Impact of MCT1 Haploinsufficiency on the Mouse Retina

Handle URI:
http://hdl.handle.net/10754/627851
Title:
Impact of MCT1 Haploinsufficiency on the Mouse Retina
Authors:
Peachey, Neal S.; Yu, Minzhong; Han, John Y. S.; Lengacher, Sylvain; Magistretti, Pierre J. ( 0000-0002-6678-320X ) ; Pellerin, Luc; Philp, Nancy J.
Abstract:
The monocarboxylate transporter 1 (MCT1) is highly expressed in the outer retina, suggesting that it plays a critical role in photoreceptors. We examined MCT1+/− heterozygotes, which express half of the normal complement of MCT1. The MCT1+/− retina developed normally and retained normal function, indicating that MCT1 is expressed at sufficient levels to support outer retinal metabolism.
KAUST Department:
Biological and Environmental Sciences and Engineering (BESE) Division; Bioscience Program
Citation:
Peachey NS, Yu M, Han JYS, Lengacher S, Magistretti PJ, et al. (2018) Impact of MCT1 Haploinsufficiency on the Mouse Retina. Advances in Experimental Medicine and Biology: 375–380. Available: http://dx.doi.org/10.1007/978-3-319-75402-4_46.
Publisher:
Springer International Publishing
Journal:
Advances in Experimental Medicine and Biology
Issue Date:
2-May-2018
DOI:
10.1007/978-3-319-75402-4_46
Type:
Book Chapter
ISSN:
0065-2598; 2214-8019
Sponsors:
This work was supported by grants from NIH (R01EY12042) and Department of Veterans Affairs (I01BX2340) and by the Foundation Fighting Blindness and Research to Prevent Blindness.
Additional Links:
http://link.springer.com/chapter/10.1007/978-3-319-75402-4_46
Appears in Collections:
Bioscience Program; Book Chapters; Biological and Environmental Sciences and Engineering (BESE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorPeachey, Neal S.en
dc.contributor.authorYu, Minzhongen
dc.contributor.authorHan, John Y. S.en
dc.contributor.authorLengacher, Sylvainen
dc.contributor.authorMagistretti, Pierre J.en
dc.contributor.authorPellerin, Lucen
dc.contributor.authorPhilp, Nancy J.en
dc.date.accessioned2018-05-14T13:37:06Z-
dc.date.available2018-05-14T13:37:06Z-
dc.date.issued2018-05-02en
dc.identifier.citationPeachey NS, Yu M, Han JYS, Lengacher S, Magistretti PJ, et al. (2018) Impact of MCT1 Haploinsufficiency on the Mouse Retina. Advances in Experimental Medicine and Biology: 375–380. Available: http://dx.doi.org/10.1007/978-3-319-75402-4_46.en
dc.identifier.issn0065-2598en
dc.identifier.issn2214-8019en
dc.identifier.doi10.1007/978-3-319-75402-4_46en
dc.identifier.urihttp://hdl.handle.net/10754/627851-
dc.description.abstractThe monocarboxylate transporter 1 (MCT1) is highly expressed in the outer retina, suggesting that it plays a critical role in photoreceptors. We examined MCT1+/− heterozygotes, which express half of the normal complement of MCT1. The MCT1+/− retina developed normally and retained normal function, indicating that MCT1 is expressed at sufficient levels to support outer retinal metabolism.en
dc.description.sponsorshipThis work was supported by grants from NIH (R01EY12042) and Department of Veterans Affairs (I01BX2340) and by the Foundation Fighting Blindness and Research to Prevent Blindness.en
dc.publisherSpringer International Publishingen
dc.relation.urlhttp://link.springer.com/chapter/10.1007/978-3-319-75402-4_46en
dc.subjectMCT1en
dc.subjectRetinaen
dc.subjectLactateen
dc.subjectTransgenic miceen
dc.subjectElectroretinogramen
dc.titleImpact of MCT1 Haploinsufficiency on the Mouse Retinaen
dc.typeBook Chapteren
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.contributor.departmentBioscience Programen
dc.identifier.journalAdvances in Experimental Medicine and Biologyen
dc.contributor.institutionDepartment of Ophthalmology, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, USAen
dc.contributor.institutionCole Eye Institute, Cleveland Clinic, Cleveland, USAen
dc.contributor.institutionLouis Stokes Cleveland VA Medical Center, Cleveland, USAen
dc.contributor.institutionDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, USAen
dc.contributor.institutionBrain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerlanden
dc.contributor.institutionDepartment of Physiology, University of Lausanne, Lausanne, Switzerlanden
kaust.authorMagistretti, Pierre J.en
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