NDLI: Involvement of Dominant-negative Spliced Variants of the Intermediate Conductance Ca2+-activated K+ Channel, KCa3.1, in Immune Function of Lymphoid Cells*

Content Provider	PubMed Central
Author	Ohya, Susumu Niwa, Satomi Yanagi, Ayano Fukuyo, Yuka Yamamura, Hisao Imaizumi, Yuji
Copyright Year	2011
Abstract	The intermediate conductance Ca2+-activated K+ channel (IKCa channel) encoded by KCa3.1 is responsible for the control of proliferation and differentiation in various types of cells. We identified novel spliced variants of KCa3.1 (human (h) KCa3.1b) from the human thymus, which were lacking the N-terminal domains of the original hKCa3.1a as a result of alternative splicing events. hKCa3.1b was significantly expressed in human lymphoid tissues. Western blot analysis showed that hKCa3.1a proteins were mainly expressed in the plasma membrane fraction, whereas hKCa3.1b was in the cytoplasmic fraction. We also identified a similar N terminus lacking KCa3.1 variants from mice and rat lymphoid tissues (mKCa3.1b and rKCa3.1b). In the HEK293 heterologous expression system, the cellular distribution of cyan fluorescent protein-tagged hKCa3.1a and/or YFP-tagged hKCa3.1b isoforms showed that hKCa3.1b suppressed the localization of hKCa3.1a to the plasma membrane. In the Xenopus oocyte translation system, co-expression of hKCa3.1b with hKCa3.1a suppressed IKCa channel activity of hKCa3.1a in a dominant-negative manner. In addition, this study indicated that up-regulation of mKCa3.1b in mouse thymocytes differentiated CD4(+)CD8(+) phenotype thymocytes into CD4(−)CD8(−) ones and suppressed concanavalin-A-stimulated thymocyte growth by down-regulation of mIL-2 transcripts. Anti-proliferative effects and down-regulation of mIL-2 transcripts were also observed in mKCa3.1b-overexpressing mouse thymocytes. These suggest that the N-terminal domain of KCa3.1 is critical for channel trafficking to the plasma membrane and that the fine-tuning of IKCa channel activity modulated through alternative splicing events may be related to the control in physiological and pathophysiological conditions in T-lymphocytes.
Related Links	http://dx.doi.org/10.1074/jbc.m110.184192
Ending Page	16952
Page Count	13
Starting Page	16940
File Format	PDF
ISSN	00219258
e-ISSN	1083351X
Journal	The Journal of Biological Chemistry
Issue Number	19
Volume Number	286
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2011-05-13
Access Restriction	Open
Rights Holder	American Society for Biochemistry and Molecular Biology
Subject Keyword	Cell Biology Biochemistry Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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