Evidence map›Paper›PMID 26733200›Full record

ArticleThe Journal of biological chemistry2016

The Transcription Factor p8 Regulates Autophagy in Response to Palmitic Acid Stress via a Mammalian Target of Rapamycin (mTOR)-independent Signaling Pathway.

Sheng-Nan Jia, Cheng Lin, Dian-Fu Chen, An-Qi Li, Li Dai, Li Zhang, Ling-Ling Zhao, Jin-Shu Yang, Fan Yang, Wei-Jun Yang

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 67 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Sheng-Nan JiaFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Cheng LinFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Dian-Fu ChenFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
An-Qi LiFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Li DaiFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Li ZhangFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Ling-Ling ZhaoFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Jin-Shu YangFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Fan YangFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China.
Wei-Jun YangFrom the College of Life Sciences, Zhejiang University, Hangzhou 310058, China w_jyang@zju.edu.cn.
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved degradative process that allows cells to maintain homoeostasis in numerous physiological situations. This process also functions as an essential protective response to endoplasmic reticulum (ER) stress, which promotes the removal and degradation of unfolded proteins. However, little is known regarding the mechanism by which autophagy is initiated and regulated in response to ER stress. In this study, different types of autophagy were identified in human gastric cancer MKN45 cells in response to the stress induced by nutrient starvation or lipotoxicity in which the regulation of these pathways is mammalian target of rapamycin (mTOR)-dependent or -independent, respectively. Interestingly, we found that p8, a stress-inducible transcription factor, was enhanced in MKN45 cells treated with palmitic acid to induce lipotoxicity. Furthermore, an increase in autophagy was observed in MKN45 cells stably overexpressing p8 using a lentivirus system, and autophagy induced by palmitic acid was blocked by p8 RNAi compared with the control. Western blotting analyses showed that autophagy was regulated by p8 or mTOR in response to the protein kinase-like endoplasmic reticulum kinase/activating transcription factor 6-mediated ER stress of lipotoxicity or the parkin-mediated mitochondrial stress of nutrient starvation, respectively. Furthermore, our results indicated that autophagy induced by palmitic acid is mTOR-independent, but this autophagy pathway was regulated by p8 via p53- and PKCα-mediated signaling in MKN45 cells. Our findings provide insights into the role of p8 in regulating autophagy induced by the lipotoxic effects of excess fat accumulation in cells.

Indexed as

AutophagyEndoplasmic Reticulum StressSignal TransductionUp-RegulationCell Line, TumorDNA-Binding ProteinsFatty Acids, NonesterifiedGreen Fluorescent ProteinsHEK293 CellsHumansMAP Kinase Signaling SystemMicroscopy, FluorescencePalmitic AcidProtein Kinase InhibitorsRecombinant Fusion ProteinsRNA InterferenceDNA-Binding Proteinsenhanced green fluorescent proteinFatty Acids, NonesterifiedGreen Fluorescent ProteinsMTOR protein, humanPalmitic AcidProtein Kinase InhibitorsRecombinant Fusion ProteinsSP8 protein, humanTOR Serine-Threonine KinasesTranscription Factorsautophagylipotoxicitymammalian target of rapamycin (mTOR)p53p8protein kinase C (PKC)

Identifiers

PMID26733200
PMCPMC4813474
OpenAlexW2234505905

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.