Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Automatic assignment of GO terms using logical inference, based on on inter-ontology links
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Cloning of three novel neuronal Cdk5 activator binding proteins.
Identification of a common protein association region in the neuronal Cdk5 activator.
Identification of a neuronal Cdk5 activator-binding protein as Cdk5 inhibitor.
Microtubule association of the neuronal p35 activator of Cdk5.
The CDK5 repressor CDK5RAP1 is a methylthiotransferase acting on nuclear and mitochondrial RNA.
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CDK5RAP1 generates ms2i6A in nuclear RNA species (polyA RNA, miRNA) as well as mitochondrial tRNA.
"By exclusion of ribosomal and transfer RNA as the source of ms2i6A, we reason that ms2i6A is indeed an RNA modification that next to mitochondrial tRNA exists also in a yet unidentified nuclear RNA species."
Quantitative high-confidence human mitochondrial proteome and its dynamics in cellular context.
Cdk5rap1-mediated 2-methylthio modification of mitochondrial tRNAs governs protein translation and contributes to myopathy in mice and humans.
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Cdk5rap1 is required for ms2 modification of mt-tRNA Ser(UCN), Phe, Tyr and Trp; loss impairs mitochondrial translation and respiration.
"In this study, we report that Cdk5 regulatory subunit-associated protein 1 (Cdk5rap1) is responsible for 2-methylthio (ms(2)) modifications of mammalian mt-tRNAs for Ser(UCN), Phe, Tyr, and Trp codons."
Cdk5rap1-mediated 2-methylthio-N6-isopentenyladenosine modification is absent from nuclear-derived RNA species.
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ms2i6A is absent from rho0 cells and restricted to mitochondrial tRNA; the MTS-less variant also lacks a conserved MTTase-domain cysteine.
"Taken together, we propose that ms2i6A is a mitochondrial tRNA-specific modification and is absent from nuclear-encoded RNA species."
Deficit of tRNA(Lys) modification by Cdkal1 causes the development of type 2 diabetes in mice.
MiaB protein is a bifunctional radical-S-adenosylmethionine enzyme involved in thiolation and methylation of tRNA.