Evidence map›Paper›PMID 27672021›Full record

ReviewJournal of cell science2016

Autophagy in adhesion and migration.

Candia M Kenific, Torsten Wittmann, Jayanta Debnath

Abstract readReview
In one paragraph

Review in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 111 citations in OpenAlex.

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  16. Integrin-Driven Axon Regeneration in the Spinal Cord Activates a Distinctive CNS Regeneration Program.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
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4 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Candia M KenificDepartment of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA 94143, USA.
Torsten WittmannDepartment of Cell and Tissue Biology, University of California San Francisco, San Francisco, CA 94143, USA.ORCID 0000-0001-9134-691X
Jayanta DebnathDepartment of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA Jayanta.Debnath@ucsf.edu.ORCID 0000-0002-8745-4069
University of California, San Francisco · US

Funding

PREDOCTORAL TRAINING IN BIOMEDICAL SCIENCEST32GM008568 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANSEL, KARL MARK · 1995 to 2019
$6.3M
Autophagy in Adhesion and MetastasisR01CA126792 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jayanta Debnath · 2009 to 2026
$5.3M
Microtubule dynamics during cell polarity and migrationR01GM079139 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WITTMANN, TORSTEN · 2008 to 2017
$2.7M
Autophagy as a microenvironmental regulator of tumorigenesis and resistanceR01CA188404 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BERGERS, GABRIELE, DEBNATH, JAYANTA · 2014 to 2018
$2.1M
Spinning disk confocal / FRAP microscope for quantitative live cell imagingS10RR026758 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WITTMANN, TORSTEN · 2010 to 2010
$500k
NCI NIH HHS R01 CA126792NCI NIH HHS R01 CA188404NCRR NIH HHS S10 RR026758NIGMS NIH HHS R01 GM079139NIGMS NIH HHS T32 GM008568
6 · The paper itself

Abstract

Autophagy, a pathway for lysosomal-mediated cellular degradation, has recently been described as a regulator of cell migration. Although the molecular mechanisms underlying autophagy-dependent motility are only beginning to emerge, new work demonstrates that selective autophagy mediated by the autophagy cargo receptor, NBR1, specifically promotes the dynamic turnover of integrin-based focal adhesion sites during motility. Here, we discuss the detailed mechanisms through which NBR1-dependent selective autophagy supports focal adhesion remodeling, and we describe the interconnections between this pathway and other established regulators of focal adhesion turnover, such as microtubules. We also highlight studies that examine the contribution of autophagy to selective degradation of proteins that mediate cellular tension and to integrin trafficking; these findings hint at further roles for autophagy in supporting adhesion and migration. Given the recently appreciated importance of selective autophagy in diverse cellular processes, we propose that further investigation into autophagy-mediated focal adhesion turnover will not only shed light onto how focal adhesions are regulated but will also unveil new mechanisms regulating selective autophagy.

Indexed as

AutophagyCell MovementAnimalsCell AdhesionFocal AdhesionsHumansIntegrinsProtein TransportIntegrinsAutophagyFocal adhesionMigrationNBR1

Identifiers

PMID27672021
PMCPMC5087656
OpenAlexW2524900504

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.