Publications by authors named "Thea Joseph"
In hypoxic and pseudohypoxic rodent models of pulmonary hypertension (PH), hypoxia-inducible factor (HIF) inhibition attenuates disease initiation. However, HIF activation alone, due to genetic alterations or use of inhibitors of prolyl hydroxylase domain (PHD) enzymes, has not been definitively shown to cause PH in humans, indicating the involvement of other mechanisms. Given the association between endothelial cell dysfunction and PH, the effects of pseudohypoxia and its underlying pathways were investigated in primary human lung endothelial cells.
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- The generation of neurons in the central nervous system involves radial glia, which are mitotic progenitors that rapidly proliferate to form a dense neurepithelium and produce different neuronal sub-types.
- Molecular mechanisms behind this process are not well understood, but a family of enzymes called GDE proteins, including GDE6, play a role in neural development.
- Research shows that overexpression of GDE6 leads to neural tube hyperplasia, abnormal neurepithelium growth, and a decrease in the production of motor neurons, indicating its important role in regulating radial glia and neurogenesis alongside GDE2.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that affects the viability of upper and lower motor neurons. Current options for treatment are limited, necessitating deeper understanding of the mechanisms underlying ALS pathogenesis. Glycerophosphodiester phosphodiesterase 2 (GDE2 or GDPD5) is a six-transmembrane protein that acts on the cell surface to cleave the glycosylphosphatidylinositol (GPI)-anchor that tethers some proteins to the membrane.
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