Evidence map›Paper›PMID 11986377›Full record

ArticleThe Journal of physiology2002

Phosphorylation and functional regulation of ClC-2 chloride channels expressed in Xenopus oocytes by M cyclin-dependent protein kinase.

Tetsushi Furukawa, Takehiko Ogura, Ya-Juan Zheng, Hiroyuki Tsuchiya, Haruaki Nakaya, Yoshifumi Katayama, Nobuya Inagaki

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2002. 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
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

20 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Functional identification of protein phosphatase 1-binding consensus residues in NBCe1-B.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018
    Article
  3. Research and progress on ClC‑2 (Review).Molecular medicine reports · 2017
    Review
  4. Article
  5. Article
  6. Chloride channelopathies of ClC-2.International journal of molecular sciences · 2013
    Review
  7. Article
  8. Phenomics of cardiac chloride channels.Comprehensive Physiology · 2013
    Review
  9. Article
  10. Article
  11. Article
  12. A synthetic prostone activates apical chloride channels in A6 epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2008
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  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

7 authors at 3 institutions in 1 country.

Tetsushi FurukawaDepartment of Physiology, Akita University School of Medicine, Akita 010-8543, Japan.
Takehiko Ogura
Ya-Juan Zheng
Hiroyuki Tsuchiya
Haruaki Nakaya
Yoshifumi Katayama
Nobuya Inagaki
Akita University · JPChiba University · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many dramatic alterations in various cellular processes during the cell cycle are known to involve ion channels. In ascidian embryos and Caenorhabditis elegans oocytes, for example, the activity of inwardly rectifying Cl(-) channels is enhanced during the M phase of the cell cycle, but the mechanism underlying this change remains to be established. We show here that the volume-sensitive Cl(-) channel, ClC-2 is regulated by the M-phase-specific cyclin-dependent kinase, p34(cdc2)/cyclin B. ClC-2 channels were phosphorylated by p34(cdc2)/cyclin B in both in vitro and cell-free phosphorylation assays. ClC-2 phosphorylation was inhibited by olomoucine and abolished by a (632)Ser-to-Ala (S632A) mutation in the C-terminus, indicating that (632)Ser is a target of phosphorylation by p34(cdc2)/cyclin B. Injection of activated p34(cdc2)/cyclin B attenuated the ClC-2 currents but not the S632A mutant channel currents expressed in Xenopus oocytes. ClC-2 currents attenuated by p34(cdc2)/cyclin B were increased by application of the cyclin-dependent kinase inhibitor, olomoucine (100 microM), an effect that was inhibited by calyculin A (5 nM) but not by okadaic acid (5 nM). A yeast two-hybrid system revealed a direct interaction between the ClC-2 C-terminus and protein phosphatase 1. These data suggest that the ClC-2 channel is also counter-regulated by protein phosphatase 1. In addition, p34(cdc2)/cyclin B decreased the magnitude of ClC-2 channel activation caused by cell swelling. As the activities of both p34(cdc2)/cyclin B and protein phosphatase 1 vary during the cell cycle, as does cell volume, the ClC-2 channel could be regulated physiologically by these factors.

Indexed as

AnimalsChloride ChannelsCLC-2 Chloride ChannelsCyclin-Dependent KinasesEnzyme InhibitorsFemaleKineticsKinetinMarine ToxinsMitosisOkadaic AcidOocytesOxazolesPhosphorylationPurinesRecombinant Proteinscalyculin AChloride ChannelsCLC-2 Chloride ChannelsCyclin-Dependent KinasesEnzyme InhibitorsKinetinMarine ToxinsOkadaic AcidolomoucineOxazolesPurinesRecombinant Proteins

Identifiers

PMID11986377
PMCPMC2290285
OpenAlexW2060535829

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.