Evidence map›Paper›PMID 24990952›Full record

ReviewThe Journal of biological chemistry2014

Phospholipase D and the maintenance of phosphatidic acid levels for regulation of mammalian target of rapamycin (mTOR).

David A Foster, Darin Salloum, Deepak Menon, Maria A Frias

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

76 citing papers in PubMed, 129 citations in OpenAlex.

  1. Article
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  5. Exploring the PLD1-tau interaction in Frontotemporal Dementia.bioRxiv : the preprint server for biology · 2026
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16 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

4 authors at 2 institutions in 1 country.

David A FosterDepartment of Biological Sciences, Hunter College of the City University of New York, New York, New York 10065. Electronic address: foster@genectr.hunter.cuny.edu.
Darin SalloumDepartment of Biological Sciences, Hunter College of the City University of New York, New York, New York 10065.
Deepak MenonDepartment of Biological Sciences, Hunter College of the City University of New York, New York, New York 10065.
Maria A FriasDepartment of Biological Sciences, Hunter College of the City University of New York, New York, New York 10065.
Hunter College · USCity University of New York · US

Funding

Role of phospholipase D in tumorigenesisR01CA046677 · NCI · HUNTER COLLEGE · PI FOSTER, DAVID A · 1997 to 2014
$3.6M
MINORITY HIGH SCHOOL STUDENT RESEARCH APPRENTICE PROGRAMS03RR003039 · NCRR · ROSALIND FRANKLIN UNIV OF MEDICINE &SCI · PI BILVAISS, BEN B · 1985 to 1985
–
NCI NIH HHS 1R01-CA046677NCI NIH HHS R01 CA046677NCRR NIH HHS RR-03039
6 · The paper itself

Abstract

Phosphatidic acid (PA) is a critical metabolite at the heart of membrane phospholipid biosynthesis. However, PA also serves as a critical lipid second messenger that regulates several proteins implicated in the control of cell cycle progression and cell growth. Three major metabolic pathways generate PA: phospholipase D (PLD), diacylglycerol kinase (DGK), and lysophosphatidic acid acyltransferase (LPAAT). The LPAAT pathway is integral to de novo membrane phospholipid biosynthesis, whereas the PLD and DGK pathways are activated in response to growth factors and stress. The PLD pathway is also responsive to nutrients. A key target for the lipid second messenger function of PA is mTOR, the mammalian/mechanistic target of rapamycin, which integrates both nutrient and growth factor signals to control cell growth and proliferation. Although PLD has been widely implicated in the generation of PA needed for mTOR activation, it is becoming clear that PA generated via the LPAAT and DGK pathways is also involved in the regulation of mTOR. In this minireview, we highlight the coordinated maintenance of intracellular PA levels that regulate mTOR signals stimulated by growth factors and nutrients, including amino acids, lipids, glucose, and Gln. Emerging evidence indicates compensatory increases in one source of PA when another source is compromised, highlighting the importance of being able to adapt to stressful conditions that interfere with PA production. The regulation of PA levels has important implications for cancer cells that depend on PA and mTOR activity for survival.

Indexed as

1-Acylglycerol-3-Phosphate O-AcyltransferaseAnimalsDiacylglycerol KinaseGlucoseGlutamineHumansPhosphatidic AcidsPhospholipase DSecond Messenger SystemsTOR Serine-Threonine Kinases1-Acylglycerol-3-Phosphate O-AcyltransferaseDiacylglycerol KinaseGlucoseGlutamineMTOR protein, humanPhosphatidic AcidsPhospholipase DTOR Serine-Threonine KinasesDiacylglycerol KinaseglycolysisLipid MetabolismLysophosphatidic Acid AcyltransferaseMammalian Target of Rapamycin (mTOR)Phosphatidic AcidPhospholipase D

Identifiers

PMID24990952
PMCPMC4132766
OpenAlexW2006896973

What Socratic 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 Socratic graph.