<?xml version="1.0"?>
<metadata xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:dc="http://purl.org/dc/elements/1.1/"><dc:title>Multifunctional roles of γ-enolase in the central nervous system</dc:title><dc:creator>Horvat,	Selena	(Avtor)
	</dc:creator><dc:creator>Kos,	Janko	(Avtor)
	</dc:creator><dc:creator>Pišlar,	Anja	(Avtor)
	</dc:creator><dc:subject>γ-enolase</dc:subject><dc:subject>neuronal marker</dc:subject><dc:subject>neurotrophic-like factor</dc:subject><dc:subject>neurodegeneration</dc:subject><dc:subject>neuroprotection</dc:subject><dc:description>Enolase, a multifunctional protein with diverse isoforms, has generally been recognized for its primary roles in glycolysis and gluconeogenesis. The shift in isoform expression from α-enolase to neuron-specific γ-enolase extends beyond its enzymatic role. Enolase is essential for neuronal survival, differentiation, and the maturation of neurons and glial cells in the central nervous system. Neuron-specific γ-enolase is a critical biomarker for neurodegenerative pathologies and neurological conditions, not only indicating disease but also participating in nerve cell formation and neuroprotection and exhibiting neurotrophic-like properties. These properties are precisely regulated by cysteine peptidase cathepsin X and scaffold protein γ1-syntrophin. Our findings suggest that γ-enolase, specifically its C-terminal part, may offer neuroprotective benefits against neurotoxicity seen in Alzheimer's and Parkinson's disease. Furthermore, although the therapeutic potential of γ-enolase seems promising, the effectiveness of enolase inhibitors is under debate. This paper reviews the research on the roles of γ-enolase in the central nervous system, especially in pathophysiological events and the regulation of neurodegenerative diseases.</dc:description><dc:date>2024</dc:date><dc:date>2024-09-06 09:49:17</dc:date><dc:type>Članek v reviji</dc:type><dc:identifier>161035</dc:identifier><dc:identifier>UDK: 616.8</dc:identifier><dc:identifier>ISSN pri članku: 2045-3701</dc:identifier><dc:identifier>DOI: 10.1186/s13578-024-01240-6</dc:identifier><dc:identifier>COBISS_ID: 197795331</dc:identifier><dc:language>sl</dc:language></metadata>
