{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T04:30:57Z","timestamp":1793421057830,"version":"4.5.0"},"reference-count":36,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1997,11,1]]},"abstract":"<jats:p>\n                    The neuronal K-Cl cotransporter isoform (KCC2) was functionally expressed in human embryonic kidney (HEK-293) cell lines. Two stably transfected HEK-293 cell lines were prepared: one expressing an epitope-tagged KCC2 (KCC2\u201322T) and another expressing the unaltered KCC2 (KCC2\u20139). The KCC2\u201322T cells produced a glycoprotein of \u223c150 kDa that was absent from HEK-293 control cells. The\n                    <jats:sup>86<\/jats:sup>\n                    Rb influx in both cell lines was significantly greater than untransfected control HEK-293 cells. The KCC2\u20139 cells displayed a constitutively active\n                    <jats:sup>86<\/jats:sup>\n                    Rb influx that could be increased further by 1 mM N-ethylmaleimide (NEM) but not by cell swelling. Both furosemide [inhibition constant ( K\n                    <jats:sub>i<\/jats:sub>\n                    ) \u223c25 \u03bcM] and bumetanide (K\n                    <jats:sub>i<\/jats:sub>\n                    \u223c55 \u03bcM) inhibited the NEM-stimulated\n                    <jats:sup>86<\/jats:sup>\n                    Rb influx in the KCC2\u20139 cells. This diuretic-sensitive\n                    <jats:sup>86<\/jats:sup>\n                    Rb influx in the KCC2\u20139 cells, operationally defined as KCC2 mediated, required external Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    but not external Na\n                    <jats:sup>+<\/jats:sup>\n                    and exhibited a high apparent affinity for external Rb\n                    <jats:sup>+<\/jats:sup>\n                    (K\n                    <jats:sup>+<\/jats:sup>\n                    ) [Michaelis constant ( K\n                    <jats:sub>m<\/jats:sub>\n                    ) = 5.2 \u00b1 0.9 (SE) mM; n = 5] but a low apparent affinity for external Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    ( K\n                    <jats:sub>m<\/jats:sub>\n                    &gt;50 mM). On the basis of thermodynamic considerations as well as the unique kinetic properties of the KCC2 isoform, it is hypothesized that KCC2 may serve a dual function in neurons: 1) the maintenance of low intracellular Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    concentration so as to allow Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    influx via ligand-gated Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    channels and 2) the buffering of external K\n                    <jats:sup>+<\/jats:sup>\n                    concentration ([K\n                    <jats:sup>+<\/jats:sup>\n                    ]\n                    <jats:sub>o<\/jats:sub>\n                    ) in the brain.\n                  <\/jats:p>","DOI":"10.1152\/ajpcell.1997.273.5.c1516","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T12:14:53Z","timestamp":1514117693000},"page":"C1516-C1525","source":"Crossref","is-referenced-by-count":350,"title":["Functional characterization of the neuronal-specific  K-Cl cotransporter: implications for [K\n                    <sup>+<\/sup>\n                    ]\n                    <sub>o<\/sub>\n                    regulation"],"prefix":"10.1152","volume":"273","author":[{"given":"John A.","family":"Payne","sequence":"first","affiliation":[{"name":"Department of Human Physiology, University of California, School of Medicine, Davis, California 95616"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1982.sp014305"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1016\/0304-3940(84)90520-2"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2736(81)90079-1"},{"key":"B5","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.107.2.261"},{"key":"B6","first-page":"89","volume":"26","author":"Delpire E.","year":"1992","journal-title":"J. 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