ArticleProceedings of the National Academy of Sciences of the United States of America2011
Trk retrograde signaling requires persistent, Pincher-directed endosomes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 67 citations in OpenAlex.
- A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.Traffic (Copenhagen, Denmark) · 2026Review
- Molecular architects of memory: BDNF/TrkB signaling and trafficking in neuronal plasticity and memory.Molecular psychiatry · 2026Review
- Centripetal Axonal Transport as a Gateway to the CNS for Veterinary Antiparasitics: Bypassing the Blood-Brain Barrier, Clinical Impact in Vulnerable Age Groups, and the Potential Facilitating Role of PFAS.Journal of toxicology · 2026Review
- Age-related changes and lack of effect of midlife resistance wheel exercise on afferent connectivity of lumbar alpha motor neurons in ageing mouse spinal cord.Biogerontology · 2025Article
- Swimming and L-arginine loaded chitosan nanoparticles ameliorates aging-induced neuron atrophy, autophagy marker LC3, GABA and BDNF-TrkB pathway in the spinal cord of rats.Pflugers Archiv : European journal of physiology · 2023Article
- Lysine acetylation regulates the interaction between proteins and membranes.Nature communications · 2021Article
- Neuronal Autophagy: Characteristic Features and Roles in Neuronal Pathophysiology.Biomolecules & therapeutics · 2021Review
- TrkA-mediated endocytosis of p75-CTF prevents cholinergic neuron death upon γ-secretase inhibition.Life science alliance · 2021Article
- EHD1 and RUSC2 Control Basal Epidermal Growth Factor Receptor Cell Surface Expression and Recycling.Molecular and cellular biology · 2020Article
- SIPA1L2 controls trafficking and local signaling of TrkB-containing amphisomes at presynaptic terminals.Nature communications · 2019Article
- Post-synaptic Release of the Neuronal Tissue-Type Plasminogen Activator (tPA).Frontiers in cellular neuroscience · 2019Article
- The many disguises of the signalling endosome.FEBS letters · 2018Review
- Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease.Free radical biology & medicine · 2018Review
- Structural insights into the activation mechanism of dynamin-like EHD ATPases.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Retrograde transport of TrkB-containing autophagosomes via the adaptor AP-2 mediates neuronal complexity and prevents neurodegeneration.Nature communications · 2017Article
- The neurotrophin receptor signaling endosome: Where trafficking meets signaling.Developmental neurobiology · 2017Review
- IL-1β impairs retrograde flow of BDNF signaling by attenuating endosome trafficking.Journal of neuroinflammation · 2017Article
- BDNF trafficking and signaling impairment during early neurodegeneration is prevented by moderate physical activity.IBRO reports · 2016Article
- Kalirin is required for BDNF-TrkB stimulated neurite outgrowth and branching.Neuropharmacology · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Target-derived neurotrophins use retrogradely transported Trk-signaling endosomes to promote survival and neuronal phenotype at the soma. Despite their critical role in neurotrophin signaling, the nature and molecular composition of these endosomes remain largely unknown, the result of an inability to specifically identify the retrograde signaling entity. Using EGF-bound nanoparticles and chimeric, EGF-binding TrkB receptors, we elucidate Trk-endosomal events involving their formation, processing, retrograde transport, and somal signaling in sympathetic neurons. By comparing retrograde endosomal signaling by Trk to the related but poorly neuromodulatory EGF-receptor, we find that Trk and EGF-receptor endosomes are formed and processed by distinct mechanisms. Surprisingly, Trk and EGF-receptors are both retrogradely transported to the soma in multivesicular bodies. However, only the Trk-multivesicular bodies rely on Pincher-dependent macroendocytosis and processing. Retrograde signaling through Pincher-generated Trk-multivesicular bodies is distinctively refractory to signal termination by lysosomal processing, resulting in sustained somal signaling and neuronal gene expression.
Indexed as
Identifiers
What Socratic 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 Socratic graph.