TNFR2: Target for therapeutics against neurodegenerative diseases?

  • Ingrid M. Nijholt*
  • , Ivica Granic
  • , Paul G. M. Luiten
  • , Ulrich L. M. Eisel
  • *Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionAcademicpeer-review

4 Citations (Scopus)

Abstract

Tumor necrosis factor α (TNFα) is a proinflammatory cytokine which acts via its two receptors TNFR1 and TNFR2. It is involved in many cell types in various cellular functions of cell growth, differentiation, and cellular apoptosis. Whereas soluble TNF has the highest affinity for TNFR1 and is therefore its main activator, the membrane standing precursor form of TNF was found to be the strongest activator of TNFR2. This may be also the simple technical reason why for a very long time hardly any TNFR2-specific response was known. In fact for a very long time TNFR2 was believed to function as ligand-passing receptor to TNFR1 or to be just a costimulator of TNFR1 signaling events. In fact under certain conditions this might be true yet a specific and TNFR1-independent signaling role was until recently not established [24].
Original languageEnglish
Title of host publicationAdvances in TNF Family Research
Subtitle of host publicationProceedings of the 12th International TNF Conference, 2009
EditorsD Wallach, A Kovalenko, M Feldman
Place of PublicationBerlin
PublisherSpringer
Chapter59
Pages567-573
Number of pages7
ISBN (Print)978-1-4419-6611-7
DOIs
Publication statusPublished - 2011
Event12th Biennial International TNF Conference - San Lorenzo del Escorial, Spain
Duration: 26-Apr-200929-Apr-2009

Publication series

NameAdvances in Experimental Medicine and Biology
PublisherSpringer Verlag Berlin
Volume691
ISSN (Print)0065-2598

Conference

Conference12th Biennial International TNF Conference
Country/TerritorySpain
CitySan Lorenzo del Escorial
Period26/04/200929/04/2009

Keywords

  • FACTOR-KAPPA-B
  • GLUTAMATE-INDUCED EXCITOTOXICITY
  • CA2+-ACTIVATED K+ CHANNELS
  • POTASSIUM CHANNEL
  • SMALL-CONDUCTANCE
  • SIGNALING PATHWAYS
  • MOUSE-BRAIN
  • NEUROPROTECTION
  • ISOFORM
  • SK2

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