Zobrazeno 1 - 3
of 3
pro vyhledávání: '"Kevin S. Bradley"'
Autor:
Amber L. Pond, Gregory H. Hockerman, Wen-Horng Wang, Mariam N. Hashmi, Kevin S. Bradley, Evan P.S. Pratt, Rod Weilbaecher, Judith K. Davie, Albert K. Urazaev, Luke B. Anderson, Sawyer M. Latour, Clayton Whitmore
Publikováno v:
Skeletal Muscle
Skeletal Muscle, Vol 10, Iss 1, Pp 1-15 (2020)
Skeletal Muscle, Vol 10, Iss 1, Pp 1-15 (2020)
Background Skeletal muscle atrophy is the net loss of muscle mass that results from an imbalance in protein synthesis and protein degradation. It occurs in response to several stimuli including disease, injury, starvation, and normal aging. Currently
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6b1a5fcef59b456a4fcaf03c441e70de
https://pubmed.ncbi.nlm.nih.gov/31948476
https://pubmed.ncbi.nlm.nih.gov/31948476
Autor:
Kevin Hannon, Kevin S. Bradley, Naoya Fujita, Wen-Horng Wang, Huahua Du, Christine B. Jaeger, Gregory H. Hockerman, Amber Pond, Carrie Nedele, Xun Wang, Claire Walther
Publikováno v:
Muscle & Nerve. 49:378-388
Introduction: We investigated the mechanism by which the MERG1a K+ channel increases ubiquitin proteasome proteolysis (UPP). Methods: Hindlimb suspension and electro-transfer of Merg1a cDNA into mouse gastrocnemius muscles induced atrophy. Results: A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::fd92f288a626c6e510a59c38dac3e6c6
https://doi.org/10.1002/mus.23924
https://doi.org/10.1002/mus.23924
Autor:
Amber L, Pond, Carrie, Nedele, Wen-Horng, Wang, Xun, Wang, Claire, Walther, Christine, Jaeger, Kevin S, Bradley, Huahua, Du, Naoya, Fujita, Gregory H, Hockerman, Kevin M, Hannon
Publikováno v:
Musclenerve. 49(3)
We investigated the mechanism by which the MERG1a K+ channel increases ubiquitin proteasome proteolysis (UPP).Hindlimb suspension and electro-transfer of Merg1a cDNA into mouse gastrocnemius muscles induced atrophy.Atrophic gastrocnemius muscles of h
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::39b6d2a2a612b576259a290edaf06a4e
https://pubmed.ncbi.nlm.nih.gov/23761265
https://pubmed.ncbi.nlm.nih.gov/23761265