding annotation with specific, mechanistically supported terms: proteasome binding for the PN projection and protein-macromolecule adaptor activity for the bridging role. Proposed replacements: proteasome binding protein-macromolecule adaptor activity Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes file:human/AKIRIN2/AKIRIN2-uniprot.txt directly binds to fully assembled 20S proteasomes at one end and to nuclear import receptor IPO9 at the other end |
| GO:0005634 nucleus | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | ACCEPT | Summary: AKIRIN2 is well supported as a predominantly nuclear protein by direct human localization data and by the mechanistic proteasome-import study. Reason: Nuclear localization is central to both AKIRIN2 proteasome-import and transcription-coregulator biology. Supporting Evidence: PMID:18066067 Antibody staining of the human cells clearly showed the nuclear localization of HsAkirin1 and HsAkirin2 PMID:34711951 nuclear import of proteasomes in vertebrates |
| GO:0006606 protein import into nucleus | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | ACCEPT | Summary: AKIRIN2 mediates nuclear import of pre-assembled proteasome complexes. Reason: This is a direct core process for the PN review because AKIRIN2 controls nuclear proteasome import. Supporting Evidence: PMID:34711951 nuclear import of proteasomes in vertebrates PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0021987 cerebral cortex development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: cerebral cortex development is inferred by orthology/by similarity; UniProt specifically describes a role in survival and proliferation of cerebral cortical progenitor cells. Reason: Retain as a contextual developmental annotation, not as a core PN proteostasis function assignment. Supporting Evidence: file:human/AKIRIN2/AKIRIN2-uniprot.txt Involved in brain development: required for the survival and proliferation of cerebral cortical progenitor cells |
| GO:0030674 protein-macromolecule adaptor activity | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | ACCEPT | Summary: AKIRIN2 bridges assembled proteasomes and IPO9 during proteasome nuclear import, matching a protein-macromolecule adaptor role. Reason: This is an appropriate core molecular-function annotation and a better functional descriptor than generic protein binding. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes file:human/AKIRIN2/AKIRIN2-uniprot.txt directly binds to fully assembled 20S proteasomes at one end and to nuclear import receptor IPO9 at the other end |
| GO:0031144 proteasome localization | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | ACCEPT | Summary: AKIRIN2 is required for proteasome relocalization/import into daughter nuclei after mitosis. Reason: Proteasome localization is a directly demonstrated core process for AKIRIN2. Supporting Evidence: PMID:34711951 AKIRIN2-dependent process PMID:34711951 Cells undergoing mitosis in the absence of AKIRIN2 |
| GO:0032755 positive regulation of interleukin-6 production | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse Akirin2 loss impairs IL-6 production downstream of TLR/IL-1R stimulation. Reason: The annotation is valid as an immune transcriptional-output context, but it is not a core PN proteostasis function. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation |
| GO:0042742 defense response to bacterium | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: defense response to bacterium is supported only indirectly/by orthology as an immune-system output of AKIRIN2 transcriptional regulation. Reason: Keep as a contextual immune/developmental annotation, not as a core AKIRIN2 molecular function or PN proteostasis projection. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0045089 positive regulation of innate immune response | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Akirin2 supports NF-kappaB-dependent innate immune gene expression in model systems, including IL-6 induction downstream of TLR/IL-1R signaling. Reason: The immune-response annotation is biologically supported but represents a regulatory output context rather than the PN core proteostasis role of AKIRIN2. Supporting Evidence: PMID:18066067 MmAkirin2, but not MmAkirin1, was responsible for the production of IL-6 in response to TLR or IL-1R stimulation PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0045944 positive regulation of transcription by RNA polymerase II | ISS GO_REF:0000024 | ACCEPT | Summary: AKIRIN2 supports NF-kappaB-dependent inducible gene expression and is conserved as a nuclear transcriptional co-regulator. Reason: The process term captures a genuine AKIRIN2 transcriptional role, though it is distinct from the PN proteasome-import function. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators PMID:18066067 Akirin is functionally and evolutionary conserved |
| GO:0071630 nuclear protein quality control by the ubiquitin-proteasome system | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | ACCEPT | Summary: AKIRIN2 acts upstream of nuclear protein quality control by maintaining nuclear proteasome availability. Reason: The qualifier is appropriate: AKIRIN2 is not a protease subunit but enables the nuclear proteasome pool needed for nuclear protein degradation. Supporting Evidence: PMID:34711951 nuclear protein degradation PMID:34711951 accumulation of MYC and other nuclear proteins |
| GO:0019899 enzyme binding | IPI PMID:23382074 A high-confidence interaction map identifies SIRT1 as a medi... | MARK AS OVER ANNOTATED | Summary: The SIRT1/enzyme-binding annotation is based on an interaction-map context and does not define a core AKIRIN2 enzymatic-adaptor function. Reason: Avoid propagating broad enzyme binding from a high-throughput interactome edge; the specific supported binding call for PN is proteasome binding. Supporting Evidence: PMID:23382074 high-confidence SIRT1 interactome PMID:34711951 directly bind to fully assembled 20S proteasomes |
| GO:0005634 nucleus | IDA PMID:18066067 Akirins are highly conserved nuclear proteins required for N... | ACCEPT | Summary: AKIRIN2 is well supported as a predominantly nuclear protein by direct human localization data and by the mechanistic proteasome-import study. Reason: Nuclear localization is central to both AKIRIN2 proteasome-import and transcription-coregulator biology. Supporting Evidence: PMID:18066067 Antibody staining of the human cells clearly showed the nuclear localization of HsAkirin1 and HsAkirin2 PMID:34711951 nuclear import of proteasomes in vertebrates |
| GO:0017053 transcription repressor complex | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Transcription repressor complex membership is inferred by similarity from a non-human ortholog and points to transcription-cofactor context rather than a defined human complex assignment. Reason: Retain as contextual but do not treat as a core AKIRIN2 complex annotation; transcription coregulator activity captures the conserved function more cleanly. Supporting Evidence: PMID:18066067 Akirins are novel important nuclear cofactors regulating the transcriptional activities of main transactivators |
| GO:0070628 proteasome binding | IDA PMID:34711951 AKIRIN2 controls the nuclear import of proteasomes in verteb... | NEW | Summary: Proposed NEW annotation from the PN proteostasis projection, independently validated by the AKIRIN2 proteasome-import paper. Reason: The PN projection maps the proteasome-adaptor group to proteasome binding, and AKIRIN2 has direct primary evidence for binding fully assembled 20S proteasomes. This is the conservative, specific MF term that captures the PN-relevant binding event without over-claiming protease activity. Supporting Evidence: PMID:34711951 directly bind to fully assembled 20S proteasomes file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_annotations.tsv AKIRIN2 Ubiquitin Proteasome System|Proteasome and associated proteins|adaptors|Akirin |
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Download this section (compressed HTML)Q: Are AKIRIN2 transcription-coregulator complexes mechanistically coupled to its nuclear proteasome-import function, or are these separable adaptor modules?
Suggested experts: de Almeida M, Zuber J, Goto A
Experiment: Compare AKIRIN2 mutants defective in the C-terminal proteasome-binding motif with mutants affecting candidate transcription-cofactor interfaces, measuring nuclear proteasome import, MYC turnover, NF-kappaB-dependent IL6 transcription, and SWI/SNF/NFKBIZ recruitment in the same human cell system.
Hypothesis: AKIRIN2 proteasome binding and IPO9 bridging are separable from its NF-kappaB/chromatin transcription-coregulator role.
Type: separation-of-function mutagenesis with imaging, degradation, and transcriptional assays
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