Evidence map›Paper›PMID 24858726›Full record

ArticleInflammation2014

The differential roles of mTOR, ERK, and JNK pathways in invariant natural killer T-cell function and survival.

Jun Tian, Li Liu, Xiangai Wang, Xuewu Sun, Suli Mu, Chuanjun Wu, Maoqiang Han

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 88% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

7 authors at 1 institution in 1 country.

Jun TianYantai Stomatological Hospital, Yantai, 264001, Shandong, China, jun-tian1990@hotmail.com.
Li Liu
Xiangai Wang
Xuewu Sun
Suli Mu
Chuanjun Wu
Maoqiang Han
Yantaishan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invariant natural killer T (iNKT) cell is a critical element for both innate and adaptive immunity. The quick responses of mature iNKT cells to TCR stimulation require activation of several different signaling pathways. However, the roles of these signaling pathways in mature iNKT cell biology remain incompletely understood. To address this issue, single signaling pathway was blocked with inhibitor in iNKT cells, and the roles of these signaling pathways were estimated. Results showed that mammalian target of rapamycin (mTOR) plays an essential role for cytokine production and survival in iNKT cells. In contrast, ERK and JNK are more important for iNKT cell effector function, but not survival. Our findings delineate the distinct roles of different signaling pathways in mature iNKT cells and therefore shed new light for modulating iNKT cell function in disease conditions.

Indexed as

AnimalsCell SurvivalCytokinesMAP Kinase Signaling SystemMiceMice, Inbred C57BLNatural Killer T-CellsSirolimusTOR Serine-Threonine KinasesCytokinesmTOR protein, mouseSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID24858726
OpenAlexW2063870660

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.