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NeuroRepair gpr17 receptor
Gpr17 Receptor, supplied by NeuroRepair, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The role of <t>GPR17</t> receptors as a specific marker of CNS damage. In the early stage of CNS tissue injury (within 24 h), an increased level of GPR17 is observed in damaged neurons and there is considerable growth in the mortality of GPR17+ neurons ( 1 ). Once 48 h have passed since axonal damage, GPR17 receptors are not located on injured neurons, but only at the limit of the nerve tissue damage due to exposition on the surface of infiltrating macrophages (activated microglial cells) ( 2 ) Once 72 h have passed since damage, a proliferation of OPCs (GPR17+) is observed. Expression of GPR17 on the surface of OPCs blocks their differentiation and maturation into myelinating OLGs. Myelination is possible after losing the GPR17 receptors by OLGs ( 3 ). One week after brain injury, the GPR17 level again enhances in the area of damage and is associated with the resumed massive infiltration of macrophage cells that previously resided on the edge of the damage site ( 4 ). Abbreviations: anti-MBP, anti-major basic protein; GPR17, G-protein coupled receptor 17; OPCs, oligodendrocyte precursor cells; OLGs, oligodendrocytes; ROS, reactive oxygen species.
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Neuropharm Ltd cns remyelination roles of purinergic signaling and the p2y-like receptor gpr17
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Cns Remyelination Roles Of Purinergic Signaling And The P2y Like Receptor Gpr17, supplied by Neuropharm Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The role of <t>GPR17</t> receptors as a specific marker of CNS damage. In the early stage of CNS tissue injury (within 24 h), an increased level of GPR17 is observed in damaged neurons and there is considerable growth in the mortality of GPR17+ neurons ( 1 ). Once 48 h have passed since axonal damage, GPR17 receptors are not located on injured neurons, but only at the limit of the nerve tissue damage due to exposition on the surface of infiltrating macrophages (activated microglial cells) ( 2 ) Once 72 h have passed since damage, a proliferation of OPCs (GPR17+) is observed. Expression of GPR17 on the surface of OPCs blocks their differentiation and maturation into myelinating OLGs. Myelination is possible after losing the GPR17 receptors by OLGs ( 3 ). One week after brain injury, the GPR17 level again enhances in the area of damage and is associated with the resumed massive infiltration of macrophage cells that previously resided on the edge of the damage site ( 4 ). Abbreviations: anti-MBP, anti-major basic protein; GPR17, G-protein coupled receptor 17; OPCs, oligodendrocyte precursor cells; OLGs, oligodendrocytes; ROS, reactive oxygen species.
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Verlag GmbH orphan receptor gpr17
The role of <t>GPR17</t> receptors as a specific marker of CNS damage. In the early stage of CNS tissue injury (within 24 h), an increased level of GPR17 is observed in damaged neurons and there is considerable growth in the mortality of GPR17+ neurons ( 1 ). Once 48 h have passed since axonal damage, GPR17 receptors are not located on injured neurons, but only at the limit of the nerve tissue damage due to exposition on the surface of infiltrating macrophages (activated microglial cells) ( 2 ) Once 72 h have passed since damage, a proliferation of OPCs (GPR17+) is observed. Expression of GPR17 on the surface of OPCs blocks their differentiation and maturation into myelinating OLGs. Myelination is possible after losing the GPR17 receptors by OLGs ( 3 ). One week after brain injury, the GPR17 level again enhances in the area of damage and is associated with the resumed massive infiltration of macrophage cells that previously resided on the edge of the damage site ( 4 ). Abbreviations: anti-MBP, anti-major basic protein; GPR17, G-protein coupled receptor 17; OPCs, oligodendrocyte precursor cells; OLGs, oligodendrocytes; ROS, reactive oxygen species.
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The role of GPR17 receptors as a specific marker of CNS damage. In the early stage of CNS tissue injury (within 24 h), an increased level of GPR17 is observed in damaged neurons and there is considerable growth in the mortality of GPR17+ neurons ( 1 ). Once 48 h have passed since axonal damage, GPR17 receptors are not located on injured neurons, but only at the limit of the nerve tissue damage due to exposition on the surface of infiltrating macrophages (activated microglial cells) ( 2 ) Once 72 h have passed since damage, a proliferation of OPCs (GPR17+) is observed. Expression of GPR17 on the surface of OPCs blocks their differentiation and maturation into myelinating OLGs. Myelination is possible after losing the GPR17 receptors by OLGs ( 3 ). One week after brain injury, the GPR17 level again enhances in the area of damage and is associated with the resumed massive infiltration of macrophage cells that previously resided on the edge of the damage site ( 4 ). Abbreviations: anti-MBP, anti-major basic protein; GPR17, G-protein coupled receptor 17; OPCs, oligodendrocyte precursor cells; OLGs, oligodendrocytes; ROS, reactive oxygen species.

Journal: International Journal of Molecular Sciences

Article Title: The GPR17 Receptor—A Promising Goal for Therapy and a Potential Marker of the Neurodegenerative Process in Multiple Sclerosis

doi: 10.3390/ijms21051852

Figure Lengend Snippet: The role of GPR17 receptors as a specific marker of CNS damage. In the early stage of CNS tissue injury (within 24 h), an increased level of GPR17 is observed in damaged neurons and there is considerable growth in the mortality of GPR17+ neurons ( 1 ). Once 48 h have passed since axonal damage, GPR17 receptors are not located on injured neurons, but only at the limit of the nerve tissue damage due to exposition on the surface of infiltrating macrophages (activated microglial cells) ( 2 ) Once 72 h have passed since damage, a proliferation of OPCs (GPR17+) is observed. Expression of GPR17 on the surface of OPCs blocks their differentiation and maturation into myelinating OLGs. Myelination is possible after losing the GPR17 receptors by OLGs ( 3 ). One week after brain injury, the GPR17 level again enhances in the area of damage and is associated with the resumed massive infiltration of macrophage cells that previously resided on the edge of the damage site ( 4 ). Abbreviations: anti-MBP, anti-major basic protein; GPR17, G-protein coupled receptor 17; OPCs, oligodendrocyte precursor cells; OLGs, oligodendrocytes; ROS, reactive oxygen species.

Article Snippet: Therefore, GPR17 receptors may be recognized as the potential goal in creating innovative therapies for the treatment of the neurodegenerative process in MS, based on the acceleration of the remyelination processes.

Techniques: Marker, Expressing

Phases of GPR17 differentiation. GPR17 as an inner timer of oligodendrocyte differentiation and the myelination process. GPR17 is expressed in the oligodendrocyte lineage cells, and its level is increased during differentiation of NG2+ OPCs into O4-pre-myelinating oligodendrocytes. It is evidently downregulated during the terminal maturation of myelinating oligodendrocytes, which express MBP.

Journal: International Journal of Molecular Sciences

Article Title: The GPR17 Receptor—A Promising Goal for Therapy and a Potential Marker of the Neurodegenerative Process in Multiple Sclerosis

doi: 10.3390/ijms21051852

Figure Lengend Snippet: Phases of GPR17 differentiation. GPR17 as an inner timer of oligodendrocyte differentiation and the myelination process. GPR17 is expressed in the oligodendrocyte lineage cells, and its level is increased during differentiation of NG2+ OPCs into O4-pre-myelinating oligodendrocytes. It is evidently downregulated during the terminal maturation of myelinating oligodendrocytes, which express MBP.

Article Snippet: Therefore, GPR17 receptors may be recognized as the potential goal in creating innovative therapies for the treatment of the neurodegenerative process in MS, based on the acceleration of the remyelination processes.

Techniques: