Primary over-expression of AßPP in muscle does not lead to the development of inclusion body myositis in a new lineage of the MCK-AßPP transgenic mouse.
Luo, Yue-Bei; Johnsen, Russell D; Griffiths, Lisa; Needham, Merrilee; Fabian, Victoria A; Fletcher, Sue; Wilton, Steve D; Mastaglia, Frank L.
Int J Exp Pathol
; 94(6): 418-25, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-24205796
Exercise Inducible Lactate Dehydrogenase B Regulates Mitochondrial Function in Skeletal Muscle.
Chaperone-like effect of the linker on the isolated C-terminal domain of rabbit muscle creatine kinase.
IL-10 prevents aging-associated inflammation and insulin resistance in skeletal muscle.
Top-Down Proteomics of Large Proteins up to 223 kDa Enabled by Serial Size Exclusion Chromatography Strategy.
Effects of the single point genetic mutation D54G on muscle creatine kinase activity, structure and stability.
New Developments in the Genetics of Inclusion Body Myositis.
Similar mitochondrial activation kinetics in wild-type and creatine kinase-deficient fast-twitch muscle indicate significant Pi control of respiration.
Role of the linker between the N- and C-terminal domains in the stability and folding of rabbit muscle creatine kinase.
Immunohistochemical and ultrastructural analysis of sporadic inclusion body myositis: a case series.
Single nucleotide polymorphisms in the myostatin (MSTN) and muscle creatine kinase (CKM) genes are not associated with elite endurance performance.