Evidence map›Paper›PMID 24516149›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Mechanistic target of rapamycin complex 1 is critical for invariant natural killer T-cell development and effector function.

Jinwook Shin, Shang Wang, Wenhai Deng, Jinhong Wu, Jimin Gao, Xiao-Ping Zhong

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
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

41 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. iNKT subsets differ in their developmental and functional requirements on Foxo1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Insulin-mediated immune dysfunction in the development of preeclampsia.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  8. Role of TSC1 in physiology and diseases.Molecular and cellular biochemistry · 2021
    Review
  9. Article
  10. Mitochondrial metabolism is essential for invariant natural killer T cell development and function.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Differential Control ofFrontiers in immunology · 2019
    Article
  18. Article
  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

6 authors.

Jinwook ShinDepartments of Pediatrics and Immunology, Duke University Medical Center, Durham, NC 27710.
Shang Wang
Wenhai Deng
Jinhong Wu
Jimin Gao
Xiao-Ping Zhong

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI DONNA NIEDZWIECKI · 1985 to 2026
$174.8M
Regulation of peripheral T cell toleranceR01AI079088 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2008 to 2019
$3.5M
TSC1-mTOR signaling and T cell toleranceR01AI101206 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2012 to 2016
$1.9M
A Murine Model of Chronic Autoimmune Hepatitis and Liver FibrosisR01AI076357 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2008 to 2012
$1.5M
Regulating peripheral T cell toleranceR56AI079088 · NIAID · DUKE UNIVERSITY · PI ZHONG, XIAOPING · 2020 to 2020
$309k
NCI NIH HHS P30 CA014236NIAID NIH HHS AI076357NIAID NIH HHS AI079088NIAID NIH HHS AI101206NIAID NIH HHS R01 AI076357NIAID NIH HHS R01 AI079088NIAID NIH HHS R01 AI101206NIAID NIH HHS R56 AI079088
6 · The paper itself

Abstract

The mechanisms that control invariant natural killer T (iNKT)-cell development and function are still poorly understood. The mechanistic or mammalian target of rapamycin (mTOR) integrates various environmental signals/cues to regulate cell growth, proliferation, metabolism, and survival. We report here that ablation of mTOR complex 1 (mTORC1) signaling by conditionally deleting Raptor causes severe defects in iNKT-cell development at early stages, leading to drastic reductions in iNKT-cell numbers in the thymus and periphery. In addition, loss of Raptor impairs iNKT-cell proliferation and production of cytokines upon α-galactosylceramide stimulation in vitro and in vivo, and inhibits liver inflammation in an iNKT cell-mediated hepatitis model. Furthermore, Raptor deficiency and rapamycin treatment lead to aberrant intracellular localization and functional impairment of promyelocytic leukemia zinc-finger, a transcription factor critical for iNKT-cell development and effector programs. Our findings define an essential role of mTORC1 to direct iNKT-cell lineage development and effector function.

Indexed as

Analysis of VarianceAnimalsBlotting, WesternBone Marrow TransplantationBromodeoxyuridineCell DeathCell DifferentiationCell ProliferationChromatin ImmunoprecipitationDNA PrimersFlow CytometryGenes, T-Cell ReceptorIntranuclear SpaceKruppel-Like Transcription FactorsMechanistic Target of Rapamycin Complex 1MiceBromodeoxyuridineDNA PrimersKruppel-Like Transcription FactorsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPromyelocytic Leukemia Zinc Finger ProteinTOR Serine-Threonine KinasesZbtb16 protein, mouseIFN-γIL-4PLZFTNFα

Identifiers

PMID24516149
PMCPMC3939904

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.