Zobrazeno 1 - 10
of 36
pro vyhledávání: '"Rajalekshmy, Shyam"'
Autor:
Paloma B. Liton, Kathleen Boesze-Battaglia, Michael E. Boulton, Patricia Boya, Thomas A. Ferguson, Ian G. Ganley, Anu Kauppinnen, Gordon W. Laurie, Noboru Mizushima, Hideaki Morishita, Rossella Russo, Jaya Sadda, Rajalekshmy Shyam, Debasish Sinha, Debra A. Thompson, David N. Zacks
Publikováno v:
Autophagy Reports, Vol 2, Iss 1 (2023)
Autophagy is a catabolic self-degradative pathway that promotes the degradation and recycling of intracellular material through the lysosomal compartment. Although first believed to function in conditions of nutritional stress, autophagy is emerging
Externí odkaz:
https://doaj.org/article/061946d58aef4da69c2648d6e73ee4f8
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 11 (2023)
Externí odkaz:
https://doaj.org/article/a33373b62d2e456e85d7d38a42406755
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:
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:
Journal of Clinical and Translational Science, Vol 3, Pp 4-4 (2019)
OBJECTIVES/SPECIFIC AIMS: Purpose - The goal of this study is to understand how loss of the membrane protein SLC4A11 alters endothelial cell metabolism thereby producing Corneal Endothelial Dystrophy. Studies from our lab indicated that glutamine-dep
Externí odkaz:
https://doaj.org/article/81b63653f51a4d689ddaa8e6562f6ff3
Publikováno v:
Frontiers in cell and developmental biology. 10
Recent studies from
Publikováno v:
Investigative Ophthalmology & Visual Science
Purpose The Slc4a11 knock out (KO) mouse model recapitulates the human disease phenotype associated with congenital hereditary endothelial dystrophy (CHED). Increased mitochondrial reactive oxygen species (ROS) in the Slc4a11 KO mouse model is a majo
Publikováno v:
PLoS ONE, Vol 9, Iss 4, p e92845 (2014)
Myocilin (MYOC) is a gene linked directly to juvenile- and adult-onset open angle glaucoma. Mutations including Pro370Leu (P370L) and Gln368stop (Q368X) have been identified in patients. In the present study, we investigated the processing of myocili
Externí odkaz:
https://doaj.org/article/b3cef52033db498fa78bae00798ed59f
Autor:
Rajalekshmy Shyam, Diego G. Ogando, Joseph A. Bonanno, Chia-Yang Liu, Yen-Chiao Wang, Edward T. Kim
Publikováno v:
Investigative ophthalmologyvisual science. 62(7)
Purpose The conventional Slc4a11 knockout (KO) shows significant corneal edema at eye opening, a fact that complicates the study of the initial events leading to edema. An inducible KO would provide opportunities to examine early events following los