{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T01:23:35Z","timestamp":1760059415895,"version":"build-2065373602"},"reference-count":59,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T00:00:00Z","timestamp":1749600000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Helmut Ecker Stiftung"},{"name":"Open Access Publication Fund of UKE\u2014Universit\u00e4tsklinikum Hamburg-Eppendorf"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>The Na,K-ATPase is a heterodimeric ion pump consisting of various combinations of a catalytic \u03b1-subunit (\u03b11, \u03b12, \u03b13, or \u03b14, encoded by ATP1A1\u2013ATP1A4) and a \u03b2-subunit (\u03b21, \u03b22, or \u03b23, encoded by ATP1B1\u2013ATP1B3). We have previously shown that Atp1b2 knock-out (ko) mice exhibit rapid photoreceptor cell degeneration, whereas Atp1b2Atp1b1 knock-in (ki) mice, which express the \u03b21-subunit instead of the \u03b22-subunit under regulatory elements of the Atp1b2 gene, exhibit slowly progressive retinal dystrophy. Here, we performed a detailed analysis of the retinal phenotype of the Atp1b2Atp1b1 ki mouse. We found that the number of cone photoreceptor cells in the mutant retinas was significantly reduced by postnatal day 28. The retinas of 4-month-old mice were almost devoid of cones. The early onset and rapid loss of cones was followed by a slowly progressive degeneration of rods. Other retinal cell types were unaffected. Nonradioactive in situ hybridization and immunohistochemistry revealed that wild-type photoreceptors expressed \u03b23 and high levels of \u03b22, while Atp1b2Atp1b1 ki photoreceptor cells expressed \u03b23 and low levels of transgenic \u03b21. Additionally, levels of retinoschisin, a secreted retina-specific protein that interacts directly with the \u03b22-subunit, were greatly reduced in mutant retinas. The results demonstrate that the \u03b21-subunit can functionally compensate, at least in part, for the absence of the \u03b22-subunit. The results also show that cones are more susceptible to Na,K-ATPase dysfunction than rods. Taken together, the present study identifies the Atp1b2Atp1b1 ki mutant as a novel animal model of an early-onset and rapidly progressive cone\u2013rod dystrophy.<\/jats:p>","DOI":"10.3390\/cells14120878","type":"journal-article","created":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T03:44:58Z","timestamp":1749613498000},"page":"878","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Atp1b2Atp1b1 Knock-In Mice Exhibit a Cone\u2013Rod Dystrophy-Like Phenotype"],"prefix":"10.3390","volume":"14","author":[{"given":"Susanne","family":"Bartsch","sequence":"first","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yevgeniya","family":"Atiskova","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefanie","family":"Schlichting","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Elke","family":"Becker","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maike","family":"Herrmann","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3227-7568","authenticated-orcid":false,"given":"Udo","family":"Bartsch","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, Experimental Ophthalmology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2025,6,11]]},"reference":[{"key":"ref_1","first-page":"F633","article-title":"Isozymes of the Na-K-ATPase: Heterogeneity in structure, diversity in function","volume":"275","author":"Blanco","year":"1998","journal-title":"Am. 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