Evidence map›Paper›PMID 22012253›Full record

ArticleCell death & disease2011

The tumour-suppressive function of CLU is explained by its localisation and interaction with HSP60.

K-A Chaiwatanasirikul, A Sala

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 24% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. The role and function of CLU in cancer biology and therapy.Clinical and experimental medicine · 2023
    Review
  8. The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022
    Review
  9. Mitochondrial chaperones in human health and disease.Free radical biology & medicine · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
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  20. 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

2 authors at 2 institutions in 2 countries.

K-A ChaiwatanasirikulMolecular Haematology and Cancer Biology Unit, UCL Institute of Child Health, London, UK.
A Sala
Institute of Cancer Research · GBUniversity College London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The product of the CLU gene promotes or inhibits tumourigenesis in a context-dependent manner. It has been hypothesised that different CLU isoforms have different and even opposing biological functions, but this theory has not been experimentally validated. Here we show that molecules involved in survival pathways are differentially modulated by the intracellular or secreted forms of CLU. Secreted CLU, which is selectively increased after transformation, activates the survival factor AKT, whereas intracellular CLU inhibits the activity of the oncogenic transcription factor nuclear factor kappa B. Furthermore, intracellular CLU is inactivated by the pro-proliferative and pro-survival activity of the chaperone protein HSP60 in neuroblastoma cells by forming a physical complex. Thus, localisation is key for CLU physiology, explaining the wide range of effects in cell survival and transformation.

Indexed as

AnimalsApoptosisCell SurvivalCell Transformation, NeoplasticChaperonin 60Child, PreschoolClusterinFemaleHumansMaleMiceProtein IsoformsTransfectionChaperonin 60ClusterinProtein Isoforms

Identifiers

PMID22012253
PMCPMC3219095
OpenAlexW2040846354

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.