Please use this identifier to cite or link to this item:
https://open.uns.ac.rs/handle/123456789/11318
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Nguyen L. | en |
dc.contributor.author | Petri, Edward | en |
dc.contributor.author | Huynh L. | en |
dc.contributor.author | Ehrlich B. | en |
dc.date.accessioned | 2020-03-03T14:43:54Z | - |
dc.date.available | 2020-03-03T14:43:54Z | - |
dc.date.issued | 2019-01-01 | en |
dc.identifier.issn | 00219258 | en |
dc.identifier.uri | https://open.uns.ac.rs/handle/123456789/11318 | - |
dc.description.abstract | © 2019 Nguyen et al. Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc. Inositol 1,4,5-trisphosphate receptors (InsP3Rs) are endoplasmic reticulum-localized channels that mediate Ca2+ release from the endoplasmic reticulum into the cytoplasm. We previously reported that an EF-hand Ca2+-binding protein, neuronal calcium sensor 1 (NCS1), binds to the InsP3R and thereby increases channel open probability, an event associated with chemotherapy-induced peripheral neuropathy. However, the exact NCS1-binding site on InsP3R remains unknown. Using protein docking, co-immunoprecipitation, and blocking peptides, we mapped the NCS1-binding site to residues 66 -110 on the suppressor domain of InsP3R type 1 (InsP3R1). We also identified Leu-89, a residue in the hydrophobic pocket of NCS1, as being critical for facilitating the NCS1-InsP3R1 interaction. Overexpression of WT NCS1 in MDA-MB231 breast cancer cells increased Ca2+ signaling and survival, whereas overexpression of Leu-89 NCS1 variants decreased Ca2+ signaling and survival, further suggesting the importance of this residue in the NCS1-InsP3R1 interaction. In conclusion, we show that NCS1-InsP3R1 interaction enhances intracellular Ca2+ signaling in cells and can be modulated by altering or occluding the hydrophobic pocket of NCS1. This improved understanding of the NCS1-InsP3R1 interaction may facilitate the development of management strategies for diseases resulting from aberrant NCS1 expression. | en |
dc.relation.ispartof | Journal of Biological Chemistry | en |
dc.title | Characterization of NCS1-InsP3R1 interaction and its functional significance | en |
dc.type | Journal/Magazine Article | en |
dc.identifier.doi | 10.1074/jbc.RA119.009736 | en |
dc.identifier.pmid | 294 | en |
dc.identifier.scopus | 2-s2.0-85076331438 | en |
dc.identifier.url | https://api.elsevier.com/content/abstract/scopus_id/85076331438 | en |
dc.relation.lastpage | 18933 | en |
dc.relation.firstpage | 18923 | en |
dc.relation.issue | 49 | en |
dc.relation.volume | 294 | en |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
crisitem.author.dept | Prirodno-matematički fakultet, Departman za biologiju i ekologiju | - |
crisitem.author.parentorg | Prirodno-matematički fakultet | - |
Appears in Collections: | PMF Publikacije/Publications |
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