How does Nogo-A signalling influence mitochondrial function during multiple sclerosis pathogenesis?-Reference-Cited by-同舟云学术

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How does Nogo-A signalling influence mitochondrial function during multiple sclerosis pathogenesis?

Published:2024-08 Issue: Volume:163 Page:105767
ISSN:0149-7634
Container-title:Neuroscience & Biobehavioral Reviews
language:en
Short-container-title:Neuroscience & Biobehavioral Reviews

Author:

Nheu Danica,Petratos Steven^ORCID

Funder

MS Research Australia

Publisher

Elsevier BV

Reference238 articles.

1. Transient axonal injury in the absence of demyelination: a correlate of clinical disease in acute experimental autoimmune encephalomyelitis;Aboul-Enein;Acta Neuropathol.,2006

2. Monocyte-derived and M1 macrophages from ankylosing spondylitis patients released higher TNF-α and expressed more IL1B in response to BzATP than macrophages from healthy subjects;Akhtari;Sci. Rep.,2021

3. Nogo receptor expression in microglia/macrophages during experimental autoimmune encephalomyelitis progression;Alrehaili;Neural Regen. Res,2018

4. Phosphorylation of Collapsin Response Mediator Protein-2 by Rho-kinase: EVIDENCE FOR TWO SEPARATE SIGNALING PATHWAYS FOR GROWTH CONE COLLAPSE*;Arimura;J. Biol. Chem.,2000

5. Phosphorylation by Rho kinase regulates CRMP-2 activity in growth cones;Arimura;Mol. Cell Biol.,2005

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