Zobrazeno 1 - 10
of 32
pro vyhledávání: '"Diego G Ogando"'
Publikováno v:
Cells, Vol 12, Iss 11, p 1528 (2023)
Purpose: Inducible Slc4a11 KO leads to corneal edema by disruption of the pump and barrier functions of the corneal endothelium (CE). The loss of Slc4a11 NH3-activated mitochondrial uncoupling leads to mitochondrial membrane potential hyperpolarizati
Externí odkaz:
https://doaj.org/article/a410014bf61d4a0d88a2bfeefddd1547
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 10 (2022)
Recent studies from Slc4a11−/− mice have identified glutamine-induced mitochondrial dysfunction as a significant contributor toward oxidative stress, impaired lysosomal function, aberrant autophagy, and cell death in this Congenital Hereditary En
Externí odkaz:
https://doaj.org/article/0dc3388e17e84ec78583a12641908973
Autor:
Rajalekshmy Shyam, PhD, Diego G. Ogando, PhD, Edward T. Kim, BS, Subashree Murugan, BOptom, Moonjung Choi, PhD, Joseph A. Bonanno, OD, PhD
Publikováno v:
Ophthalmology Science, Vol 2, Iss 1, Pp 100084- (2022)
Purpose: Congenital hereditary endothelial dystrophy (CHED) is a rare condition that manifests at an early age showing corneal edema, increased oxidative stress, mitochondrial dysfunction, and eventually apoptosis of the endothelium due to loss of fu
Externí odkaz:
https://doaj.org/article/1bdfc09091034259b4b4ac32e785d473
Publikováno v:
Cells, Vol 11, Iss 2, p 197 (2022)
Solute-linked cotransporter, SLC4A11, a member of the bicarbonate transporter family, is an electrogenic H+ transporter activated by NH3 and alkaline pH. Although SLC4A11 does not transport bicarbonate, it shares many properties with other members of
Externí odkaz:
https://doaj.org/article/31a5cd4d2698483eae384aeb2b9518a3
Autor:
Wenlin Zhang, Hongde Li, Diego G. Ogando, Shimin Li, Matthew Feng, Francis W. Price, Jr, Jason M. Tennessen, Joseph A. Bonanno
Publikováno v:
EBioMedicine, Vol 16, Iss C, Pp 292-301 (2017)
Corneal endothelium (CE) is among the most metabolically active tissues in the body. This elevated metabolic rate helps the CE maintain corneal transparency by its ion and fluid transport properties, which when disrupted, leads to visual impairment.
Externí odkaz:
https://doaj.org/article/05d493b6c4604c87a19d3ac27673e71e
Publikováno v:
Redox Biology, Vol 26, Iss , Pp - (2019)
SLC4A11 is a NH3 sensitive membrane transporter with H+ channel-like properties that facilitates Glutamine catabolism in Human and Mouse corneal endothelium (CE). Loss of SLC4A11 activity induces oxidative stress and cell death, resulting in Congenit
Externí odkaz:
https://doaj.org/article/69dfe717fa094bcab95fcfab5458b6d2
Publikováno v:
Cells; Volume 12; Issue 11; Pages: 1528
Purpose: Inducible Slc4a11 KO leads to corneal edema by disruption of the pump and barrier functions of the corneal endothelium (CE). The loss of Slc4a11 NH3-activated mitochondrial uncoupling leads to mitochondrial membrane potential hyperpolarizati
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=multidiscipl::be740de3b320a963bd10f32a3a0d7dd4
Purpose: Inducible Slc4a11 KO leads to corneal edema by disruption of the pump and barrier functions of the corneal endothelium (CE). The loss of Slc4a11 NH3-activated mitochondrial uncoupling leads to mitochondrial membrane potential hyperpolarizati
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::fd714d0cf384d90de5270d383ec04f50
https://doi.org/10.20944/preprints202305.1059.v1
https://doi.org/10.20944/preprints202305.1059.v1
Publikováno v:
Frontiers in cell and developmental biology. 10
Recent studies from
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::44a5f2ceb5b7b5fc8beb913cc2dcb2ba
https://pubmed.ncbi.nlm.nih.gov/35557943
https://pubmed.ncbi.nlm.nih.gov/35557943
Autor:
Diego G. Ogando, Joseph A. Bonanno
Publikováno v:
Exp Eye Res
Slc4a11 KO mice show significant corneal edema, altered endothelial morphology, and mitochondrial ROS at an early age without a decrease in endothelial cell density. We examined the differential gene expression profile between wild type (WT) and KO w
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c42d15f458d461b4891e325e4155012
https://pubmed.ncbi.nlm.nih.gov/34871568
https://pubmed.ncbi.nlm.nih.gov/34871568