Gene Ontology annotation through association of InterPro records with GO terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Germline mutations in DIS3L2 cause the Perlman syndrome of overgrowth and Wilms tumor susceptibility.
Exonuclease hDIS3L2 specifies an exosome-independent 3'-5' degradation pathway of human cytoplasmic mRNA.
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Human DIS3L2 is a processive 3′–5′ exoribonuclease that can degrade structured RNA substrates and functions outside the RNA exosome in the tested preparations.
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Human-cell depletion slows selected mRNA decay; endogenous and tagged protein show a soluble cytoplasmic pool, and XRN1 co-recovery is RNA dependent.
Mammalian DIS3L2 exoribonuclease targets the uridylated precursors of let-7 miRNAs.
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Human 885-residue DIS3L2 binds oligo(U) RNA and catalyses divalent-metal-dependent RNA degradation; a D391N substitution abolishes the measured cleavage.
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Human-cell and biochemical experiments identify uridylated pre-let-7 as a substrate, with oligo(U) preference but not an absolute inability to degrade other substrates.
The exoribonuclease Dis3L2 defines a novel eukaryotic RNA degradation pathway.
A role for the Perlman syndrome exonuclease Dis3l2 in the Lin28-let-7 pathway.
Mechanism of Dis3l2 substrate recognition in the Lin28-let-7 pathway.
Characterization of a TUTase/RNase complex required for Drosophila gametogenesis.
Nuclear poly(A) binding protein 1 (PABPN1) mediates zygotic genome activation-dependent maternal mRNA clearance during mouse early embryonic development.
DIS3L2 source, substrate and propagation guide