Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Analysis of the C. elegans Argonaute family reveals that distinct Argonautes act sequentially during RNAi.
In vitro analyses of the production and activity of secondary small interfering RNAs in C. elegans.
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CSR-1 is an experimentally active secondary-siRNA-directed slicer.
"An Argonaute protein, CSR-1, is responsible for the Slicer activity induced by secondary-type siRNAs."
The Argonaute CSR-1 and its 22G-RNA cofactors are required for holocentric chromosome segregation.
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CSR-1 associates with 22G guides and chromosome-associated target loci; tested targets in this context were not generally downregulated.
"the CSR-1-interacting small RNAs (22G-RNAs) are antisense to thousands of germline-expressed protein-coding genes."
A conserved PUF-Ago-eEF1A complex attenuates translation elongation.
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CSR-1 participates with FBF/eEF1A in translational repression, independently supporting a repressive role.
"Nematode CSR-1 (Ago) promoted repression of FBF (PUF) target mRNAs in in vivo assays"
CSR-1 RNAi pathway positively regulates histone expression in C. elegans.
ELLI-1, a novel germline protein, modulates RNAi activity and P-granule accumulation in Caenorhabditis elegans.
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The study includes direct csr-1 mutant granule phenotypes, despite its ELLI-1 title.
"Loss of CSR-1 complex components results in a very specific, enlarged P-granule phenotype."
The C. elegans CSR-1 argonaute pathway counteracts epigenetic silencing to promote germline gene expression.
Protection of germline gene expression by the C. elegans Argonaute CSR-1.
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RNA recruitment demonstrates active protection/licensing beyond a necessity phenotype.
"the recruitment of CSR-1 to a transcript licenses expression of the transcript, protecting it from piRNA-mediated silencing."
Two isoforms of the essential C. elegans Argonaute CSR-1 differentially regulate sperm and oocyte fertility.
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Isoforms share catalytic residues but differ in expression, small-RNA targets and biological roles.
"both CSR-1 isoforms possess the same catalytic tetrad within the PIWI domain"
Arginine methylation promotes siRNA-binding specificity for a spermatogenesis-specific isoform of the Argonaute protein CSR-1.
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Isoform-specific guide choice depends on the long isoform arginine-modified extension.
"multiple dimethylarginine modifications, which are necessary for the preferential binding of CSR-1A to spermatogenesis-specific 22G-RNAs."
OpenScientist CSR-1 identity and transcription-factor/metabolic-prediction adjudication
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The report identifies the stale accession as LARP-1 and resolves CSR-1 to F20D12.1/H2KZD5/Q27GU1. Independent live accession and UniParc snapshots corroborate the identity correction.
"Q21992 is DELETED"
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Its RNA-effector and gene-expression findings inform the biological summary, but its broad-metabolic-term preference does not refute broad true processes. It contains no miRNA-binding adjudication.
"CSR-1 directly binds histone mRNA"
Actual PTHR22891 lineage and ancestral assertions for H2KZD5
Traceable CSR-1 three-way identity correction and original/replacement source hashes
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The old canonical source rows were for NHR-47 Q17370; old review id Q21992 was deleted LARP-1; exact H2KZD5 snapshots replace the source files while preserving the originals.
"verified_input_identity_correction"
Falcon report generated from the original Q17370/NHR-47 input, retained for provenance
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This report identifies its intended target as nhr-47, corroborating that the original research input was the wrong gene for this folder.
"The research target is the *C. elegans* nuclear hormone receptor gene **nhr-47**"
OpenScientist focused assessment of CSR-1 miRNA-binding specificity
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The report confirms the selective 22G-RNA literature and identifies the unquantified miRNA fraction as a remaining primary-data gap. This supports calibrated uncertainty, not a negative binding assertion.
"Published IPs report 22G-RNAs; miRNA fraction not explicitly quantified/excluded"
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The focused investigation used database records and PubMed abstracts, limiting conclusions about unreported negative assays.
"findings rest on public UniProt, PANTHER v19, and QuickGO records plus the cited PubMed abstracts."