Evidence map›Paper›PMID 39261742›Full record

ArticleEMBO reports2024

CaMKII suppresses proteotoxicity by phosphorylating BAG3 in response to proteasomal dysfunction.

Chenliang Zhang, Huanji Xu, Qiulin Tang, Yichun Duan, Hongwei Xia, Huixi Huang, Di Ye, Feng Bi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO reports, 2024. 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
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.

  1. Structural insights into HRI kinase activity and inhibition.Biochemical Society transactions · 2026
    Review
  2. Review
  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

8 authors.

Chenliang Zhang *Division of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.ORCID 0000-0003-2274-2657
Huanji Xu *Division of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Qiulin TangDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Yichun DuanDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Hongwei XiaDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Huixi HuangDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Di YeDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Feng BiDivision of Abdominal Tumor Multimodality Treatment, Department of Medical Oncology, Cancer Center and Laboratory of Molecular Targeted Therapy in Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China. bifeng@scu.edu.cn.ORCID 0000-0002-0527-5105

Funding

1.1.3.5 Project for Disciplines of excellence, West China Hospital, Sichuan University ZYGD18005MOST | National Natural Science Foundation of China (NSFC) 32000533MOST | National Natural Science Foundation of China (NSFC) 82073059
6 · The paper itself

Abstract

Protein quality control serves as the primary defense mechanism for cells against proteotoxicity induced by proteasome dysfunction. While cells can limit the build-up of ubiquitinated misfolded proteins during proteasome inhibition, the precise mechanism is unclear. Here, we find that protein kinase Ca

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCalcium-Calmodulin-Dependent Protein Kinase Type 2Proteasome Endopeptidase ComplexAnimalsCell Line, TumorEukaryotic Initiation Factor-2FemaleHumansMicePhosphorylationProteasome InhibitorsSignal TransductionAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanCalcium-Calmodulin-Dependent Protein Kinase Type 2Eukaryotic Initiation Factor-2Proteasome Endopeptidase ComplexProteasome InhibitorsBAG3CaMKIIHRIParaptosisProteasome Inhibition

Identifiers

PMID39261742
PMCPMC11466968

What OpenQuestion holds

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Registered trials

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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.