| First Author | Liu QH | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 1 | Pages | 68-79 |
| PubMed ID | 15611229 | Mgi Jnum | J:95865 |
| Mgi Id | MGI:3527413 | Doi | 10.4049/jimmunol.174.1.68 |
| Citation | Liu QH, et al. (2005) Distinct calcium channels regulate responses of primary B lymphocytes to B cell receptor engagement and mechanical stimuli. J Immunol 174(1):68-79 |
| abstractText | Intracellular Ca(2+) plays a central role in controlling lymphocyte function. Nonetheless, critical gaps remain in our understanding of the mechanisms that regulate its concentration. Although Ca(2+)-release-activated calcium (CRAC) channels are the primary Ca(2+) entry pathways in T cells, additional pathways appear to be operative in B cells. Our efforts to delineate these pathways in primary murine B cells reveal that Ca(2+)-permeant nonselective cation channels (NSCCs) operate in a cooperative fashion with CRAC. Interestingly, these non-CRAC channels are selectively activated by mechanical stress, although the mechanism overlaps with BCR-activated pathways, suggesting that they may operate in concert to produce functionally diverse Ca(2+) signals. NSCCs also regulate the membrane potential, which activates integrin-dependent binding of B cells to extracellular matrix elements involved in their trafficking and localization within secondary lymphoid organs. Thus, CRAC and distinct Ca(2+) permeant NSCCs are differentially activated by the BCR and mechanical stimuli and regulate distinct aspects of B cell physiology. |
