Evidence map›Paper›PMID 27151460›Full record

ArticleNature communications2016

14-3-3 proteins regulate Tctp-Rheb interaction for organ growth in Drosophila.

Thao Phuong Le, Linh Thuong Vuong, Ah-Ram Kim, Ya-Chieh Hsu, Kwang-Wook Choi

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. 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
2.8field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. UsingCells · 2023
    Review
  7. Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Pterostilbene Promotes Mean Lifespan in Both Male and FemaleOxidative medicine and cellular longevity · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. 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

5 authors at 2 institutions in 2 countries.

Thao Phuong LeDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 305-701, Korea.
Linh Thuong VuongDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 305-701, Korea.
Ah-Ram KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 305-701, Korea.
Ya-Chieh HsuDepartment of Stem Cell and Regenerative Biology, Harvard University, Sherman Fairchild 358A, 7 Divinity Avenue Cambridge, Massachusetts 02138, USA.
Kwang-Wook ChoiDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, 291 Daehak-ro, Yuseong-gu, Daejeon 305-701, Korea.
Korea Advanced Institute of Science and Technology · KRFairchild Semiconductor (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

14-3-3 family proteins regulate multiple signalling pathways. Understanding biological functions of 14-3-3 proteins has been limited by the functional redundancy of conserved isotypes. Here we provide evidence that 14-3-3 proteins regulate two interacting components of Tor signalling in Drosophila, translationally controlled tumour protein (Tctp) and Rheb GTPase. Single knockdown of 14-3-3ɛ or 14-3-3ζ isoform does not show obvious defects in organ development but causes synergistic genetic interaction with Tctp and Rheb to impair tissue growth. 14-3-3 proteins physically interact with Tctp and Rheb. Knockdown of both 14-3-3 isoforms abolishes the binding between Tctp and Rheb, disrupting organ development. Depletion of 14-3-3s also reduces the level of phosphorylated S6 kinase, phosphorylated Thor/4E-BP and cyclin E (CycE). Growth defects from knockdown of 14-3-3 and Tctp are suppressed by CycE overexpression. This study suggests a novel mechanism of Tor regulation mediated by 14-3-3 interaction with Tctp and Rheb.

Indexed as

14-3-3 ProteinsAnimalsBiomarkers, TumorDrosophilaDrosophila ProteinsGene Expression Regulation, DevelopmentalGene Knockdown TechniquesIntracellular Signaling Peptides and ProteinsRas Homolog Enriched in Brain ProteinSignal TransductionTOR Serine-Threonine Kinases14-3-3 ProteinsBiomarkers, TumorDrosophila ProteinsIntracellular Signaling Peptides and ProteinsRas Homolog Enriched in Brain ProteinRheb protein, Drosophilatarget of rapamycin protein, DrosophilaTCTP protein, DrosophilaTOR Serine-Threonine Kinases

Identifiers

PMID27151460
PMCPMC4859069
OpenAlexW2345587463

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.