Evidence map›Paper›PMID 18559421›Full record

ArticleMolecular and cellular biology2008

Identification of a posttranslational mechanism for the regulation of hERG1 K+ channel expression and hERG1 current density in tumor cells.

Leonardo Guasti, Olivia Crociani, Elisa Redaelli, Serena Pillozzi, Simone Polvani, Marika Masselli, Tommaso Mello, Andrea Galli, Amedeo Amedei, Randy S Wymore and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

38 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. The ERG1 KFrontiers in molecular neuroscience · 2022
    Review
  10. Review
  11. Ion Channel Dysregulation in Head and Neck Cancers: Perspectives for Clinical Application.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Ether-à-go-go KThe Journal of physiology · 2018
    Review
  17. Article
  18. Article
  19. Article
  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

12 authors at 4 institutions in 2 countries.

Leonardo GuastiDepartment of Experimental Pathology and Oncology, University of Florence, Viale G. B. Morgagni 50, 50134 Florence, Italy.
Olivia Crociani
Elisa Redaelli
Serena Pillozzi
Simone Polvani
Marika Masselli
Tommaso Mello
Andrea Galli
Amedeo Amedei
Randy S Wymore
Enzo Wanke
Annarosa Arcangeli
University of Florence · ITUniversity of Milano-Bicocca · ITFondazione Farmacogenomica FiorGen · ITOklahoma State University Center for Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A common feature of tumor cells is the aberrant expression of ion channels on their plasma membrane. The molecular mechanisms regulating ion channel expression in cancer cells are still poorly known. K(+) channels that belong to the human ether-a-go-go-related gene 1 (herg1) family are frequently misexpressed in cancer cells compared to their healthy counterparts. We describe here a posttranslational mechanism for the regulation of hERG1 channel surface expression in cancer cells. This mechanism is based on the activity of hERG1 isoforms containing the USO exon. These isoforms (i) are frequently overexpressed in human cancers, (ii) are retained in the endoplasmic reticulum, and (iii) form heterotetramers with different proteins of the hERG family. (iv) The USO-containing heterotetramers are retained intracellularly and undergo ubiquitin-dependent degradation. This process results in decreased hERG1 current (I(hERG1)) density. We detailed such a mechanism in heterologous systems and confirmed its functioning in tumor cells that endogenously express hERG1 proteins. The silencing of USO-containing hERG1 isoforms induces a higher I(hERG1) density in tumors, an effect that apparently regulates neurite outgrowth in neuroblastoma cells and apoptosis in leukemia cells.

Indexed as

Ion Channel GatingProtein Processing, Post-TranslationalAlternative SplicingApoptosisCell Line, TumorCell MembraneCloning, MolecularDNA, ComplementaryEther-A-Go-Go Potassium ChannelsGene Expression Regulation, NeoplasticGene SilencingHealthHumansIntracellular SpaceModels, BiologicalMolecular Sequence DataDNA, ComplementaryEther-A-Go-Go Potassium ChannelsKCNH1 protein, humanProtein IsoformsRNA, Messenger

Identifiers

PMID18559421
PMCPMC2519704
OpenAlexW2127707929

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.