Loss of neuronal Miro1 disrupts mitophagy and induces hyperactivation of the integrated stress response

zu Verbundenen Objekten

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch

Erschienen in
Loss of neuronal Miro1 disrupts mitophagy and induces hyperactivation of the integrated stress response ; day:21 ; month:06 ; year:2021 ; extent:20
The EMBO journal / European Molecular Biology Organization ; (21.06.2021) (gesamt 20)

Urheber
López‐Doménech, Guillermo
Howden, Jack H.
Covill‐Cooke, Christian
Morfill, Corinne
Patel, Jigna V.
Bürli, Roland
Crowther, Damian
Birsa, Nicol
Brandon, Nicholas J.
Kittler, Josef T.

DOI
10.15252/embj.2018100715
URN
urn:nbn:de:101:1-2021062415083031678457
Rechteinformation
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
14.08.2025, 11:00 MESZ

Datenpartner

Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Original beim Datenpartner anzeigen

Beteiligte

  • López‐Doménech, Guillermo
  • Howden, Jack H.
  • Covill‐Cooke, Christian
  • Morfill, Corinne
  • Patel, Jigna V.
  • Bürli, Roland
  • Crowther, Damian
  • Birsa, Nicol
  • Brandon, Nicholas J.
  • Kittler, Josef T.

Ähnliche Objekte (12)

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

Loss of thymidine phosphorylase activity disrupts adipocyte differentiation and induces insulin-resistant lipoatrophic diabetes

Loss of thymidine phosphorylase activity disrupts adipocyte differentiation and induces insulin-resistant lipoatrophic diabetes

Aggregation of alpha-synuclein disrupts mitochondrial metabolism and induce mitophagy via cardiolipin externalization

Aggregation of alpha-synuclein disrupts mitochondrial metabolism and induce mitophagy via cardiolipin externalization

iPLA2β loss leads to age-related cognitive decline and neuroinflammation by disrupting neuronal mitophagy

iPLA2β loss leads to age-related cognitive decline and neuroinflammation by disrupting neuronal mitophagy

GPR50 regulates neuronal development as a mitophagy receptor

GPR50 regulates neuronal development as a mitophagy receptor

Gonococcal OMV-delivered PorB induces epithelial cell mitophagy

Gonococcal OMV-delivered PorB induces epithelial cell mitophagy

Impaired mitophagy induces antimicrobial responses in macrophages infected with Mycobacterium tuberculosis

Impaired mitophagy induces antimicrobial responses in macrophages infected with Mycobacterium tuberculosis

HPV/E7 induces chemotherapy‐mediated tumor suppression by ceramide‐dependent mitophagy

HPV/E7 induces chemotherapy‐mediated tumor suppression by ceramide‐dependent mitophagy

STX17 dynamically regulated by Fis1 induces mitophagy via hierarchical macroautophagic mechanism

STX17 dynamically regulated by Fis1 induces mitophagy via hierarchical macroautophagic mechanism

NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway

NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway

Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior

Loss of calsyntenin paralogs disrupts interneuron stability and mouse behavior

Acute inactivation of the serine-threonine kinase Stk25 disrupts neuronal migration

Acute inactivation of the serine-threonine kinase Stk25 disrupts neuronal migration

Verbundene Objekte