The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Store-Independent Activation of Orai1 by SPCA2 in Mammary Tumors
Open accessAbstract
SUMMARY Ca2+ is an essential and ubiquitous second messenger. Changes in cytosolic Ca2+ trigger events critical for tumorigenesis, such as cellular motility, proliferation and apoptosis. We show that an isoform of Secretory Pathway Ca2+-ATPase, SPCA2, is upregulated in breast cancer-derived cells and human breast tumors, and suppression of SPCA2 attenuated basal Ca2+ levels and tumorigenicity. Contrary to its conventional role in Golgi Ca2+ sequestration, expression of SPCA2 increased Ca2+ influx by a mechanism dependent on the store-operated Ca2+ channel Orai1. Unexpectedly, SPCA2-Orai1 signaling was independent of ER Ca2+ stores or STIM1 and STIM2 sensors, and uncoupled from Ca2+-ATPase activity of SPCA2. Binding of SPCA2 amino terminus to Orai1 enabled access of its carboxyl terminus to Orai1 and activation of Ca2+ influx. Our findings reveal a signaling pathway in which Orai1-SPCA2 complex elicits constitutive store-independent Ca2+ signaling that promotes tumorigenesis.
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Metadata
- Authors
- Feng, M., Grice, D. M., Faddy, H. M., Nguyen, N., Leitch, S., Wang, Y., Muend, S., Kenny, P. A., Sukumar, S., Roberts-Thomson, S. J., Monteith, G. R., & Rao, R.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 143
- Issue
- 1
- Pages
- 84-98
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2020033048
- Cited by
- 306
- References
- 57
- FWCI
- 10.75
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Feng, M., Grice, D. M., Faddy, H. M., Nguyen, N., Leitch, S., Wang, Y., Muend, S., Kenny, P. A., Sukumar, S., Roberts-Thomson, S. J., Monteith, G. R., & Rao, R. (2010). Store-Independent Activation of Orai1 by SPCA2 in Mammary Tumors. Cell. https://doi.org/10.1016/j.cell.2010.08.040
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