Protection of TRPC7 cation channels from calcium inhibition by closely associated SERCA pumps Loïc Lemonnier, Mohamed Trebak, Jean-Philippe Lievremont 1 , Gary S. Bird and James W. Putney, Jr. 2 National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina, USA 2 Correspondence: NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709 USA. E-mail: putney@niehs.nih.gov <h3>SPECIFIC AIMS</h3> Among the different structures involved in the regulation of Ca 2+ homeostasis, the transient receptor potential (TRP) channels superfamily is one of the most intensively studied. TRPs were first cloned from Drosophila melanogaster as a gene necessary for normal visual signal transduction. Numerous studies have demonstrated that members of the TRP superfamily of channels are involved in regulated Ca 2+ entry, in some instances as store-operated channels, in others as non-store-operated channels. Most Ca 2+ -permeable channels are themselves regulated by Ca 2+ , often in complex ways. In the current study, we have investigated the regulation of TRPC7, stably expressed in human embryonic kidney (HEK293) cells by Ca 2+ , and more specifically by sarcoplasmic-endoplasmic reticulum calcium ATPase (SERCA) pumps. TRPC7 was chosen for this study because it is a channel known
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