ArticleMolecular biology of the cell2008
A novel juxtamembrane domain in tumor necrosis factor receptor superfamily molecules activates Rac1 and controls neurite growth.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Fas acts as a T cell co-stimulatory receptor via both death domain-independent and -dependent mechanisms.Cell death and differentiation · 2026Article
- CD95/Fas stoichiometry in future precision medicine.Cell death and differentiation · 2025Review
- Charge-based immunoreceptor signalling in health and disease.Nature reviews. Immunology · 2025Review
- Collaborative Roles for RAC1, ERM Proteins and PTEN During Adult Sensory Axon Regeneration.Molecular neurobiology · 2025Article
- Review
- Review
- Role of metalloproteases in the CD95 signaling pathways.Frontiers in immunology · 2022Review
- An unexpected turn of fortune: targeting TRAIL-Rs in KRAS-driven cancer.Cell death discovery · 2020Review
- Exploring the TRAILs less travelled: TRAIL in cancer biology and therapy.Nature reviews. Cancer · 2017Review
- Modulation of hippocampal neuroplasticity by Fas/CD95 regulatory protein 2 (Faim2) in the course of bacterial meningitis.Journal of neuropathology and experimental neurology · 2014Article
- Life in the Fas lane: differential outcomes of Fas signaling.Cellular and molecular life sciences : CMLS · 2013Review
- TROY (TNFRSF19) promotes glioblastoma survival signaling and therapeutic resistance.Molecular cancer research : MCR · 2013Article
- Article
- The tumor necrosis factor receptor stalk regions define responsiveness to soluble versus membrane-bound ligand.Molecular and cellular biology · 2012Article
- The actin cytoskeleton as a sensor and mediator of apoptosis.Bioarchitecture · 2012Article
- The activation of ezrin-radixin-moesin proteins is regulated by netrin-1 through Src kinase and RhoA/Rho kinase activities and mediates netrin-1-induced axon outgrowth.Molecular biology of the cell · 2011Article
- The death receptor CD95 activates the cofilin pathway to stimulate tumour cell invasion.EMBO reports · 2011Article
- Fas/CD95 regulatory protein Faim2 is neuroprotective after transient brain ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- The role of tumor necrosis factor receptor superfamily members in mammalian brain development, function and homeostasis.Reviews in the neurosciences · 2011Review
- TROY (TNFRSF19) is overexpressed in advanced glial tumors and promotes glioblastoma cell invasion via Pyk2-Rac1 signaling.Molecular cancer research : MCR · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the tumor necrosis factor receptor (TNFR) superfamily control cell fate determination, including cell death and differentiation. Fas (CD95) is the prototypical "death receptor" of the TNFR superfamily and signals apoptosis through well established pathways. In the adult nervous system, Fas induces apoptosis in the context of neuropathology such as stroke or amyotrophic lateral sclerosis. However, during nervous system development, Fas promotes neurite growth and branching. The molecular mechanisms underlying Fas-induced process formation and branching have remained unknown to date. Here, we define the molecular pathway linking Fas to process growth and branching in cell lines and in developing neurons. We describe a new cytoplasmic membrane proximal domain (MPD) that is essential for Fas-induced process growth and that is conserved in members of the TNFR superfamily. We show that the Fas MPD recruits ezrin, a molecule that links transmembrane proteins to the cytoskeleton, and activates the small GTPase Rac1. Deletion of the MPD, but not the death domain, abolished Rac1 activation and process growth. Furthermore, an ezrin-derived inhibitory peptide prevented Fas-induced neurite growth in primary neurons. Our results define a new domain, topologically and functionally distinct from the death domain, which regulates neuritogenesis via recruitment of ezrin and activation of Rac1.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.