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Cited by 63Cell death mechanisms and regulationNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

The DOI matches its Crossref record.

CD95–CD95L: can the brain learn from the immune system?

Becher, Burkhard, Owens, Trevor, Antel, Jack P., Barker, Philip A.·1998·Trends in Neurosciences
DOI 10.1016/s0166-2236(97)01180-6
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Abstract

Members of the tumor necrosis factor/nerve growth factor receptor superfamily of cell-surface molecules can play the dual role of mediating either cytotoxicity or cell survival, both in the immune system and in the nervous system. A member of this superfamily, CD95 (also known as ApoI or Fas), was initially identified in the immune system and has been shown to mediate receptor-dependent programmed cell death and to be expressed in the nervous system. In neurodegenerative disorders, CD95-CD95 ligand expression on glial cells might precede receptor-mediated apoptosis by cells of the CNS. It is now being recognized that CD95 signaling by immune cells mediates effects other than apoptosis, such as cell survival and under inflammatory conditions expression of this protein promotes neural-immune interactions. Both neuroscientists and immunologists can contribute to defining the mechanisms underlying these divergent effects and utilize such knowledge to aid understanding of cell death and survival.

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Crossref · 10.1016/s0166-2236(97)01180-6

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  • FASLG induces cell death by binding to its receptor FAS, leading to caspase-dependent apoptosis.

    “FASLG induces cell death by binding to its receptor, FAS, leading to caspase-dependant apoptosis [16, 17].”

    From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [16]

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Metadata

Authors
Becher, B., Owens, T., Antel, J. P., & Barker, P. A.
Affiliations
Montreal Neurological Institute and Hospital (CA)
ORCID
Venue
Trends in Neurosciences
Publisher
Elsevier BV
Published
1998-03
Volume
21
Issue
3
Pages
114-116
ISSN
0166-2236 (ISSN-L)
DOI
10.1016/s0166-2236(97)01180-6
OpenAlex
W2043639971
Cited by
63
References
0
Citations by year
2023: 1 · 2016: 1 · 2015: 1
FWCI
0.80
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Trends in Neurosciences (publishedVersion)
  • PubMed (publishedVersion)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
Fas, Fas ligand, TNF receptor superfamily, apoptosis, cell survival, neurodegenerative diseases, glial cells, neuroimmune interactions, neuroinflammation, programmed cell death
MeSH terms
Brain, Humans, Immune System, Ligands, Apoptosis, fas Receptor

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