Evidence map›Paper›PMID 25113562›Full record

ArticleMolecular and cellular biology2014

Piwil2 inhibits keratin 8 degradation through promoting p38-induced phosphorylation to resist Fas-mediated apoptosis.

Siyuan Jiang, Lianfang Zhao, Yilu Lu, Meiling Wang, Yuan Chen, Dachang Tao, Yunqiang Liu, Huaqin Sun, Sizhong Zhang, Yongxin Ma

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 32 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 2 institutions in 1 country.

Siyuan JiangDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Lianfang ZhaoDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yilu LuDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Meiling WangDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yuan ChenDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Dachang TaoDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yunqiang LiuDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Huaqin SunSichuan University-The Chinese University of Hong Kong Joint Laboratory for Reproductive Medicine, West China Institute of Women and Children's Health, West China Second University Hospital, Sichuan University, Chengdu, China.
Sizhong ZhangDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Yongxin MaDepartment of Medical Genetics and Division of Morbid Genomics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China mayongxin@gmail.com.
State Key Laboratory of BiotherapySichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The piwi-like 2 (piwil2) gene is widely expressed in tumors and protects cells from apoptosis induced by a variety of stress stimuli. However, the role of Piwil2 in Fas-mediated apoptosis remains unknown. Here, we present evidence that Piwil2 inhibits Fas-mediated apoptosis. By a bacterial two-hybrid screening, we identify a new Piwil2-interacting partner, keratin 8 (K8), a major intermediate filament protein protecting the cell from Fas-mediated apoptosis. Our results show that Piwil2 binds to K8 and p38 through its PIWI domain and forms a Piwil2/K8/P38 triple protein-protein complex. Thus, Piwil2 increases the phosphorylation level of K8 Ser-73 and then inhibits ubiquitin-mediated degradation of K8. As a result, the knockdown of Piwil2 increases the Fas protein level at the membrane. In addition to our previous finding that Piwil2 inhibits the expression of p53 through the Src/STAT3 pathway, here we demonstrate that Piwil2 represses p53 phosphorylation through p38. Our present study indicates that Piwil2 plays a role in Fas-mediated apoptosis for the first time and also can affect p53 phosphorylation in tumor cells, revealing a novel mechanism of Piwil2 in apoptosis, and supports that Piwil2 plays an active role in tumorigenesis.

Indexed as

ApoptosisArgonaute ProteinsBinding Sitesfas ReceptorGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeLa CellsHep G2 CellsHumansKeratin-8p38 Mitogen-Activated Protein KinasesPhosphorylationSerineSignal TransductionTumor Suppressor Protein p53Argonaute ProteinsFAS protein, humanfas ReceptorKeratin-8KRT8 protein, humanp38 Mitogen-Activated Protein KinasesPIWIL2 protein, humanSerineTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25113562
PMCPMC4386451
OpenAlexW1977477337

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.