Evidence map›Paper›PMID 21824394›Full record

ArticleBMC molecular biology2011

Increased complexity of Tmem16a/Anoctamin 1 transcript alternative splicing.

Kate E O'Driscoll, Rachel A Pipe, Fiona C Britton

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022
    Review
  5. Review
  6. Article
  7. Differential Regulation of CaInternational journal of molecular sciences · 2021
    Article
  8. Allosteric modulation of alternatively spliced CaProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  9. Article
  10. Review
  11. Direct repression of anoctamin 1 (FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  12. Article
  13. Anoctamin Channels in Human Myometrium: A Novel Target for Tocolysis.Reproductive sciences (Thousand Oaks, Calif.) · 2018
    Article
  14. Article
  15. Functional comparison of anoctamin 1 antagonists on human uterine smooth muscle contractility and excitability.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2018
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Kate E O'DriscollDepartment of Physiology and Cell Biology, 1664 North Virginia Street, University of Nevada School of Medicine, Reno, Nevada 89557-0046, USA.
Rachel A Pipe
Fiona C Britton
University of Nevada, Reno · US

Funding

Bestrophin Channel Function in HeartR01HL091238 · NHLBI · UNIVERSITY OF NEVADA RENO · PI BRITTON, FIONA CATHERINE · 2008 to 2012
$2.0M
NHLBI NIH HHS 1R01HL091238NHLBI NIH HHS R01 HL091238
6 · The paper itself

Abstract

backgroundTMEM16A (Anoctamin 1; ANO1) is an eight transmembrane protein that functions as a calcium-activated chloride channel. TMEM16A in human exhibits alternatively spliced exons (6b, 13 and 15), which confer important roles in the regulation of channel function. Mouse Tmem16a is reported to consist of 25 exons that code for a 956 amino acid protein. In this study our aim was to provide details of mouse Tmem16a genomic structure and to investigate if Tmem16a transcript undergoes alternative splicing to generate channel diversity.

resultsWe identified Tmem16a transcript variants consisting of alternative exons 6b, 10, 13, 14, 15 and 18. Our findings indicate that many of these exons are expressed in various combinations and that these splicing events are mostly conserved between mouse and human. In addition, we confirmed the expression of these exon variants in other mouse tissues. Additional splicing events were identified including a novel conserved exon 13b, tandem splice sites of exon 1 and 21 and two intron retention events.

conclusionOur results suggest that Tmem16a gene is significantly more complex than previously described. The complexity is especially evident in the region spanning exons 6 through 16 where a number of the alternative splicing events are thought to affect calcium sensitivity, voltage dependence and the kinetics of activation and deactivation of this calcium-activated chloride channel. The identification of multiple Tmem16a splice variants suggests that alternative splicing is an exquisite mechanism that operates to diversify TMEM16A channel function in both physiological and pathophysiological conditions.

Indexed as

Alternative SplicingAmino Acid SequenceAnimalsAnoctamin-1Chloride ChannelsComputational BiologyExonsHumansIntronsMiceMolecular Sequence DataANO1 protein, mouseAnoctamin-1Chloride Channels

Identifiers

PMID21824394
PMCPMC3170211
OpenAlexW2049539545

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.