Evidence map›Paper›PMID 29048431›Full record

ArticleCell death & disease2017

HSPB1 facilitates ERK-mediated phosphorylation and degradation of BIM to attenuate endoplasmic reticulum stress-induced apoptosis.

Donna Kennedy, Katarzyna Mnich, Deepu Oommen, Reka Chakravarthy, Leonardo Almeida-Souza, Michiel Krols, Svetlana Saveljeva, Karen Doyle, Sanjeev Gupta, Vincent Timmerman and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 56 citations in OpenAlex.

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  6. Cold-blooded vertebrate utilizes behavioral fever to alleviate T cell apoptosis and optimize antimicrobial immunity.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

13 authors at 3 institutions in 2 countries.

Donna KennedyApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Katarzyna MnichApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Deepu OommenApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Reka ChakravarthyApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Leonardo Almeida-SouzaPeripheral Neuropathy Research Group, University of Antwerp, Antwerpen, Belgium.
Michiel KrolsPeripheral Neuropathy Research Group, University of Antwerp, Antwerpen, Belgium.
Svetlana SaveljevaApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Karen DoyleDiscipline of Physiology, NUI Galway, Galway, Ireland.
Sanjeev GuptaDiscipline of Pathology, School of Medicine, NUI Galway, Galway, Ireland.
Vincent TimmermanPeripheral Neuropathy Research Group, University of Antwerp, Antwerpen, Belgium.
Sophie JanssensUnit Immunoregulation and Mucosal Immunology, VIB Inflammation Research Centre, Ghent University, Gent, Belgium.
Adrienne M GormanApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.
Afshin SamaliApoptosis Research Centre, Biomedical Sciences, NUI Galway, Galway, Ireland.ORCID 0000-0002-8610-8375
Ollscoil na Gaillimhe – University of Galway · IEUniversity of Antwerp · BEGhent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BIM, a pro-apoptotic BH3-only protein, is a key regulator of the intrinsic (or mitochondrial) apoptosis pathway. Here, we show that BIM induction by endoplasmic reticulum (ER) stress is suppressed in rat PC12 cells overexpressing heat shock protein B1 (HSPB1 or HSP27) and that this is due to enhanced proteasomal degradation of BIM. HSPB1 and BIM form a complex that immunoprecipitates with p-ERK1/2. We found that HSPB1-mediated proteasomal degradation of BIM is dependent on MEK-ERK signaling. Other studies have shown that several missense mutations in HSPB1 cause the peripheral neuropathy, Charcot-Marie-Tooth (CMT) disease, which is associated with nerve degeneration. Here we show that cells overexpressing CMT-related HSPB1 mutants exhibited increased susceptibility to ER stress-induced cell death and high levels of BIM. These findings identify a novel function for HSPB1 as a negative regulator of BIM protein stability leading to protection against ER stress-induced apoptosis, a function that is absent in CMT-associated HSPB1 mutants.

Indexed as

AnimalsApoptosisBcl-2-Like Protein 11Endoplasmic ReticulumEndoplasmic Reticulum StressGene Expression RegulationHSP27 Heat-Shock ProteinsMitochondriaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PC12 CellsPhosphorylationProteasome Endopeptidase ComplexProtein BindingProteolysisRatsBcl2l11 protein, ratBcl-2-Like Protein 11HSP27 Heat-Shock ProteinsHspb1 protein, ratMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proteasome Endopeptidase ComplexRNA, Small Interfering

Identifiers

PMID29048431
PMCPMC5596589
OpenAlexW2750773786

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.