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The lipid acyltransferase LYCAT controls phosphatidylinositol‐3,4,5‐trisphosphate (PIP3) signaling

2019· article· en· W3173282525 on OpenAlexafffundabout
Costin N. Antonescu, Leslie N. Bone, Saba Khuffash, Yasmin Awadeh, Gizem Esra Genç, Marina S. Defferrari, Roberto J. Botelho

Bibliographic record

VenueThe FASEB Journal · 2019
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicProtein Kinase Regulation and GTPase Signaling
Canadian institutionsToronto Metropolitan University
FundersNatural Sciences and Engineering Research Council of CanadaCanadian Institutes of Health Research
KeywordsPhosphatidylinositolCell biologyPhosphorylationCell signalingInositolSignal transductionPTENPI3K/AKT/mTOR pathwayBiologyProtein kinase BBiochemistryChemistryReceptor

Abstract

fetched live from OpenAlex

Phosphatidylinositol‐3,4,5‐trisphospate (PIP3) is a potent signaling lipid that exerts key control over cell growth, survival, adhesion and migration. PIP3 signaling is often disrupted in various cancers, making understanding the regulation of PIP3 signaling an important priority. Much has been learned from the study of phosphorylation of the inositol headgroup of phosphoinositides, such as the phosphorylation of phosphatidylinositol‐4,5‐bisphospate (PIP2) to produce PIP3, as well as negative regulation of PIP3 by phosphoinositide phosphatases such as PTEN. However, much less is known about another key dimension of control of phosphoinositide action, the regulation of the fatty acyl profile of these lipids. Indeed, phosphatidylinositol and phosphoinositides exhibit remarkable selectivity of acyl chains (>50% harboring 1‐stearoyl, 2‐arachidonoyl), an acyl profile quite distinct from other phospholipids. This suggests that control of fatty acyl profile of phosphoinositides may be an important determinant of the function of these lipids that has to date remained largely unexplored. We recently uncovered that the acyltransferase LYCAT is a key regulator of the acyl profile of specific phosphoinositides such as PIP2, thus exerting control over membrane traffic phenomena dependent on these phosphoinositides (Bone LN et al 2017 Mol Biol Cell . 28:161–172). We now examine how LYCAT controls PIP3 signaling and PIP3‐dependent control of cell physiology, including the activation of Akt and control of actin dynamics. We find that LYCAT perturbation impairs the activation of Akt and the activation of a number of Akt substrates, which in turn impacts cell growth and survival. Furthermore, LYCAT perturbation elicits dramatic changes in actin filament morphology, cell migration and cancer cell invasion. These results indicate that control of phosphoinositide acyl chain profile is an important novel dimension of regulation of PIP3 signaling, impacting proliferative, growth and migration signaling, and as such may be a novel dimension to control of cancer cell growth and progression. Support or Funding Information This work was supported by an Ontario Early Researcher Award, a Canada Research Chair Award, and a Natural Sciences and Engineering Research Council Grant to R.J.B, and a Project Grant and New Investigator Salary Award from the Canadian Institutes of Health Research to C.N.A. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.001
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.042
Threshold uncertainty score0.622

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0010.000
Scholarly communication0.0000.000
Open science0.0010.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.007
GPT teacher head0.225
Teacher spread0.218 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one teacher head, not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations1
Published2019
Admission routes3
Has abstractyes

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