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
Gene Ontology annotation based on curation of immunofluorescence data
Labeling of heterochronic ribosomes reveals C1ORF109 and SPATA5 control a late step in human ribosome assembly.
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AIRIM/C1orf109 was identified in an unbiased genome-wide screen as a previously uncharacterised ribosome biogenesis factor.
"These efforts identify two functionally uncharacterized genes, C1orf109 and SPATA5."
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AIRIM controls a late, cytoplasmic step of pre-60S maturation together with CINP and SPATA5L1.
"We provide evidence that these factors, together with CINP and SPATA5L1, control a late step of human pre-60S maturation in the cytoplasm."
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Loss of AIRIM impairs global protein synthesis.
"Loss of either C1orf109 or SPATA5 impairs global protein synthesis."
The SPATA5-SPATA5L1 ATPase complex directs replisome proteostasis to ensure genome integrity.
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AIRIM/C1orf109 is one of four subunits of the 55LCC complex, with AAA+ ATPases SPATA5-SPATA5L1 and CINP.
"Here, we identify replisome factor interactions with a protein complex composed of AAA+ ATPases SPATA5-SPATA5L1 together with heterodimeric partners C1orf109-CINP (55LCC)."
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AIRIM and CINP form a funnel-like structure above the ATPase motor, establishing AIRIM's role as structural rather than catalytic.
"An integrative structural biology approach revealed a molecular architecture of SPATA5-SPATA5L1 N-terminal domains interacting with C1orf109-CINP to form a funnel-like structure above a cylindrically shaped ATPase motor."
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55LCC ATPase activity is enhanced by replication fork DNA and coupled to protease-dependent cleavage of replisome substrates.
"55LCC showed ATPase activity that was specifically enhanced by replication fork DNA and was coupled to cysteine protease-dependent cleavage of replisome substrates in response to replication fork damage."
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Loss of the complex causes ubiquitin-independent proteotoxicity, replication stress and chromosome instability.
"Deficiency in the 55LCC complex elicited ubiquitin-independent proteotoxicity, replication stress, and severe chromosome instability."
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The authors define the complex's role as replisome proteostasis required for fork progression and genome stability.
"These findings define 55LCC-mediated proteostasis as critical for replication fork progression and genome stability"
Cryo-EM structure of the AAA+ SPATA5 complex and its role in human cytoplasmic pre-60S maturation.
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The assembly is 4:2:2:2 (SPATA5:SPATA5L1:C1orf109:CINP), so 'heterohexameric' describes the motor rather than the whole complex.
"Here we reveal that SPATA5 forms a 4:2:2:2 complex with SPATA5L1, C1orf109, and CINP."
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AIRIM/C1orf109 and CINP form the N-terminal ring above two hexameric AAA+ ATPase rings - the structural contribution this review annotates as GO:0005198.
"This complex features an N-terminal ring made of C1orf109, CINP and NTDs of SPATA5/SPATA5L1, and two hexameric AAA+ ATPase rings."
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Recognition of the pre-60S particle is mediated by CINP, not by AIRIM.
"the recognition of the pre-60S particle is mediated by human-specific factor CINP, through two distinct sets of interactions: one with GTPBP4 and the other with ES27A."
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C1orf109 makes no direct contact with the pre-60S particle - docking onto the particle is CINP's contribution. This bounds AIRIM's role but does not remove it: AIRIM binds the substrate RLP24 inside the funnel, which is a different interaction from the one this sentence is about.
"CINP contributes to both the interfaces between the SPATA5 complex and the pre-60S particle, while C1orf109 does not interact with the pre-60S particle directly"
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The paper's own conclusion about what AIRIM does: it is an adapter protein bringing the motor and its substrate RLP24 together.
"these data collectively support that CINP and C1orf109 are adapter proteins to mediate the interaction between the SPATA5 complex and its substrate RLP24"
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Co-immunoprecipitation evidence for that adapter role - an RLP24 fragment pulls down C1orf109.
