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ocular hypertension/phosphatase
Nuoroda įrašoma į mainų sritį
6 rezultatus
A study of histology and enzymatic histochemistry on rabbit's retina in acute ocular hypertension.
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Prisijungti Registracija
The changes of activities of enzymes relating to energy metabolism in rabbit's retina in acute ocular hypertension were observed. The activities of succinate dehydrogenase and adenosine triphosphatase were found to be reduced, while the activities of the lactatic dehydrogenase and
Targeting the vascular-specific phosphatase PTPRB protects against retinal ganglion cell loss in a pre-clinical model of glaucoma.
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Elevated intraocular pressure (IOP) due to insufficient aqueous humor outflow through the trabecular meshwork and Schlemm's canal (SC) is the most important risk factor for glaucoma, a leading cause of blindness worldwide. We previously reported loss of function mutations in the receptor tyrosine
Changes of serum calcium, phosphorus, and parathyroid hormone concentrations and ocular findings among patients undergoing hemodialysis.
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Prisijungti Registracija
There are various reports of ocular abnormalities in metabolic disorders. This study was done with the aim to investigate the relationships between the amounts of serum calcium, phosphorus, and parathyroid hormone concentrations and ocular findings in patients undergoing hemodialysis. Fifty eight
Improved immunohistochemical detection of phosphorylated mitogen-activated protein kinases in the injured rat optic nerve head.
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The activity of mitogen-activated protein kinases (MAPKs) is largely controlled by addition or removal of phosphate groups, which are carried out by kinase or phosphatase enzymes, respectively. Determining the phosphorylation status of MAPK isoenzymes, therefore, aids elucidation of the
Lysophosphatidic Acid Induces ECM Production via Activation of the Mechanosensitive YAP/TAZ Transcriptional Pathway in Trabecular Meshwork Cells.
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UNASSIGNED
Lysophosphatidic acid (LPA), a bioactive lipid, has been shown to increase resistance to aqueous humor outflow (AH) through the trabecular meshwork (TM). The molecular basis for this response of the TM to LPA, however, is not completely understood. In this study, we explored the possible
Calcineurin activation causes retinal ganglion cell degeneration.
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OBJECTIVE
We previously reported that calcineurin, a Ca(2+)/calmodulin-dependent serine/threonine phosphatase, is activated and proposed that it participates in retinal ganglion cell (RGC) apoptosis in two rodent ocular hypertension models. In this study, we tested whether calcineurin activation by
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