Evidence map›Paper›PMID 33111211›Full record

ArticleMolecular and cellular biochemistry2021

TAK1 is involved in sodium L-lactate-stimulated p38 signaling and promotes apoptosis.

Qingen Da, Zilong Yan, Zhangfu Li, Zhen Han, Mingming Ren, Lei Huang, Xiaowei Zhang, Jikui Liu, Tao Wang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Qingen DaDepartment of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.ORCID http://orcid.org/0000-0002-1683-9922
Zilong YanDepartment of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Zhangfu LiDepartment of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Zhen HanDepartment of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, 518000, China.
Mingming RenDepartment of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, 518000, China.
Lei HuangDepartment of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, 518000, China.
Xiaowei ZhangSchool of Basic Medical Sciences, Peking University, Beijing, China.
Jikui LiuDepartment of Hepatobiliary Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, China. Liu8929@126.com.
Tao WangDepartment of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, 518000, China. szwangtao@126.com.
Hong Kong University of Science and Technology · HKPeking University · CN

Funding

the basic and applied basic research project of Guangdong (Youth fund projects) 2019A1515110111the science and technology development project of Guangdong 2017B090904010the Shenzhen municipal commission of health and family planning SZFZ2018071
6 · The paper itself

Abstract

In the present study, we found that the phosphorylation of p38 mitogen-activated protein kinase (p38) was significantly increased in L-lactate-treated HeLa cells, which is under concentration- and time-dependent manner. The protein level of Bcl-2 was significantly reduced and Bax and C-caspase3 were significantly increased in L-lactate-treated cells. qRT-PCR analysis suggested that the expression level of apoptosis-related genes Bax, C-myc, and FasL were significantly upregulated by L-lactate treatment. In addition, p38 inhibitor SB203580 blocked the L-lactate-stimulated phosphorylation of p38 (p-p38) and apoptosis, which suggested that L-lactate-stimulated apoptosis may be related to the activation of p38. Moreover, TAK1 inhibitor Takinib reduced L-lactate-triggered phosphorylation of p38 and also apoptosis; however, ASK1 inhibitor NQDI-1 did not. Cells transfected with siRNA of TAK1(siTAK1) showed similar results with Takinib inhibitor. These results suggested that the L-lactate treatment elevated activation of p38 and apoptosis was related to TAK1. In this study, we suggested that TAK1 plays an important role in L-lactate-stimulated activation of p38 affecting apoptosis in HeLa cells.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspase 3FemaleHeLa CellsHumansMAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationProto-Oncogene Proteins c-bcl-2Signal TransductionSodium LactateUterine Cervical NeoplasmsBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanCASP3 protein, humanCaspase 3MAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Sodium LactateApoptosisL-lactatep38TAK1

Identifiers

PMID33111211
OpenAlexW3096119268

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.