{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,6]],"date-time":"2026-01-06T05:26:55Z","timestamp":1767677215218},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1995,10,1]]},"abstract":"<jats:p> The SAD mouse is characterized by the expression of human SAD hemoglobin (Hb), a super S Hb with a higher tendency to polymerize than HbS due to the presence of two additional mutations, Antilles beta 23Ile and D Punjab beta 121Glu. Monovalent cation transport was studied in erythrocytes from SAD-1 (Hb SAD = 19%) and beta-thal\/SAD-1 (Hb SAD = 26%) mice. Erythrocytes containing Hb SAD exhibited dehydration, increased maximal rate of Na(+)-K+ pump, unchanged Rb+ flux via the Gardos channel, and increased K(+)-Cl- cotransport. K(+)-Cl- cotransport was defined as Cl(-)-dependent (substitution with sulfamate or methanesulfonate) okadaic acid-sensitive K+ efflux. Volume regulatory decrease via K(+)-Cl- cotransport was also increased in swollen SAD erythrocytes compared with controls. K(+)-Cl- cotransport was stimulated by staurosporine in all mouse strains, but the extent of stimulation was reduced in beta-thal\/SAD-1 mice. Treatment with dithiothreitol reduced K(+)-Cl- cotransport activity in SAD-1 and beta-thal\/SAD-1 mice to levels similar to that of control strains, indicating that reversible sulfhydryl oxidation contributes to the activated state of K(+)-Cl- cotransport in mouse erythrocytes that express transgenic human Hb SAD. <\/jats:p>","DOI":"10.1152\/ajpcell.1995.269.4.c899","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T18:24:08Z","timestamp":1514139848000},"page":"C899-C906","source":"Crossref","is-referenced-by-count":25,"title":["Sulfhydryl oxidation and activation of red cell K(+)-Cl- cotransport in the transgenic SAD mouse"],"prefix":"10.1152","volume":"269","author":[{"given":"L.","family":"De Franceschi","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, University of Verona, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"Beuzard","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Verona, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C.","family":"Brugnara","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Verona, Italy."}],"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.1995.269.4.C899","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:38:37Z","timestamp":1718653117000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajpcell.1995.269.4.C899"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,10,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1995,10,1]]}},"alternative-id":["10.1152\/ajpcell.1995.269.4.C899"],"URL":"https:\/\/doi.org\/10.1152\/ajpcell.1995.269.4.c899","relation":{},"ISSN":["0363-6143","1522-1563"],"issn-type":[{"value":"0363-6143","type":"print"},{"value":"1522-1563","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,10,1]]}}}