Evidence map›Paper›PMID 21172822›Full record

ArticleJournal of cell science2011

Depletion of nuclear actin is a key mediator of quiescence in epithelial cells.

Virginia A Spencer, Sylvain Costes, Jamie L Inman, Ren Xu, James Chen, Michael J Hendzel, Mina J Bissell

Abstract read
In one paragraph

Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

70 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Nuclear actin is a critical regulator ofbioRxiv : the preprint server for biology · 2024
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Mechanical Forces in Nuclear Organization.Cold Spring Harbor perspectives in biology · 2022
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Nuclear actin regulates cell proliferation and migration via inhibition of SRF and TEAD.Biochimica et biophysica acta. Molecular cell research · 2020
    Article
  18. Review
  19. Review
  20. Nucleoskeletal regulation of transcription: Actin on MRTF.Experimental biology and medicine (Maywood, N.J.) · 2019
    Review

10 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

7 authors at 2 institutions in 2 countries.

Virginia A SpencerLife Sciences Division, Lawrence Berkeley National Laboratory, 1 Cyclotron Road, MS 977R225A, Berkeley, CA 94720, USA. vaspencer@lbl.gov
Sylvain Costes
Jamie L Inman
Ren Xu
James Chen
Michael J Hendzel
Mina J Bissell
Lawrence Berkeley National Laboratory · USUniversity of Alberta · CA

Funding

Systems-Based Predictions of Responses to Cancer TherapyU54CA112970 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI MILLS, GORDON B. · 2004 to 2014
$27.1M
TRANS-NETWORK PROJECTSU54CA143836 · NCI · UNIVERSITY OF CALIFORNIA BERKELEY · PI LIPHARDT, JAN T. · 2009 to 2014
$15.1M
Role of Metalloproteinases in Mammary Gland RemodelingR01CA057621 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WERB, ZENA · 1993 to 2017
$9.0M
Definition of the Microenvironment in Breast CancerR01CA064786 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BISSELL, MINA · 1995 to 2020
$6.1M
Myoepithelial cell differentiation defects in ductal carcinoma in situ (DCIS)U01CA143233 · NCI · DANA-FARBER CANCER INST · PI BISSELL, MINA, POLLARD, JEFFREY W. · 2009 to 2013
$2.5M
Bioengineering 3-D Models for Organ-Specific Cancer Therapy in Lung and BreastU54CA126552 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BISSELL, MINA · 2006 to 2010
$2.2M
Definition of Microenvironment in Breast CancerR37CA064786 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI BISSELL, MINA · 2009 to 2013
$2.0M
CIHRNCI NIH HHS R01 CA057621NCI NIH HHS R01CA057621NCI NIH HHS R01 CA064786NCI NIH HHS R01CA064786NCI NIH HHS R37 CA064786NCI NIH HHS U01 CA143233NCI NIH HHS U01CA143233NCI NIH HHS U54 CA112970NCI NIH HHS U54CA112970NCI NIH HHS U54 CA126552NCI NIH HHS U54CA126552NCI NIH HHS U54 CA143836NCI NIH HHS U54CA143836
6 · The paper itself

Abstract

Functional differentiation is orchestrated by precise growth-regulatory controls conveyed by the tissue microenvironment. Cues from laminin 111 (LN1) lower transcription and suppress mammary epithelial cell growth in culture, but how LN1 induces quiescence is unknown. Recent literature points to involvement of nuclear β-actin in transcriptional regulation. Here, we show that quiescence induced by growth factor withdrawal, or LN1 addition, rapidly decreases nuclear β-actin. LN1, but not other extracellular matrix (ECM) molecules, decreases the levels of nuclear β-actin and destabilizes RNA polymerase (RNA Pol) II and III binding to transcription sites, leading to a dramatic drop in transcription and DNA synthesis. Constitutive overexpression of globular β-actin in the nucleus reverses the effect of LN1 on transcription and RNA Pol II association and prevents the cells from becoming quiescent in the presence of LN1. The physiological relevance of our findings was verified by identifying a clear spatial separation of LN1 and β-actin in developing mammary end buds. These data indicate a novel role for nuclear β-actin in growth arrest of epithelial cells and underscore the importance of the integrity of the basement membrane in homeostasis.

Indexed as

Cell CycleActinsAnimalsCell NucleusCells, CulturedEpithelial CellsGene Expression RegulationHumansLamininMiceMice, Inbred BALB CProtein BindingRNA Polymerase IIActinsLamininRNA Polymerase II

Identifiers

PMID21172822
PMCPMC3001411
OpenAlexW2156139408

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.