Microglial Function during Glucose Deprivation: Inflammatory and Neuropsychiatric Implications
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1559-1182
- Extent
-
Online-Ressource
- Language
-
Englisch
- Notes
-
online resource.
- Bibliographic citation
-
Microglial Function during Glucose Deprivation: Inflammatory and Neuropsychiatric Implications ; day:7 ; month:2 ; year:2017 ; pages:1-11
Molecular neurobiology ; (7.2.2017), 1-11
- Keyword
-
Hirnkrankheit
Neuropsychiatrie
Nervenkrankheit
- Creator
-
Churchward, Matthew A.
- Contributor
-
Tchir, Devan R.
Todd, Kathryn G.
SpringerLink (Online service)
- DOI
-
10.1007/s12035-017-0422-9
- URN
-
urn:nbn:de:1111-201703034710
- Rights
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
-
14.08.2025, 10:50 AM CEST
Data provider
This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Churchward, Matthew A.
- Tchir, Devan R.
- Todd, Kathryn G.
- SpringerLink (Online service)
Other Objects (12)
LncRNA TUG1 mediates microglial inflammatory activation by regulating glucose metabolic reprogramming
Acute glucose fluctuation impacts microglial activity, leading to inflammatory activation or self-degradation
Exosomal Mir-3613-3p derived from oxygen–glucose deprivation-treated brain microvascular endothelial cell promotes microglial M1 polarization
Sirt1 regulates microglial activation and inflammation following oxygen-glucose deprivation/reoxygenation injury by targeting the Shh/Gli-1 signaling pathway
Early glycolytic reprogramming controls microglial inflammatory activation
Glucose deprivation in tuberous sclerosis complex-related tumors
Glucose deprivation impairs hypoxia-inducible factor-1α synthesis
Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
Glucose transporter 1 critically controls microglial activation through facilitating glycolysis
LncRNA MALAT1 promotes high glucose-induced inflammatory response of microglial cells via provoking MyD88/IRAK1/TRAF6 signaling
Neuropsychiatric electrophysiology
Androgen deprivation modulates the inflammatory response induced by irradiation
LncRNA TUG1 mediates microglial inflammatory activation by regulating glucose metabolic reprogramming
Acute glucose fluctuation impacts microglial activity, leading to inflammatory activation or self-degradation
Exosomal Mir-3613-3p derived from oxygen–glucose deprivation-treated brain microvascular endothelial cell promotes microglial M1 polarization
Sirt1 regulates microglial activation and inflammation following oxygen-glucose deprivation/reoxygenation injury by targeting the Shh/Gli-1 signaling pathway
Early glycolytic reprogramming controls microglial inflammatory activation
Glucose deprivation in tuberous sclerosis complex-related tumors
Glucose deprivation impairs hypoxia-inducible factor-1α synthesis
Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
Glucose transporter 1 critically controls microglial activation through facilitating glycolysis
LncRNA MALAT1 promotes high glucose-induced inflammatory response of microglial cells via provoking MyD88/IRAK1/TRAF6 signaling
Neuropsychiatric electrophysiology
Androgen deprivation modulates the inflammatory response induced by irradiation
LncRNA TUG1 mediates microglial inflammatory activation by regulating glucose metabolic reprogramming
Acute glucose fluctuation impacts microglial activity, leading to inflammatory activation or self-degradation
Exosomal Mir-3613-3p derived from oxygen–glucose deprivation-treated brain microvascular endothelial cell promotes microglial M1 polarization
Sirt1 regulates microglial activation and inflammation following oxygen-glucose deprivation/reoxygenation injury by targeting the Shh/Gli-1 signaling pathway
Early glycolytic reprogramming controls microglial inflammatory activation
Glucose deprivation in tuberous sclerosis complex-related tumors
Glucose deprivation impairs hypoxia-inducible factor-1α synthesis
Phosphoproteomics identifies microglial Siglec‐F inflammatory response during neurodegeneration
Glucose transporter 1 critically controls microglial activation through facilitating glycolysis
LncRNA MALAT1 promotes high glucose-induced inflammatory response of microglial cells via provoking MyD88/IRAK1/TRAF6 signaling
Neuropsychiatric electrophysiology