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

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

Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara

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

A ribonucleotide reductase gene involved in a p53-dependent cell-cycle checkpoint for DNA damage.

Mammalian p53R2 protein forms an active ribonucleotide reductase in vitro with the R1 protein, which is expressed both in resting cells in response to DNA damage and in proliferating cells.

p53R2-dependent pathway for DNA synthesis in a p53-regulated cell cycle checkpoint.

Wild-type p53 regulates human ribonucleotide reductase by protein-protein interaction with p53R2 as well as hRRM2 subunits.

Characterization of enzymatic properties of human ribonucleotide reductase holoenzyme reconstituted in vitro from hRRM1, hRRM2, and p53R2 subunits.

Mutation of RRM2B, encoding p53-controlled ribonucleotide reductase (p53R2), causes severe mitochondrial DNA depletion.

Ribonucleotide reduction is a cytosolic process in mammalian cells independently of DNA damage.

ATM-mediated serine 72 phosphorylation stabilizes ribonucleotide reductase small subunit p53R2 protein against MDM2 to DNA damage.

A proteome-scale map of the human interactome network.

A massively parallel pipeline to clone DNA variants and examine molecular phenotypes of human disease mutations.

Widespread macromolecular interaction perturbations in human genetic disorders.

Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.

RNR (M1M2B) reduces nucleotide diphosphates to deoxynucleotide diphosphates (thioredoxin)

TP53 stimulates transcription of RRM2B gene

RNR (M1M2B) reduces nucleotide diphosphates to deoxynucleotide diphosphates (glutaredoxin)

UniProtKB entry Q7LG56 (RIR2B_HUMAN)