Publikationsdatum:
2005-01-08
Beschreibung:
Calcium is known to play vital roles in diverse physiological processes, and it is known that voltage-gated calcium channels (Cav) mediate calcium influx in excitable cells. However, no consensus exists on the molecular identity of the calcium channels present in nonexcitable cells such as T lymphocytes. Here, we demonstrate that T lymphocytes express both regulatory beta4 and poreforming Cav1 alpha1 subunits of Cav channels. Cav beta4-mutant T lymphocytes fail to acquire normal functions and display impairment in the calcium response, activation of the transcription factor NFAT, and cytokine production. Although Cav1 channels of lymphocytes retain their voltage dependency, T cell receptor stimulation dramatically increases channel opening, providing a new mechanism for calcium entry in lymphocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badou, Abdallah -- Basavappa, Srisaila -- Desai, Rooma -- Peng, You-Qing -- Matza, Didi -- Mehal, Wajahat Z -- Kaczmarek, Leonard K -- Boulpaep, Emile L -- Flavell, Richard A -- New York, N.Y. -- Science. 2005 Jan 7;307(5706):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15637280" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Animals
;
CD4-Positive T-Lymphocytes/*immunology/*metabolism
;
Calcium/*metabolism
;
Calcium Channels, L-Type/*metabolism
;
*Calcium Signaling
;
Cytokines/biosynthesis
;
DNA-Binding Proteins/metabolism
;
Ion Channel Gating
;
Lymphocyte Activation
;
Membrane Potentials
;
Mice
;
Mice, Inbred C3H
;
Mice, Inbred C57BL
;
Mutation
;
NFATC Transcription Factors
;
Nuclear Proteins/metabolism
;
Patch-Clamp Techniques
;
Phosphorylation
;
Protein Subunits/metabolism
;
Receptors, Antigen, T-Cell/metabolism
;
T-Lymphocytes/immunology/metabolism
;
Transcription Factors/metabolism
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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