| Literature DB >> 16691292 |
Christina Schlecker1, Wolfgang Boehmerle, Andreas Jeromin, Brenda DeGray, Anurag Varshney, Yogendra Sharma, Klara Szigeti-Buck, Barbara E Ehrlich.
Abstract
Regulation and dysregulation of intracellular calcium (Ca2+) signaling via the inositol 1,4,5-trisphosphate receptor (InsP3R) has been linked to many cellular processes and pathological conditions. In the present study, addition of neuronal calcium sensor-1 (NCS-1), a high-affinity, low-capacity, calcium-binding protein, to purified InsP3R type 1 (InsP3R1) increased the channel activity in both a calcium-dependent and -independent manner. In intact cells, enhanced expression of NCS-1 resulted in increased intracellular calcium release upon stimulation of the phosphoinositide signaling pathway. To determine whether InsP3R1/NCS-1 interaction could be functionally relevant in bipolar disorders, conditions in which NCS-1 is highly expressed, we tested the effect of lithium, a salt widely used for treatment of bipolar disorders. Lithium inhibited the enhancing effect of NCS-1 on InsP3R1 function, suggesting that InsP3R1/NCS-1 interaction is an essential component of the pathomechanism of bipolar disorder.Entities:
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Year: 2006 PMID: 16691292 PMCID: PMC1459068 DOI: 10.1172/JCI22466
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 14.808