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Molecular determinant of KCa3.1 that affects cell proliferation?
Author(s) -
Hamilton Kirk L.,
Devor Daniel C.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.884.11
Subject(s) - hek 293 cells , transfection , cell growth , cell , microbiology and biotechnology , chemistry , cell culture , potassium channel , biology , biophysics , biochemistry , genetics
It has been demonstrated that the KCa3.1, the intermediate‐conductance Ca 2+ ‐activated K + channel KCNN4, increases cell proliferation. It still remains to be determined how this occurs. Recently, we reported that wild‐type KCa3.1, a non‐conducting KCa3.1 or non‐trafficking KCa3.1 channel increased cell proliferation when transiently expressed in HEK cells (Millership et al., Am J. Physiol Cell Physiol 300:C792‐C802, 2011). In the present study, we have used chimeric channels of KCa3.1 (IK) and KCa2.2 (SK; has no affect on cell proliferation) to uncover the potential molecular portion of KCa3.1 that alters cell proliferation. Transient transfection of HEK cells with IK increased cell number after 3 days to 131±7% (n = 7) compared to mock‐transfected cells (n = 7) while SK had no effect on cell number (n = 4). HEK cells transfected with a chimeric channel of SK‐200IK (SK+S5‐pore‐ S6‐C‐terminus of IK) significantly increased cell number to 119±3% (n = 5) when compared with mock‐transfected cells, however, SK‐287IK (SK+C‐terminus of IK) did not increase cell count (n = 3). We are currently exploring other chimeric and mutated channels to further define the portion of KCa3.1 responsible for altered cell proliferation. At present, our data suggest that the S5‐pore‐S6 portion of KCa3.1 is crucial for modulation of cell proliferation. This work was funded by Department of Physiology at UoO (KLH) and NIH (DCD).