Evidence map›Paper›PMID 23530222›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Phosphatidylinositol 5-phosphate 4-kinase (PIP4K) regulates TOR signaling and cell growth during Drosophila development.

Amit Gupta, Sarah Toscano, Deepti Trivedi, David R Jones, Swarna Mathre, Jonathan H Clarke, Nullin Divecha, Padinjat Raghu

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

48 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. PIP4K attenuates PIP5K lipid kinase activity by disrupting membrane-mediated dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Pss knockdown in the midgut causes growth retardation in Drosophila similar to that in human LMHD.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
  4. Subcellular Cartography of the Phosphoinositide Multiverse.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 25 Years of PI5P.Frontiers in cell and developmental biology · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Pharmacological inhibition of PI5P4Kα/β disrupts cell energy metabolism and selectively kills p53-null tumor cells.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Article
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  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

8 authors at 6 institutions in 2 countries.

Amit GuptaNational Centre for Biological Sciences, Tata Institute of Fundamental Research, Gandhi Krishi Vignana Kendra Campus, Bangalore 560065, India.
Sarah Toscano
Deepti Trivedi
David R Jones
Swarna Mathre
Jonathan H Clarke
Nullin Divecha
Padinjat Raghu
Babraham Institute · GBCancer Research UK Manchester Institute · GBNational Centre for Biological Sciences · INTata Institute of Fundamental Research · INUniversity of Cambridge · GBUniversity of Manchester · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

During development, Drosophila larvae undergo a dramatic increase in body mass wherein nutritional and developmental cues are transduced into growth through the activity of complex signaling pathways. Class I phosphoinositide 3-kinases have an established role in this process. In this study we identify Drosophila phosphatidylinositol 5-phosphate 4-kinase (dPIP4K) as a phosphoinositide kinase that regulates growth during larval development. Loss-of-function mutants in dPIP4K show reduced body weight and prolonged larval development, whereas overexpression of dPIP4K results both in an increase in body weight and shortening of larval development. The growth defect associated with dPIP4K loss of function is accompanied by a reduction in the average cell size of larval endoreplicative tissues. Our findings reveal that these phenotypes are underpinned by changes in the signaling input into the target of rapamycin (TOR) signaling complex and changes in the activity of its direct downstream target p70 S6 kinase. Together, these results define dPIP4K activity as a regulator of cell growth and TOR signaling during larval development.

Indexed as

Amino Acid SequenceAnimalsCell ProliferationDrosophila melanogasterDrosophila ProteinsGene Expression Regulation, DevelopmentalMicroscopy, ConfocalMinor Histocompatibility AntigensMolecular Sequence DataPhosphotransferases (Alcohol Group Acceptor)Protein Interaction Domains and MotifsSequence Analysis, DNASequence Homology, Amino AcidTOR Serine-Threonine KinasesDrosophila ProteinsMinor Histocompatibility Antigensphosphatidylinositol phosphate 4-kinasePhosphotransferases (Alcohol Group Acceptor)target of rapamycin protein, DrosophilaTOR Serine-Threonine Kinases

Identifiers

PMID23530222
PMCPMC3625332
OpenAlexW2010905069

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.