Evidence map›Paper›PMID 30275345›Full record

ArticleMolecular and cellular biology2018

Hsp70 Interacts with Mitogen-Activated Protein Kinase (MAPK)-Activated Protein Kinase 2 To Regulate p38MAPK Stability and Myoblast Differentiation during Skeletal Muscle Regeneration.

Wei Fan, Xiu Kui Gao, Xi Sheng Rao, Yin Pu Shi, Xiao Ceng Liu, Fei Ya Wang, Yu Fen Liu, Xiao Xia Cong, Min Yi He, Shui Bo Xu and 9 more

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. MK2 degradation as a sensor of signal intensity that controls stress-induced cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

19 authors at 5 institutions in 2 countries.

Wei Fan *Department of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Xiu Kui Gao *Department of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Xi Sheng Rao *Department of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Yin Pu ShiDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Xiao Ceng LiuDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Fei Ya WangDepartment of Pathology, Hospital of Pingdingshan Coal Industry Group, Pingdingshan, China.
Yu Fen LiuDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Xiao Xia CongDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Min Yi HeDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Shui Bo XuDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Wei Liang ShenDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Yue ShenDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Shi Gui YanDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Yan LuoDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China.
Boon Chuan LowMechanobiology Institute, Department of Biological Sciences, National University of Singapore, Singapore, Singapore.
Hongwei OuyangKey Laboratory of Tissue Engineering and Regenerative Medicine of Zhejiang Province, Dr. Li Dak Sum & Yip Yio Chin Center for Stem Cell and Regenerative Medicine, Zhejiang University School of Medicine, Hangzhou, China.
Zhang BaoDepartment of Respiratory Medicine, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Li Ling ZhengDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China zhengliling@zju.edu.cn zhouyt@zju.edu.cn.
Yi Ting ZhouDepartment of Biochemistry and Molecular Biology, Zhejiang University School of Medicine, Hangzhou, China zhengliling@zju.edu.cn zhouyt@zju.edu.cn.ORCID 0000-0003-4543-3099
Second Affiliated Hospital of Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CNNational University of Singapore · SGPingdingshan University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The regenerative process of injured muscle is dependent on the fusion and differentiation of myoblasts derived from muscle stem cells. Hsp70 is important for maintaining skeletal muscle homeostasis and regeneration, but the precise cellular mechanism remains elusive. In this study, we found that Hsp70 was upregulated during myoblast differentiation. Depletion or inhibition of Hsp70/Hsc70 impaired myoblast differentiation. Importantly, overexpression of p38 mitogen-activated protein kinase α (p38MAPKα) but not AKT1 rescued the impairment of myogenic differentiation in Hsp70- or Hsc70-depleted myoblasts. Moreover, Hsp70 interacted with MK2, a substrate of p38MAPK, to regulate the stability of p38MAPK. Knockdown of Hsp70 also led to downregulation of both MK2 and p38MAPK in intact muscles and during cardiotoxin-induced muscle regeneration. Hsp70 bound MK2 to regulate MK2-p38MAPK interaction in myoblasts. We subsequently identified the essential regions required for Hsp70-MK2 interaction. Functional analyses showed that MK2 is essential for both myoblast differentiation and skeletal muscle regeneration. Taken together, our findings reveal a novel role of Hsp70 in regulating myoblast differentiation by interacting with MK2 to stabilize p38MAPK.

Indexed as

AnimalsCell DifferentiationCell LineDown-RegulationHSP70 Heat-Shock ProteinsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2MiceMice, Inbred C57BLMuscle DevelopmentMuscle, SkeletalMyoblastsp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesRegenerationUp-RegulationHSP70 Heat-Shock ProteinsIntracellular Signaling Peptides and ProteinsMAP-Kinase-Activated Kinase 2p38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesHsp70/Hsc70MAPKAPK2muscle regenerationmyoblast differentiationmyogenesisp38MAPK

Identifiers

PMID30275345
PMCPMC6275188
OpenAlexW2895227942

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.