{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,12]],"date-time":"2025-12-12T13:31:10Z","timestamp":1765546270647},"reference-count":0,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1996,3,1]]},"abstract":"<jats:p> The decreased osmotic fragility and reduced K+ content of BXD-31 mouse erythrocytes arise from variation at a single genetic locus. We compared ion transport in erythrocytes from BXD-31 mice and the parental strain, DBA\/2J. The strains had similar rates for Na-K pump, Na\/H exchange, Na-K-2Cl cotransport, Ca2+ activated K+ channel, or AE1-mediated SO4 transport. In contrast, K-Cl cotransport was twice as active in BXD-31 as in DBA\/2J cells. Cl- dependent K+ efflux from BXD-31 cells displayed steep activation by acid pH (with maximal transport occurring at pH 6.75), whereas DBA\/2J erythrocytes displayed a far less dramatic response to pH. Both strains displayed regulatory volume decrease in response to cell swelling. However, a 62% greater loss of cell K+ via K-Cl cotransport was observed in the BXD-31 strain. Furthermore the decreased osmotic fragility of BXD-31 red blood cells was normalized by treatment with nystatin to achieve normal cell K+ and water content. Thus upregulated K-Cl cotransport induces cell dehydration and K+ deficit in BXD-31 erythrocytes and causes their characteristic resistance to osmotic lysis. <\/jats:p>","DOI":"10.1152\/ajpcell.1996.270.3.c866","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T19:04:07Z","timestamp":1514142247000},"page":"C866-C877","source":"Crossref","is-referenced-by-count":19,"title":["Resistance to osmotic lysis in BXD-31 mouse erythrocytes: association with upregulated K-Cl cotransport"],"prefix":"10.1152","volume":"270","author":[{"given":"C. C.","family":"Armsby","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, The Children's Hospital, Boston,Massachusetts 02115, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A. K.","family":"Stuart-Tilley","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, The Children's Hospital, Boston,Massachusetts 02115, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. L.","family":"Alper","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, The Children's Hospital, Boston,Massachusetts 02115, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Brugnara","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, The Children's Hospital, Boston,Massachusetts 02115, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Cell Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajpcell.1996.270.3.C866","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:35:22Z","timestamp":1718652922000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajpcell.1996.270.3.C866"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,3,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,3,1]]}},"alternative-id":["10.1152\/ajpcell.1996.270.3.C866"],"URL":"https:\/\/doi.org\/10.1152\/ajpcell.1996.270.3.c866","relation":{},"ISSN":["0363-6143","1522-1563"],"issn-type":[{"value":"0363-6143","type":"print"},{"value":"1522-1563","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,3,1]]}}}