Evidence map›Paper›PMID 23825572›Full record

ArticlePloS one2013

Dynamics and molecular determinants of cytoplasmic lipid droplet clustering and dispersion.

David J Orlicky, Jenifer Monks, Adrianne L Stefanski, James L McManaman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Lipid droplet velocity is a microenvironmental sensor of aggressive tumors regulated by V-ATPase and PEDF.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  4. Alcohol-induced microtubule acetylation leads to the accumulation of large, immobile lipid droplets.American journal of physiology. Gastrointestinal and liver physiology · 2019
    Article
  5. Article
  6. Article
  7. Article
  8. Lipid droplet functions beyond energy storage.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. The cell biology of fat expansion.The Journal of cell biology · 2015
    Review
  18. Article
  19. Lipid transport in the lactating mammary gland.Journal of mammary gland biology and neoplasia · 2014
    Review
  20. Article
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.

David J OrlickyDepartment of Pathology, University of Colorado School of Medicine, Aurora, Colorado, United States of America.
Jenifer Monks
Adrianne L Stefanski
James L McManaman
University of Colorado Denver · US

Funding

The functional role of microRNAs in the normal mammary glandP01HD038129 · NICHD · UNIVERSITY OF COLORADO DENVER · PI ANDERSON, STEVEN M · 2000 to 2015
$15.2M
MECHANISMS OF MILK LIPID SECRETIONR01HD045965 · NICHD · UNIVERSITY OF COLORADO DENVER · PI MCMANAMAN, JAMES LEWIS · 2004 to 2013
$2.8M
North Carolina Collaborative PPRU NetworkU10HD045962 · NICHD · DUKE UNIVERSITY · PI BENJAMIN, DANIEL K. · 2004 to 2009
$2.1M
NICHD NIH HHS P01 HD038129NICHD NIH HHS P01-HD38129NICHD NIH HHS R01-HD045962NICHD NIH HHS R01 HD045965NICHD NIH HHS U10 HD045962
6 · The paper itself

Abstract

Perilipin-1 (Plin1), a prominent cytoplasmic lipid droplet (CLD) binding phosphoprotein and key physiological regulator of triglyceride storage and lipolysis in adipocytes, is thought to regulate the fragmentation and dispersion of CLD that occurs in response to β-adrenergic activation of adenylate cyclase. Here we investigate the dynamics and molecular determinants of these processes using cell lines stably expressing recombinant forms of Plin1 and/or other members of the perilipin family. Plin1 and a C-terminal CLD-binding fragment of Plin1 (Plin1CT) induced formation of single dense CLD clusters near the microtubule organizing center, whereas neither an N-terminal CLD-binding fragment of Plin1, nor Plin2 or Plin3 induced clustering. Clustered CLD coated by Plin1, or Plin1CT, dispersed in response to isoproterenol, or other agents that activate adenylate cyclase, in a process inhibited by the protein kinase A inhibitor, H89, and blocked by microtubule disruption. Isoproterenol-stimulated phosphorylation of CLD-associated Plin1 on serine 492 preceded their dispersion, and live cell imaging showed that cluster dispersion involved initial fragmentation of tight clusters into multiple smaller clusters, which then fragmented into well-dispersed individual CLD. siRNA knockdown of the cortical actin binding protein, moesin, induced disaggregation of tight clusters into multiple smaller clusters, and inhibited the reaggregation of dispersed CLD into tight clusters. Together these data suggest that the clustering and dispersion processes involve a complex orchestration of phosphorylation-dependent, microtubule-dependent and independent, and microfilament dependent steps.

Indexed as

AnimalsCytoplasmHEK293 CellsHumansIsoproterenolLipid MetabolismMiceMicrofilament ProteinsMicrotubulesMutationOrganellesPhosphoproteinsPhosphorylationIsoproterenolMicrofilament ProteinsmoesinPhosphoproteins

Identifiers

PMID23825572
PMCPMC3692517
OpenAlexW1992521638

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.