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Data suggest that calnuc (nucleobindin 1) is possibly involved in controlling protein unfolding diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), prion disease, and type II diabetes.
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Calnuc depletion causes the misdelivery to and degradation in lysosomes of cationic-independent mannose-6-phosphate receptor and Sortilin .
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nesfatin-1 has a role in thyroid dysfunction in patients with T2DM
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The serine protease activity of calnuc is allosterically regulated by Zn2+ binding and its interaction with G protein alpha subunit.
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postulate that the engineered forms of NUCB1 prevent hIAPP fibril formation by a mechanism where protofibril-like species are "capped" to prevent further fibril assembly and maturation
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structural basis for the properties of Calnuc and NUCB2 binding to Galpha subunits and its regulation by calcium ions.
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Nucleobindin 1 is a calcium-regulated guanine nucleotide dissociation inhibitor of G{alpha}i1.
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Comparison between the structure of nucleobindin and other EF-hand proteins sheds light into the dual function of nucleobindin as Ca2+ storage (buffer) and Ca2+ sensor.
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Calnuc protein may be a tumor-associated antigen (TAA) that induces autoantibody response in human cancers
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NUCB1 is the first-identified, Golgi-localized negative feedback regulator in the ATF6-mediated branch of the UPR
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results suggest that the functions of nucleobindins could be modulated by caspase-mediated cleavage in apoptosis
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Proline residue at the +2-position (Pro(+2)) from the signal peptide cleavage site is the determinant of NUCB1 protein export from the ER and subsequent transport to the Golgi.
