Evidence map›Paper›PMID 9660883›Full record

ArticleThe Journal of physiology1998

Regulation of Ca2+-dependent Cl- conductance in a human colonic epithelial cell line (T84): cross-talk between Ins(3,4,5,6)P4 and protein phosphatases.

W Xie, K R Solomons, S Freeman, M A Kaetzel, K S Bruzik, D J Nelson, S B Shears

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  9. Article
  10. How versatile are inositol phosphate kinases?The Biochemical journal · 2004
    Review
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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

7 authors at 6 institutions in 2 countries.

W XieDepartment of Neurology, MC2030, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637, USA.
K R Solomons
S Freeman
M A Kaetzel
K S Bruzik
D J Nelson
S B Shears
University of Manchester · GBNational Institute of Environmental Health Sciences · USNational Institutes of Health · USUniversity of Chicago · USUniversity of Cincinnati Medical Center · USUniversity of Illinois Chicago · US

Funding

ROLE OF ION CHANNELS IN MONONUCLEAR PHAGOCYTE ACTIVATIONR01GM036823 · NIGMS · UNIVERSITY OF CHICAGO · PI NELSON, DEBORAH J. · 1986 to 2012
$3.2M
MUSCARINIC GATED ATRIAL K+ CHANNELR01GM054266 · NIGMS · UNIVERSITY OF CHICAGO · PI NELSON, DEBORAH J. · 1996 to 1999
–
NIGMS NIH HHS R01 GM036823NIGMS NIH HHS R01 GM36823NIGMS NIH HHS R01 GM54266
6 · The paper itself

Abstract

1. We have studied the regulation of whole-cell chloride current in T84 colonic epithelial cells by inositol 3,4,5,6-tetrakisphosphate (Ins(3,4,5,6)P4). New information was obtained using (a) microcystin and okadaic acid to inhibit serine/threonine protein phosphatases, and (b) a novel functional tetrakisphosphate analogue, 1, 2-bisdeoxy-1,2-bisfluoro-Ins(3,4,5,6)P4 (i.e. F2-Ins(3,4,5,6)P4). 2. Calmodulin-dependent protein kinase II (CaMKII) increased chloride current 20-fold. This current (ICl,CaMK) continued for 7 +/- 1.2 min before its deactivation, or running down, by approximately 60 %. This run-down was prevented by okadaic acid, whereupon ICl,CaMK remained near its maximum value for >= 14.3 +/- 0.6 min. 3. F2-Ins(3, 4,5,6)P4 inhibited ICl,CaMK (IC50 = 100 microM) stereo-specifically, since its enantiomer, F2-Ins(1,4,5,6)P4 had no effect at >= 500 microM. Dose-response data (Hill coefficient = 1.3) showed that F2-Ins(3,4,5,6)P4 imitated only the non-co-operative phase of inhibition by Ins(3,4,5,6)P4, and not the co-operative phase. 4. Ins(3,4,5,6)P4 was prevented from blocking ICl,CaMK by okadaic acid (IC50 = 1.5 nM) and microcystin (IC50 = 0.15 nM); these data lead to the novel conclusion that, in situ, protein phosphatase activity is essential for Ins(3,4,5,6)P4 to function. The IC50 values indicate that more than one species of phosphatase was required. One of these may be PP1, since F2-Ins(3,4,5,6)P4-dependent current blocking was inhibited by okadaic acid and microcystin with IC50 values of 70 nM and 0.15 nM, respectively.

Indexed as

CalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell CommunicationCell LineChloride ChannelsColonElectric StimulationElectrophysiologyEnzyme InhibitorsEpithelial CellsHumansInositol PhosphatesMembrane PotentialsOkadaic AcidPatch-Clamp TechniquesCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Chloride ChannelsEnzyme Inhibitorsinositol-3,4,5,6-tetrakisphosphateInositol PhosphatesOkadaic AcidPhosphoprotein Phosphatases

Identifiers

PMID9660883
PMCPMC2231076
OpenAlexW1989678156

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.