Publications by authors named "Shen-Yan Huang"
Huntington's disease (HD) is a hereditary neurodegenerative disorder characterized by involuntary movements, cognitive deficits, and psychiatric symptoms. Currently, there is no cure, and only limited treatments are available to manage the symptoms and to slow down the disease's progression. The molecular and cellular mechanisms of HD's pathogenesis are complex, involving immune cell activation, altered protein turnover, and disturbance in brain energy homeostasis.
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- The immune synapse is a crucial structure for T cell activation, connecting T lymphocytes with antigen-presenting cells (APCs).
- Research reveals that INPP5E, a protein associated with the sensory organelle called cilia, is concentrated at the immune synapse in Jurkat T-cells during specific types of T cell activation.
- Silencing INPP5E hampers key signaling processes, affecting the proper function of TCR signaling and reducing the secretion of IL-2, an important immune response factor.
An increasing amount of evidence emphasizes the role of metabolic reprogramming in immune cells to fight infections. However, little is known about the regulation of metabolite transporters that facilitate and support metabolic demands. In this study, we found that the expression of equilibrative nucleoside transporter 3 (ENT3, encoded by solute carrier family 29 member 3, Slc29a3) is part of the innate immune response, which is rapidly upregulated upon pathogen invasion.
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