{
    "uniprot_canonical_ac": "A2AT37-1", 
    "publication_count": 8, 
    "reported_interactions": 0, 
    "record_type": "protein", 
    "predicted_glycosites": 0, 
    "protein_names_refseq": "nonsense mRNA reducing factor 2; up-frameshift suppressor 2 homolog; regulator of nonsense transcripts 2", 
    "refseq_ac": "NP_001074601.1", 
    "reported_n_glycosites": 0, 
    "refseq_name": "regulator of nonsense transcripts 2", 
    "record_id": "A2AT37-1", 
    "protein_names_uniprotkb": "Regulator of nonsense transcripts 2; Nonsense mRNA reducing factor 2; Regulator of nonsense transcripts 2; Up-frameshift suppressor 2 homolog; Upf2", 
    "pathway": " (mmu:326622); Nonsense Mediated Decay (NMD) enhanced by the Exon Junction Complex (EJC) (R-MMU-975957)", 
    "function": "Hematopoietic-specific deletion of Upf2, a core NMD factor, led to the rapid, complete, and lasting cell-autonomous extinction of all hematopoietic stem and progenitor populations., [RefSeq]; Involved in nonsense-mediated decay (NMD) of mRNAs containing premature stop codons by associating with the nuclear exon junction complex (EJC). Recruited by UPF3B associated with the EJC core at the cytoplasmic side of the nuclear envelope and the subsequent formation of an UPF1-UPF2-UPF3 surveillance complex (including UPF1 bound to release factors at the stalled ribosome) is believed to activate NMD. In cooperation with UPF3B stimulates both ATPase and RNA helicase activities of UPF1. Binds spliced mRNA., [UniProtKB]; Our findings indicate that impaired UPF2-dependent nonsense-mediated decay leads to neurodevelopmental dysfunction, [RefSeq]; Study find that loss of Upf2 during fetal liver development is incompatible with postnatal life due to failure of terminal differentiation. Moreover, deletion of Upf2 in the adult liver results in hepatosteatosis and disruption of liver homeostasis. Publication Status: Online-Only, [RefSeq]; Upon removal of TDRD6, the association of several mRNAs with UPF1 and UPF2 is disturbed, and the long 3' UTR-stimulated but not the downstream exon-exon junction triggered pathway of NMD is impaired.This function depends on TDRD6-promoted assembly of mRNA and decay enzymes in Chromatoid bodies . Publication Status: Online-Only, [RefSeq]; We report that UPF2-mediated nonsense-mediated mRNA decay (NMD) plays an essential role in male germ cells by eliminating ubiquitous genes-derived, longer 3'UTR transcripts, and that this role is independent of its canonical role in degrading 'premature termination codon' (PTC)-containing transcripts in somatic cell lineages Publication Status: Online-Only, [RefSeq]", 
    "protein_name": "Regulator of nonsense transcripts 2", 
    "reported_mutagensis": 0, 
    "reported_phosphosites": 1, 
    "reported_o_glycosites_with_glycan": 0, 
    "tax_id": 10090, 
    "organism": "Mus musculus", 
    "disease": "", 
    "reported_glycation": 0, 
    "reported_snv": 0, 
    "mass": 147553.0, 
    "gene_names_uniprotkb": "Upf2", 
    "reported_n_glycosites_with_glycan": 0, 
    "reported_o_glycosites": 0, 
    "gene_names_refseq": "Upf2", 
    "gene_name": "Upf2"
}