Evidence map›Paper›PMID 23471296›Full record

ArticleCellular and molecular life sciences : CMLS2013

TRPM7 is regulated by halides through its kinase domain.

Haijie Yu, Zheng Zhang, Annette Lis, Reinhold Penner, Andrea Fleig

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. TRP Channels in Digestive Tract Cancers.International journal of molecular sciences · 2020
    Review
  9. Physiology of Astroglial Excitability.Function (Oxford, England) · 2020
    Article
  10. TRPM7, Magnesium, and Signaling.International journal of molecular sciences · 2019
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Intracellular Cl- as a signaling ion that potently regulates Na+/HCO3- transporters.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  17. Article
  18. Article
  19. Article
  20. TRPM7.Handbook of experimental pharmacology · 2014
    Review
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

5 authors at 3 institutions in 1 country.

Haijie YuCenter for Biomedical Research, The Queen's Medical Center, 1301 Punchbowl St., Honolulu, HI 96813, USA.
Zheng Zhang
Annette Lis
Reinhold Penner
Andrea Fleig
Queen's Medical Center · USUniversity of Hawaiʻi at Mānoa · USUniversity of Hawaii System · US

Funding

University of Hawaii Cancer Center CCSGP30CA071789 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI Xin Chen · 1996 to 2026
$56.2M
Regulation of Metal Ion Homeostasis by Channel KinasesP01GM078195 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI FLEIG, ANDREA · 2007 to 2011
$8.7M
NCI NIH HHS P30 CA071789NIGMS NIH HHS P01 GM078195NIGMS NIH HHS P01GM078195
6 · The paper itself

Abstract

Transient receptor potential melastatin 7 (TRPM7) is a divalent-selective cation channel fused to an atypical α-kinase. TRPM7 is a key regulator of cell growth and proliferation, processes accompanied by mandatory cell volume changes. Osmolarity-induced cell volume alterations regulate TRPM7 through molecular crowding of solutes that affect channel activity, including magnesium (Mg(2+)), Mg-nucleotides and a further unidentified factor. Here, we assess whether chloride and related halides can act as negative feedback regulators of TRPM7. We find that chloride and bromide inhibit heterologously expressed TRPM7 in synergy with intracellular Mg(2+) ([Mg(2+)]i) and this is facilitated through the ATP-binding site of the channel's kinase domain. The synergistic block of TRPM7 by chloride and Mg(2+) is not reversed during divalent-free or acidic conditions, indicating a change in protein conformation that leads to channel inactivation. Iodide has the strongest inhibitory effect on TRPM7 at physiological [Mg(2+)]i. Iodide also inhibits endogenous TRPM7-like currents as assessed in MCF-7 breast cancer cells, where upregulation of SLC5A5 sodium-iodide symporter enhances iodide uptake and inhibits cell proliferation. These results indicate that chloride could be an important factor in modulating TRPM7 during osmotic stress and implicate TRPM7 as a possible molecular mechanism contributing to the anti-proliferative characteristics of intracellular iodide accumulation in cancer cells.

Indexed as

Adenosine TriphosphateBromidesCell ProliferationChloridesDNA, ComplementaryDose-Response Relationship, DrugFeedback, PhysiologicalGene Expression RegulationHEK293 CellsHumansHydrogen-Ion ConcentrationInhibitory Concentration 50IodidesMCF-7 CellsPatch-Clamp TechniquesProtein Serine-Threonine KinasesAdenosine TriphosphateBromidesChloridesDNA, ComplementaryIodidesProtein Serine-Threonine KinasesSodium-Iodide SymportersSymportersTRPM7 protein, humanTRPM Cation Channels

Identifiers

PMID23471296
PMCPMC3710292
OpenAlexW2088138990

What OpenQuestion holds

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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.