Journal article
A mouse model of creatine transporter deficiency reveals impaired motor function and muscle energy metabolism
- Abstract:
-
Creatine serves as fast energy buffer in organs of high-energy demand such as brain and skeletal muscle. L-Arginine:glycine amidinotransferase (AGAT) and guanidinoacetate N-methyltransferase are responsible for endogenous creatine synthesis. Subsequent uptake into target organs like skeletal muscle, heart and brain is mediated by the creatine transporter (CT1, SLC6A8). Creatine deficiency syndromes are caused by defects of endogenous creatine synthesis or transport and are mainly characterize...
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- Publication status:
- Published
- Peer review status:
- Peer reviewed
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Authors
Funding
+ Deutsche Forschungsgemeinschaft
More from this funder
Funding agency for:
Isbrandt, D
Neu, A
Choe, C
Grant:
CH872/1-1
CH872/1-1
5/86, C-UC
Bibliographic Details
- Publisher:
- Frontiers Media Publisher's website
- Journal:
- Frontiers in Physiology Journal website
- Volume:
- 9
- Article number:
- 773
- Publication date:
- 2018-06-22
- Acceptance date:
- 2018-06-04
- DOI:
- ISSN:
-
1664-042X
Item Description
- Pubs id:
-
pubs:864783
- UUID:
-
uuid:6b05eacc-7fa8-4da5-b5ee-9145ab85422c
- Local pid:
- pubs:864783
- Source identifiers:
-
864783
- Deposit date:
- 2018-07-12
Terms of use
- Copyright holder:
- © 2018 Stockebrand, et al
- Copyright date:
- 2018
- Notes:
- This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
- Licence:
- CC Attribution (CC BY)
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