Hochschulschrift
Analysis of mitochondrial metabolism during the pro-inflammatory activation of macrophages
- Location
-
Deutsche Nationalbibliothek Frankfurt am Main
- Dimensions
-
21 cm
- Extent
-
325 Seiten
- Language
-
Englisch
- Notes
-
Illustrationen, Diagramme
Enthält Sonderabdrucke
Technische Universität Carolo-Wilhelmina zu Braunschweig, Dissertation, 2018
- Classification
-
Biowissenschaften, Biologie
- Event
-
Veröffentlichung
- (where)
-
Braunschweig
- (when)
-
2019
- Creator
-
Nonnenmacher, Yannic
- Table of contents
- Rights
-
Bei diesem Objekt liegt nur das Inhaltsverzeichnis digital vor. Der Zugriff darauf ist unbeschränkt möglich.
- Last update
-
11.03.2025, 11:52 AM CET
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.
Object type
- Hochschulschrift
Associated
- Nonnenmacher, Yannic
Time of origin
- 2019
Other Objects (12)
Mitochondrial reactive oxygen species license pro-inflammatory signaling in infected macrophages via disulfide linkage of NEMO
Role of mitochondrial metabolism during the immunometabolic response of inflammatory macrophages to bacterial pathogens
Regulatory Roles of the Mitochondrial Metabolism and the Nuclear Repressor BACH1 in Inflammatory Macrophages
Mitofusin 2 deficiency causes pro-inflammatory effects in human primary macrophages
Hypoxia potentiates palmitate-induced pro-inflammatory activation of primary human macrophages
Adipocyte death triggers a pro-inflammatory response and induces metabolic activation of resident macrophages
The influence of serum amyloid A on pro-inflammatory signaling in monocytes/macrophages cell lines
Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells
Mitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing
Hyperoxia/Hypoxia Exposure Primes a Sustained Pro-Inflammatory Profile of Preterm Infant Macrophages Upon LPS Stimulation
Pharmacological LRH-1/Nr5a2 inhibition limits pro-inflammatory cytokine production in macrophages and associated experimental hepatitis
Macrophage mechanosensing during their pro-inflammatory response
Mitochondrial reactive oxygen species license pro-inflammatory signaling in infected macrophages via disulfide linkage of NEMO
Role of mitochondrial metabolism during the immunometabolic response of inflammatory macrophages to bacterial pathogens
Regulatory Roles of the Mitochondrial Metabolism and the Nuclear Repressor BACH1 in Inflammatory Macrophages
Mitofusin 2 deficiency causes pro-inflammatory effects in human primary macrophages
Hypoxia potentiates palmitate-induced pro-inflammatory activation of primary human macrophages
Adipocyte death triggers a pro-inflammatory response and induces metabolic activation of resident macrophages
The influence of serum amyloid A on pro-inflammatory signaling in monocytes/macrophages cell lines
Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells
Mitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing
Hyperoxia/Hypoxia Exposure Primes a Sustained Pro-Inflammatory Profile of Preterm Infant Macrophages Upon LPS Stimulation
Pharmacological LRH-1/Nr5a2 inhibition limits pro-inflammatory cytokine production in macrophages and associated experimental hepatitis
Macrophage mechanosensing during their pro-inflammatory response
Mitochondrial reactive oxygen species license pro-inflammatory signaling in infected macrophages via disulfide linkage of NEMO
Role of mitochondrial metabolism during the immunometabolic response of inflammatory macrophages to bacterial pathogens
Regulatory Roles of the Mitochondrial Metabolism and the Nuclear Repressor BACH1 in Inflammatory Macrophages
Mitofusin 2 deficiency causes pro-inflammatory effects in human primary macrophages
Hypoxia potentiates palmitate-induced pro-inflammatory activation of primary human macrophages
Adipocyte death triggers a pro-inflammatory response and induces metabolic activation of resident macrophages
The influence of serum amyloid A on pro-inflammatory signaling in monocytes/macrophages cell lines
Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells
Mitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing
Hyperoxia/Hypoxia Exposure Primes a Sustained Pro-Inflammatory Profile of Preterm Infant Macrophages Upon LPS Stimulation
Pharmacological LRH-1/Nr5a2 inhibition limits pro-inflammatory cytokine production in macrophages and associated experimental hepatitis