Journal article
Dampened activity of ryanodine receptor channels in mutant skeletal muscle lacking TRIC-A
- Abstract:
-
TRIC-A is a major component of the nuclear and sarcoplasmic reticulum (SR) membranes of cardiac and skeletal muscle, and is localised closely with RyR channels in the SR terminal cisternae. The skeletal muscle of Tric-a KO mice is characterised by Ca2+ overloaded and swollen SR and by changes in the properties of SR Ca2+ release. We therefore investigated if RyR1 gating behaviour is modified in the SR from Tric-a KO mice by incorporating native RyR1 into planar phospholipid bilayers under vol...
Expand abstract
- Publication status:
- Published
- Peer review status:
- Peer reviewed
Actions
Access Document
- Files:
-
-
(Version of record, pdf, 1.3MB)
-
- Publisher copy:
- 10.1113/JP273550
Why is the content I wish to access not available via ORA?
Bibliographic data (the information relating to research outputs) and full-text items (e.g. articles, theses, reports, etc.) arrive in ORA from several different sources. Unfortunately we are not able to make available the full-text for every research output.
Please contact the ORA team (
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
) if you have queries regarding unavailable content OR if you are aware of a full-text copy we can make available.
Content may be unavailable for the following four reasons
-
Version unsuitable
-
We have not obtained a suitable full-text for a given research output. See this page for more information.
-
Recently completed
-
Sometimes content is held in ORA but is unavailable for a fixed period of time to comply with the policies and wishes of rights holders.
-
Permissions
-
All content made available in ORA should comply with relevant rights, such as copyright. See this page for more information.
-
Clearance
-
Some thesis volumes scanned as part of the digitisation scheme funded by Dr Leonard Polonsky are currently unavailable due to sensitive material or uncleared third-party copyright content. We are attempting to contact authors whose theses are affected.
Alternative access to the full-text
You may be able to access the full-text directly from the publisher's website using the 'Publisher Copy' link in the 'Links & Downloads' box from a research output's ORA record page. This method may require an institutional or individual subscription to the journal/resource.
Authors
Funding
Bibliographic Details
- Publisher:
- John Wiley & Sons Ltd Publisher's website
- Journal:
- Journal of Physiology Journal website
- Volume:
- 595
- Issue:
- 14
- Pages:
- 4769–4784
- Publication date:
- 2017-05-23
- Acceptance date:
- 2017-03-29
- DOI:
- EISSN:
-
1469-7793
- ISSN:
-
0022-3751
Item Description
- Keywords:
- Pubs id:
-
pubs:688938
- UUID:
-
uuid:cf4fafe6-49e8-4ca2-a932-a5d488d99e3f
- Local pid:
- pubs:688938
- Deposit date:
- 2017-04-10
Terms of use
- Copyright holder:
- El-Ajouz et al
- Copyright date:
- 2017
- Notes:
-
Copyright © 2017 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
- Licence:
- CC Attribution (CC BY)
If you are the owner of this record, you can report an update to it here: Report update to this record