Evidence map›Paper›PMID 29079782›Full record

ArticleNature communications2017

CaMKII-mediated Beclin 1 phosphorylation regulates autophagy that promotes degradation of Id and neuroblastoma cell differentiation.

Xuan Li, Xiao-Qi Wu, Rong Deng, Dan-Dan Li, Jun Tang, Wen-Dan Chen, Jing-Hong Chen, Jiao Ji, Lin Jiao, Shan Jiang and 17 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. The Biological Role and Clinical Significance of BECLIN-1 in Cancer.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Autophagy-mediated ID1 turnover dictates chemo-resistant fate in ovarian cancer stem cells.Journal of experimental & clinical cancer research : CR · 2024
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

8 more citing papers are in PubMed but not listed here.

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

27 authors at 8 institutions in 2 countries.

Xuan LiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Xiao-Qi WuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Rong DengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Dan-Dan LiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Jun TangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Wen-Dan ChenState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Jing-Hong ChenDepartment of Hematology, The Second Affiliated Hospital, Guangzhou Medical University, 510260, Guangzhou, China.
Jiao JiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Lin JiaoState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Shan JiangDepartment of Oncology, The First Affiliated Hospital, Chongqing Medical University, 400016, Chongqing, China.
Fen YangDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, 211166, Nanjing, China.
Gong-Kan FengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Ravichandran SenthilkumarState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Fei YueInstitute of Biosciences and Technology, Texas A&M University Health Science Center, Houston, TX, 77030, USA.
Hai-Liang ZhangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Rui-Yan WuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Yan YuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Xue-Lian XuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Jia MaiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Zhi-Ling LiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Xiao-Dan PengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Yun HuangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Xiang HuangThe School of Medicine, Jinan University, 510632, Guangzhou, China.
Ning-Fang MaKey Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, 511436, Guangzhou, China.
Qian TaoSir YK Pao Cancer Centre, Department of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong SAR, China.
Yi-Xin ZengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China.
Xiao-Feng ZhuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Cancer Center, Sun Yat-sen University, 510060, Guangzhou, China. zhuxfeng@mail.sysu.edu.cn.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNGuangzhou Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNJinan University · CNNanjing Medical University · CNPrince of Wales Hospital · CNTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a degradative pathway that delivers cellular components to the lysosome for degradation. The role of autophagy in cell differentiation is poorly understood. Here we show that CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy. Meanwhile, CaMKII can also promote K63-linked ubiquitination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6. Ubiquitinated Id-1/Id-2 can then bind to p62 and be transported to autolysosomes for degradation. Id degradation promotes the differentiation of neuroblastoma cells and reduces the proportion of stem-like cells. Our study proposes a mechanism by which autophagic degradation of Id proteins can regulate cell differentiation. This suggests that targeting of CaMKII and the regulation of autophagic degradation of Id may be an effective therapeutic strategy to induce cell differentiation in neuroblastoma.

Indexed as

AnimalsAutophagyBeclin-1Calcium-Calmodulin-Dependent Protein Kinase Type 2Cell DifferentiationFibroblastsHEK293 CellsHumansInhibitor of Differentiation Protein 1Inhibitor of Differentiation Protein 2Intracellular Signaling Peptides and ProteinsLysineLysosomesMiceNeuroblastomaPhosphorylationBeclin-1BECN1 protein, humanCalcium-Calmodulin-Dependent Protein Kinase Type 2ID1 protein, humanID2 protein, humanInhibitor of Differentiation Protein 1Inhibitor of Differentiation Protein 2Intracellular Signaling Peptides and ProteinsLysineP62 protein, humanRNA-Binding ProteinsSerineTifab protein, humanTNF Receptor-Associated Factor 6

Identifiers

PMID29079782
PMCPMC5660092
OpenAlexW2765467346

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.