Evidence map›Paper›PMID 28049841›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

TRAIL-death receptor endocytosis and apoptosis are selectively regulated by dynamin-1 activation.

Carlos R Reis, Ping-Hung Chen, Nawal Bendris, Sandra L Schmid

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 78 citations in OpenAlex.

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  4. Inactivation of PI3K-C2α deregulates cell death pathways and sensitizes to endotoxic shock.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Carlos R ReisDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Ping-Hung ChenDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Nawal BendrisDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Sandra L SchmidDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390 sandra.schmid@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

EARLY STEPS IN RECEPTOR-MEDIATED ENDOCYTOSISR01GM042455 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI METTLEN, MARCEL BERNARD · 1989 to 2020
$8.2M
Request for administrative supplement to Parent R01 GM073165 entitled "Mechanisms regulating clathrin-mediated endocytosis"R01GM073165 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI METTLEN, MARCEL BERNARD · 2006 to 2022
$6.8M
NIGMS NIH HHS R01 GM042455NIGMS NIH HHS R01 GM073165
6 · The paper itself

Abstract

Clathrin-mediated endocytosis (CME) constitutes the major pathway for uptake of signaling receptors into eukaryotic cells. As such, CME regulates signaling from cell-surface receptors, but whether and how specific signaling receptors reciprocally regulate the CME machinery remains an open question. Although best studied for its role in membrane fission, the GTPase dynamin also regulates early stages of CME. We recently reported that dynamin-1 (Dyn1), previously assumed to be neuron-specific, can be selectively activated in cancer cells to alter endocytic trafficking. Here we report that dynamin isoforms differentially regulate the endocytosis and apoptotic signaling downstream of TNF-related apoptosis-inducing ligand-death receptor (TRAIL-DR) complexes in several cancer cells. Whereas the CME of constitutively internalized transferrin receptors is mainly dependent on the ubiquitously expressed Dyn2, TRAIL-induced DR endocytosis is selectively regulated by activation of Dyn1. We show that TRAIL stimulation activates ryanodine receptor-mediated calcium release from endoplasmic reticulum stores, leading to calcineurin-mediated dephosphorylation and activation of Dyn1, TRAIL-DR endocytosis, and increased resistance to TRAIL-induced apoptosis. TRAIL-DR-mediated ryanodine receptor activation and endocytosis is dependent on early caspase-8 activation. These findings delineate specific mechanisms for the reciprocal crosstalk between signaling and the regulation of CME, leading to autoregulation of endocytosis and signaling downstream of surface receptors.

Indexed as

ApoptosisCalcium SignalingCaspase 8Cell Line, TumorClathrinDynamin IEndocytosisHumansModels, BiologicalRyanodine Receptor Calcium Release ChannelSignal TransductionTNF-Related Apoptosis-Inducing LigandCASP8 protein, humanCaspase 8ClathrinDynamin IRyanodine Receptor Calcium Release ChannelTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humancalcineurincaspasesclathrin-mediated endocytosisprogrammed cell deathryanodine receptor

Identifiers

PMID28049841
PMCPMC5255607
OpenAlexW2562330232

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.