Evidence map›Paper›PMID 25682866›Full record

ArticleOncotarget2015

A Golgi-based KDELR-dependent signalling pathway controls extracellular matrix degradation.

Carmen Ruggiero, Giorgia Fragassi, Mauro Grossi, Benedetta Picciani, Rosaria Di Martino, Mirco Capitani, Roberto Buccione, Alberto Luini, Michele Sallese

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  13. The Function of KDEL Receptors as UPR Genes in Disease.International journal of molecular sciences · 2021
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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

9 authors at 3 institutions in 2 countries.

Carmen RuggieroUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Giorgia FragassiUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Mauro GrossiUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Benedetta PiccianiUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Rosaria Di MartinoInstitute of Protein Biochemistry National Research Council, Naples, Italy.
Mirco CapitaniUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Roberto BuccioneLaboratory of Tumour Cell Invasion, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Alberto LuiniInstitute of Protein Biochemistry National Research Council, Naples, Italy.
Michele SalleseUnit of Genomic Approaches to Membrane Traffic, Fondazione Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy.
Mario Negri Sud Foundation · ITInstitute of Protein Biochemistry · ITCentre National de la Recherche Scientifique · FR

Funding

Telethon GGP12220
6 · The paper itself

Abstract

We recently identified an endomembrane-based signalling cascade that is activated by the KDEL receptor (KDELR) on the Golgi complex. At the Golgi, the KDELR acts as a traffic sensor (presumably via binding to chaperones that leave the ER) and triggers signalling pathways that balance membrane fluxes between ER and Golgi. One such pathway relies on Gq and Src. Here, we examine if KDELR might control other cellular modules through this pathway. Given the central role of Src in extracellular matrix (ECM) degradation, we investigated the impact of the KDELR-Src pathway on the ability of cancer cells to degrade the ECM. We find that activation of the KDELR controls ECM degradation by increasing the number of the degradative structures known as invadopodia. The KDELR induces Src activation at the invadopodia and leads to phosphorylation of the Src substrates cortactin and ASAP1, which are required for basal and KDELR-stimulated ECM degradation. This study furthers our understanding of the regulatory circuitry underlying invadopodia-dependent ECM degradation, a key phase in metastases formation and invasive growth.

Indexed as

Signal TransductionAdaptor Proteins, Signal TransducingCell Line, TumorCell MovementCortactinEnzyme ActivationExtracellular MatrixGolgi ApparatusHumansNeoplasm InvasivenessNeoplasmsPhosphorylationPodosomesReceptors, PeptideRNA Interferencesrc-Family KinasesAdaptor Proteins, Signal TransducingASAP1 protein, humanCortactinCTTN protein, humanKDELR1 protein, humanKDELR2 protein, humanReceptors, Peptidesrc-Family KinasesVesicular Transport Proteins

Identifiers

PMID25682866
PMCPMC4413660
OpenAlexW1806042694

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.