Evidence map›Paper›PMID 20018880›Full record

ArticleThe Journal of biological chemistry2010

Cross-talk between remodeling and de novo pathways maintains phospholipid balance through ubiquitination.

Phillip L Butler, Rama K Mallampalli

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
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  4. Mosquito metabolomics reveal that dengue virus replication requires phospholipid reconfiguration via the remodeling cycle.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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  17. Targeting F box protein Fbxo3 to control cytokine-driven inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  18. Article
  19. Surfactant phospholipid metabolism.Biochimica et biophysica acta · 2013
    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

2 authors at 1 institution in 1 country.

Phillip L ButlerDepartment of Biochemistry, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242, USA.
Rama K Mallampalli
VA Pittsburgh Healthcare System · US

Funding

TNF-alpha Control of a Surfactant Enzyme in Lung InjuryR01HL081784 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2006 to 2024
$5.4M
F box-Induced Acute Lung Injury and ParkinR01HL096376 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2010 to 2025
$5.1M
Sepsis-Associated Immune Suppression and F-box ProteinsR01HL097376 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2009 to 2025
$5.1M
Stabilizing mitochondria in sepsisR01HL098174 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2010 to 2021
$3.6M
TNFalpha-Lipoprotein Control of a Surfactant EnzymeR01HL068135 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MALLAMPALLI, RAMA K · 2001 to 2010
$2.7M
NHLBI NIH HHS R01 HL068135NHLBI NIH HHS R01 HL081784NHLBI NIH HHS R01 HL096376NHLBI NIH HHS R01 HL097376NHLBI NIH HHS R01 HL098174
6 · The paper itself

Abstract

Phosphatidylcholine (PtdCho), the major phospholipid of animal membranes, is generated by its remodeling and de novo synthesis. Overexpression of the remodeling enzyme, LPCAT1 (acyl-CoA:lysophosphatidylcholine acyltransferase) in epithelia decreased de novo PtdCho synthesis without significantly altering cellular PtdCho mass. Overexpression of LPCAT1 increased degradation of CPT1 (cholinephosphotransferase), a resident Golgi enzyme that catalyzes the terminal step for de novo PtdCho synthesis. CPT1 degradation involved its multiubiquitination and processing via the lysosomal pathway. CPT1 mutants harboring arginine substitutions at multiple carboxyl-terminal lysines exhibited proteolytic resistance to effects of LPCAT1 overexpression in cells and restored de novo PtdCho synthesis. Thus, cross-talk between phospholipid remodeling and de novo pathways involves ubiquitin-lysosomal processing of a key molecular target that mechanistically provides homeostatic control of cellular PtdCho content.

Indexed as

Homeostasis1-Acylglycerophosphocholine O-AcyltransferaseAnimalsCells, CulturedDiacylglycerol CholinephosphotransferaseEpithelial CellsLungLysosomesMicePhosphatidylcholinesPhospholipidsReceptor Cross-TalkSignal TransductionUbiquitinUbiquitination1-Acylglycerophosphocholine O-AcyltransferaseDiacylglycerol CholinephosphotransferaseLpcat1 protein, mousePhosphatidylcholinesPhospholipidsUbiquitin

Identifiers

PMID20018880
PMCPMC2825420
OpenAlexW2020552116

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.