| Autor: |
Grissmer, S, Lewis, RS, Cahalan, MD |
| Jazyk: |
angličtina |
| Rok vydání: |
1992 |
| Zdroj: |
Grissmer, S; Lewis, RS; & Cahalan, MD. (1992). Ca2+-activated K+channels in human leukemic T cells. Journal of General Physiology, 99(1), 63-84. doi: 10.1085/jgp.99.1.63. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/3w28t5vp |
| DOI: |
10.1085/jgp.99.1.63. |
| Popis: |
Using the patch-clamp technique, we have identified two types of Ca2+-activated K+(K(Ca)) channels in the human leukemic T cell line, Jurkat. Substances that elevate the intracellular Ca2+concentration ([Ca2+]i), such as ionomycin or the mitogenic lectin phytohemagglutinin (PHA), as well as whole-cell dialysis with pipette solutions containing elevated [Ca2+]i, activate a voltage-independent K+conductance. Unlike the voltage-gated (type n) K+channels in these cells, the majority of K(Ca) channels are insensitive to block by charybdotoxin (CTX) or 4-aminopyridine (4-AP), but are highly sensitive to block by apamin (Kd< 1 nM). Channel activity is strongly dependent on [Ca2+]i, suggesting that multiple Ca2+binding sites may be involved in channel opening. The Ca2+concentration at which half of the channels are activated is 400 nM. These channels show little voltage dependence over a potential range of - 100 to 0 mV and have a unitary conductance of 4-7 pS in symmetrical 170 mM K+. In the presence of 10 nM apamin, a less prevalent type of K(Ca) channel with a unitary conductance of 40-60 pS can be observed. These larger-conductance channels are sensitive to block by CTX. Pharmacological blockade of K(Ca) channels and voltage-gated type n channels inhibits oscillatory Ca2+signaling triggered by PHA. These results suggest that K(Ca) channels play a supporting role during T cell activation by sustaining dynamic patterns of Ca2+signaling. © 1992, Rockefeller University Press., All rights reserved. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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