ArticleThe Journal of physiology2004
CaT1 knock-down strategies fail to affect CRAC channels in mucosal-type mast cells.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 44 citations in OpenAlex.
- Bovine Leukemia Virus Infection Affects Host Gene Expression Associated with DNA Mismatch Repair.Pathogens (Basel, Switzerland) · 2020Article
- Canonical transient receptor potential (TRPC) 1 acts as a negative regulator for vanilloid TRPV6-mediated Ca2+ influx.The Journal of biological chemistry · 2012Article
- The Role of TRP Proteins in Mast Cells.Frontiers in immunology · 2012Article
- Intracellular Ca Mobilization and Beta-hexosaminidase Release Are Not Influenced by 60 Hz-electromagnetic Fields (EMF) in RBL 2H3 Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2011Article
- Blunted IgE-mediated activation of mast cells in mice lacking the serum- and glucocorticoid-inducible kinase SGK3.American journal of physiology. Cell physiology · 2010Article
- CRAC channelopathies.Pflugers Archiv : European journal of physiology · 2010Review
- Dynamic but not constitutive association of calmodulin with rat TRPV6 channels enables fine tuning of Ca2+-dependent inactivation.The Journal of physiology · 2006Article
- A severe defect in CRAC Ca2+ channel activation and altered K+ channel gating in T cells from immunodeficient patients.The Journal of experimental medicine · 2005Article
- A store-operated nonselective cation channel in human lymphocytes.Cellular and molecular neurobiology · 2005Article
- STIM1, an essential and conserved component of store-operated Ca2+ channel function.The Journal of cell biology · 2005Article
- Structure-function analysis of TRPV channels.Naunyn-Schmiedeberg's archives of pharmacology · 2005Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CaT1, the calcium transport protein 1 encoded by TRPV6, is able to generate a Ca(2+) conductance similar but not identical to the classical CRAC current in mucosal-type mast cells. Here we show that CaT1-derived Ca(2+) entry into HEK293 cells is effectively inhibited either by expression of various dominant negative N-terminal fragments of CaT1 (N(334)-CaT1, N(198)-CaT1 and N(154)-CaT1) or by antisense suppression. By contrast, the endogenous CRAC current of the mast cells was unaffected by CaT1 antisense and siRNA knockdown but markedly suppressed by two (N(334)-CaT1, N(198)-CaT1) of the dominant negative N-CaT1 fragments. Inhibition of CRAC current was not an unspecific, toxic effect, as inward rectifier K(+) and MagNuM currents of the mast cells were not significantly affected by these N-CaT1 fragments. The shortest N(154)-CaT1 fragment inhibited CaT1-derived currents in mast cells, but failed to inhibit CRAC currents. Thus, the structural requirements of rCaT N-terminal fragments for inhibition of rCaT1 and CRAC channels are different. These results together with the lack of CaT1 antisense and siRNA effects on currents render it unlikely that CaT1 is a component of native CRAC channels in mast cells. The data further demonstrate a novel strategy for CRAC current inhibition by an N-terminal structure of CaT1.
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