Evidence map›Paper›PMID 22952941›Full record

ArticlePloS one2012

The PICALM protein plays a key role in iron homeostasis and cell proliferation.

Paula B Scotland, Jessica L Heath, Amanda E Conway, Natasha B Porter, Michael B Armstrong, Jennifer A Walker, Mitchell L Klebig, Catherine P Lavau, Daniel S Wechsler

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. CXCR4 Mediates Enhanced Cell Migration inFrontiers in oncology · 2021
    Article
  18. Review
  19. Article
  20. Review
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 1 country.

Paula B ScotlandDivision of Pediatric Hematology-Oncology, Duke University Medical Center, Durham, North Carolina, USA.
Jessica L Heath
Amanda E Conway
Natasha B Porter
Michael B Armstrong
Jennifer A Walker
Mitchell L Klebig
Catherine P Lavau
Daniel S Wechsler
Duke Medical Center · USDuke University Hospital · USMayo Clinic · US

Funding

Mechanisms of Leukemogenic Transformation by MLL-CALMR01CA109281 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WECHSLER, DANIEL STEVEN · 2005 to 2009
$1.3M
NCI NIH HHS R01 CA 109281NCI NIH HHS R01 CA109281
6 · The paper itself

Abstract

The ubiquitously expressed phosphatidylinositol binding clathrin assembly (PICALM) protein associates with the plasma membrane, binds clathrin, and plays a role in clathrin-mediated endocytosis. Alterations of the human PICALM gene are present in aggressive hematopoietic malignancies, and genome-wide association studies have recently linked the PICALM locus to late-onset Alzheimer's disease. Inactivating and hypomorphic Picalm mutations in mice cause different degrees of severity of anemia, abnormal iron metabolism, growth retardation and shortened lifespan. To understand PICALM's function, we studied the consequences of PICALM overexpression and characterized PICALM-deficient cells derived from mutant fit1 mice. Our results identify a role for PICALM in transferrin receptor (TfR) internalization and demonstrate that the C-terminal PICALM residues are critical for its association with clathrin and for the inhibitory effect of PICALM overexpression on TfR internalization. Murine embryonic fibroblasts (MEFs) that are deficient in PICALM display several characteristics of iron deficiency (increased surface TfR expression, decreased intracellular iron levels, and reduced cellular proliferation), all of which are rescued by retroviral PICALM expression. The proliferation defect of cells that lack PICALM results, at least in part, from insufficient iron uptake, since it can be corrected by iron supplementation. Moreover, PICALM-deficient cells are particularly sensitive to iron chelation. Taken together, these data reveal that PICALM plays a critical role in iron homeostasis, and offer new perspectives into the pathogenesis of PICALM-associated diseases.

Indexed as

HomeostasisAmino AcidsAnimalsCell MembraneCell ProliferationClathrinEmbryo, MammalianEndocytosisFibroblastsGene Expression RegulationHEK293 CellsHumansIntracellular SpaceIronIron Chelating AgentsIron DeficienciesAmino AcidsClathrinIronIron Chelating AgentsMonomeric Clathrin Assembly ProteinsPICALM protein, humanPICALM protein, mouseReceptors, TransferrinRNA, Messenger

Identifiers

PMID22952941
PMCPMC3431333
OpenAlexW2133691274

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.