Gene Ontology annotation through association of InterPro records with GO terms
Use of the ND evidence code for Gene Ontology (GO) terms
Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
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
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Defining the membrane proteome of NK cells.
CDK5 regulatory subunit-associated protein 1-like 1 (CDKAL1) is a tail-anchored protein in the endoplasmic reticulum (ER) of insulinoma cells.
A proteome-scale map of the human interactome network.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
CDKAL1:4Fe-4S methylthiolates N6-threonylcarbamoyladenosine-37 in tRNA yielding 2-methylthio-N6-threonylcarbamoyladenosine-37
Identification of eukaryotic and prokaryotic methylthiotransferase for biosynthesis of 2-methylthio-N6-threonylcarbamoyladenosine in tRNA.
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Human CDKAL1 expressed in a miaB-deficient E. coli strain converts t6A to ms2t6A in tRNA; the radical SAM CxxxCxxC cysteines are required.
"These results demonstrate that B. subtilis YqeV/MtaB and human CDKAL1/e-MtaB proteins are both functional in vivo and selectively involved in the conversion of t 6 A to ms 2 t 6 A."
Deficit of tRNA(Lys) modification by Cdkal1 causes the development of type 2 diabetes in mice.
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Mouse Cdkal1 is required for ms2t6A37 in tRNA-Lys(UUU); loss causes Lys misreading in proinsulin, impaired insulin secretion and glucose intolerance.
"These results demonstrate that mouse Cdkal1 is a methylthiolase that converts t 6 A to ms 2 t 6 A in tRNA Lys (UUU)."
Irp2 regulates insulin production through iron-mediated Cdkal1-catalyzed tRNA modification.
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Iron deficiency in Irp2-null beta cells lowers Fe-S-dependent Cdkal1 activity, causing Lys misreading in proinsulin.
"As a consequence of reduced Cdkal1 function in Irp2−/− β cells, lysine codons in proinsulin are misread and proinsulin processing is impaired, reducing insulin content and secretion."
Two Fe-S clusters catalyze sulfur insertion by radical-SAM methylthiotransferases.