"our immunoprecipitation experiments show that a fragment (residues 85–163) of RLP24 was indeed able to immunoprecipitate both CINP and C1orf109"
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The structural counterpart: RLP24's last two helices bind C1orf109.
"the last two helices (residues 80–163) of RLP24 are able to bind to both CINP and C1orf109"
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AIRIM and CINP build the inner wall of the funnel the substrate is drawn into.
"the helical bundles of CINP and C1orf109 constitute the inner wall of the funnel"
A programmed decline in ribosome levels governs human early neurodevelopment.
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Variants in AIRIM/C1orf109 are primarily associated with neurodevelopmental disorders - the source for the disease statement in the description, which was previously uncited.
"Here we describe variants in the ribosome biogenesis factor AIRIM/C1orf109 that are primarily associated with neurodevelopmental disorders."
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The developmental defects caused by AIRIM variants are suppressed by enhancing mTOR activity.
"Enhancing mTOR activity suppresses the growth and developmental defects associated with AIRIM/C1orf109 variants."
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Why reduced ribosome biogenesis produces tissue-specific defects is the open question this work addresses, and it frames why a housekeeping factor has a neural phenotype.
"How reductions in ribosome biogenesis can result in tissue- and developmental-specific defects remains unclear."
C1orf109L binding DHX9 promotes DNA damage depended on the R-loop accumulation and enhances camptothecin chemosensitivity.
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A distinct, isoform-specific activity: the long isoform C1orf109L binds DHX9 and promotes R-loop-dependent DNA damage.
"C1orf109L binding DHX9 promotes DNA damage depended on the R-loop accumulation"
Identification and characterization of a novel gene, c1orf109, encoding a CK2 substrate that is involved in cancer cell proliferation.
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C1ORF109 localises to both nucleus and cytoplasm by immunofluorescence and immunogold.
"The protein C1ORF109 was mainly located in the nucleus and cytoplasm."
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C1ORF109 is a phosphoprotein in vivo and a CK2 substrate in vitro.
"C1ORF109 was a phosphoprotein in vivo and could be phosphorylated by the protein kinase CK2 in vitro"
A reference map of the human binary protein interactome.
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HuRI is a proteome-scale all-by-all binary interactome map, not a study of AIRIM.
"Here we present a human 'all-by-all' reference interactome map of human binary protein interactions, or 'HuRI'."
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Its scale is roughly four times the curated small-scale literature, which is why a single gene can accumulate over a hundred generic protein-binding rows from it.
"With approximately 53,000 protein-protein interactions, HuRI has approximately four times as many such interactions as there are high-quality curated interactions from small-scale studies."
A proteome-scale map of the human interactome network.
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HI-II-14 is a systematic proteome-scale binary interaction map rather than a study of AIRIM.
"Here, we describe a systematic map of ~14,000 high-quality human binary protein-protein interactions."
Architecture of the human interactome defines protein communities and disease networks.
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BioPlex 2.0 is a single-pipeline affinity-purification mass spectrometry interactome, not a study of AIRIM; it independently recovers the AIRIM-CINP association.
"BioPlex 2.0 is the largest collection of human co-complex data assembled from a single pipeline to date, containing 56,553 interactions from 10,961 proteins"
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
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BioPlex 3.0 is a proteome-scale AP-MS interaction network; it also recovers the AIRIM-CINP association.
"Through affinity-purification mass spectrometry, we have created two proteome-scale, cell-line-specific interaction networks."
Affinage mechanistic annotation for AIRIM (human)
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The affinage record independently identifies AIRIM as a structural subunit of the 55LCC complex, matching the conclusion of this review.
"AIRIM (C1orf109) is a structural subunit of the eumetazoan-specific 55LCC complex"
Next-generation sequencing to generate interactome datasets.
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A high-throughput yeast two-hybrid methodology study, not a study of AIRIM's function.
"test the strategy in a high-throughput yeast two-hybrid (Y2H) system"