ARF1 controls STING activation and recycling to prevent chronic type I IFN signalling
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
Ulm, Universität Ulm, Dissertation, 2024
- Schlagwort
-
Signaltransduktion
Interferon
Autoaggressionskrankheit
Angeborene Immunität
Mitochondrium
- Ereignis
-
Veröffentlichung
- (wo)
-
Ulm
- (wer)
-
Universität Ulm
- (wann)
-
2024
- Urheber
- DOI
-
10.18725/OPARU-53029
- URN
-
urn:nbn:de:bsz:289-oparu-53105-6
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
- 14.08.2025, 10:48 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek.
Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Hirschenberger, Maximilian
- Universität Ulm
Entstanden
- 2024
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TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN
PRV UL13 inhibits cGAS–STING-mediated IFN-β production by phosphorylating IRF3
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Aryl hydrocarbon receptor suppresses STING-mediated type I IFN expression in triple-negative breast cancer
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STING signalling is terminated through ESCRT-dependent microautophagy of vesicles originating from recycling endosomes
Clathrin-associated AP-1 controls termination of STING signalling
DUSP4 modulates RIG-I- and STING-mediated IRF3-type I IFN response
TLR9 and STING agonists synergistically induce innate and adaptive type‐II IFN
PRV UL13 inhibits cGAS–STING-mediated IFN-β production by phosphorylating IRF3
Influenza C virus NS1 protein counteracts RIG-I-mediated IFN signalling
Monocyte-derived macrophages aggravate pulmonary vasculitis via cGAS/STING/IFN-mediated nucleic acid sensing
Aryl hydrocarbon receptor suppresses STING-mediated type I IFN expression in triple-negative breast cancer
SGLT2 inhibitor activates the STING/IRF3/IFN-β pathway and induces immune infiltration in osteosarcoma
Sting
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