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Literature summary for 3.4.24.61 extracted from

  • Nishi, K.; Sato, Y.; Ohno, M.; Hiraoka, Y.; Saijo, S.; Sakamoto, J.; Chen, P.M.; Morita, Y.; Matsuda, S.; Iwasaki, K.; Sugizaki, K.; Harada, N.; Mukumoto, Y.; Kiyonari, H.; Furuyama, K.; Kawaguchi, Y.; Uemoto, S.; Kita, T.; Inagaki, N.; Kimura, T.; Nishi, E.
    Nardilysin is required for maintaining pancreatic beta-cell function (2016), Diabetes, 65, 3015-3027 .
    View publication on PubMed
Search for more literature for 3.4.24.61

Organism

Organism UniProt Comment Textmining
Mus musculus Q8BHG1
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-

Synonyms

Synonyms Comment Organism
N-Arginine dibasic convertase
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 Mus musculus
Nrd1 and NRDc
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 Mus musculus

General Information

General Information Comment Organism
malfunction Nrd1-/- mice show glucose intolerance and severely decreased glucose-stimulated insulin secretion (GSIS). Islets isolated from Nrd1-/- mice exhibit reduced insulin content and impaired GSIS in vitro. Moreover, beta-cell-specific NRDc-deficient (Nrd1delbeta) mice show a diabetic phenotype with markedly reduced GSIS. MafA is specifically downregulated in islets from Nrd1delbeta mice Mus musculus
physiological function nardilysin controls beta-cell function via regulation of the Islet-1-MafA pathway. Overexpression of NRDc upregulates MafA and insulin expression in INS832/13 cells Mus musculus