Evidence map›Paper›PMID 33872315›Full record

ArticlePLoS genetics2021

The actin nucleation factors JMY and WHAMM enable a rapid Arp2/3 complex-mediated intrinsic pathway of apoptosis.

Virginia L King, Nathan K Leclair, Alyssa M Coulter, Kenneth G Campellone

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  8. The multiple links between actin and mitochondria.Nature reviews. Molecular cell biology · 2023
    Review
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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.

Virginia L KingDepartment of Molecular and Cell Biology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut, United States of America.ORCID 0000-0002-9493-5426
Nathan K LeclairDepartment of Molecular and Cell Biology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut, United States of America.ORCID 0000-0002-0401-2549
Alyssa M CoulterDepartment of Molecular and Cell Biology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut, United States of America.ORCID 0000-0002-6147-4408
Kenneth G CampelloneDepartment of Molecular and Cell Biology, Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut, United States of America.ORCID 0000-0002-3178-9804
University of Connecticut · US

Funding

Cytoskeletal control of membrane remodelingR01GM107441 · NIGMS · UNIVERSITY OF CONNECTICUT STORRS · PI CAMPELLONE, KENNETH G · 2014 to 2018
$1.4M
Cytoskeletal functions in cell aging and diseaseK02AG050774 · NIA · UNIVERSITY OF CONNECTICUT STORRS · PI CAMPELLONE, KENNETH G · 2016 to 2021
$838k
NIA NIH HHS K02 AG050774NIGMS NIH HHS R01 GM107441
6 · The paper itself

Abstract

The actin cytoskeleton is a well-known player in most vital cellular processes, but comparably little is understood about how the actin assembly machinery impacts programmed cell death pathways. In the current study, we explored roles for the human Wiskott-Aldrich Syndrome Protein (WASP) family of actin nucleation factors in DNA damage-induced apoptosis. Inactivation of each WASP-family gene revealed that two of them, JMY and WHAMM, are necessary for rapid apoptotic responses. JMY and WHAMM participate in a p53-dependent cell death pathway by enhancing mitochondrial permeabilization, initiator caspase cleavage, and executioner caspase activation. JMY-mediated apoptosis requires actin nucleation via the Arp2/3 complex, and actin filaments are assembled in cytoplasmic territories containing clusters of cytochrome c and active caspase-3. The loss of JMY additionally results in significant changes in gene expression, including upregulation of the WHAMM-interacting G-protein RhoD. Depletion or deletion of RHOD increases cell death, suggesting that RhoD normally contributes to cell survival. These results give rise to a model in which JMY and WHAMM promote intrinsic cell death responses that can be opposed by RhoD.

Indexed as

Actin CytoskeletonActin-Related Protein 2Actin-Related Protein 2-3 ComplexActin-Related Protein 3ApoptosisCytochromes cDNA DamageHumansMembrane ProteinsMicrotubule-Associated ProteinsMitochondriaNuclear Proteinsrho GTP-Binding ProteinsRNA, Small InterferingTrans-ActivatorsTumor Suppressor Protein p53Actin-Related Protein 2Actin-Related Protein 2-3 ComplexActin-Related Protein 3ACTR3 protein, humanCytochromes cJMY protein, humanMembrane ProteinsMicrotubule-Associated ProteinsNuclear ProteinsRHOD protein, humanrho GTP-Binding ProteinsRNA, Small InterferingTP53 protein, humanTrans-ActivatorsTumor Suppressor Protein p53WAS protein, humanWHAMM protein, humanWiskott-Aldrich Syndrome Protein

Identifiers

PMID33872315
PMCPMC8084344
OpenAlexW3156058707

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.