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1 pitulated by respiratory chain inhibition in cultured myotubes.
2 prevents lipid-induced insulin resistance in cultured myotubes.
3 ation and the dispersion of AChR clusters in cultured myotubes.
4 can (rhBGN) increases utrophin expression in cultured myotubes.
5 on of the illuminated AChRs from clusters on cultured myotubes.
6 e and HDAC4 knockdown enhances glycolysis in cultured myotubes.
7 e inhibition of UPR causes severe atrophy in cultured myotubes.
8 ay arise from the NMJ basement membrane with cultured myotubes.
9 and cardiac muscles, murine limb muscle, and cultured myotubes.
10 ression in mouse limb muscles in vivo and in cultured myotubes.
11 -4) inhibit agrin-induced AChR clustering on cultured myotubes.
12 gulating mitochondrial oxidative function in cultured myotubes.
13 calcium in agrin-induced AChR clustering on cultured myotubes.
14 on associated with AChR cluster dispersal in cultured myotubes.
15 s and triggers formation of AChR clusters on cultured myotubes.
16 vated AMPK and stimulated lipid oxidation in cultured myotubes.
17 e receptor (AChR) clusters on the surface of cultured myotubes.
20 agrin and neuregulin-1 (Nrg-1) signaling in cultured myotubes and developing muscle fibers in vivo.
21 nduced reactive oxygen species production in cultured myotubes and improved insulin-stimulated glucos
23 endogenous AChR beta-subunit transcripts in cultured myotubes and in vivo, and this binding is incre
24 number of lipid-challenged models including cultured myotubes and isolated muscles strips incubated
27 tes was comparable between muscle tissue and cultured myotubes, and temporal lipid profiles correlate
29 s increased in skeletal muscle tissue and in cultured myotubes basally and in response to insulin in
35 maging of acetylcholine receptors (AChRs) in cultured myotubes differentiated ex vivo from immortaliz
36 exposure on glucose and lipid metabolism in cultured myotubes established from people with normal gl
38 as supported by elevated oxidative stress in cultured myotubes exposed to palmitate in the presence o
39 mparisons with changes in gene expression in cultured myotubes following treatment with a non-damagin
42 ell as IL-6 secretion, was unaltered between cultured myotubes from normal glucose tolerant or type 2
43 f transcription 3 (STAT3) phosphorylation in cultured myotubes from normal glucose tolerant subjects.
44 athies, the relatively relaxed zebrafish and cultured myotubes from patients with RYR1-related myopat
46 tractility and Ca(2+) release from the SR of cultured myotubes from Stac3 mutant mice could be restor
47 hen TrkB-mediated signaling was disrupted in cultured myotubes in the absence of motor nerve terminal
48 rs (AChRs) at laminin-associated clusters on cultured myotubes in the absence or presence of the nerv
50 y, forced expression of Gadd45a in muscle or cultured myotubes induces atrophy in the absence of upst
52 e acetylcholine receptor (AChR) synthesis in cultured myotubes, is a member of the neuregulin family
54 Recombinant human IL-6 (rhIL-6) treatment of cultured myotubes only minimally increased SOCS3, howeve
55 was used to monitor Ca2+ signals in primary-cultured myotubes, prepared from forelimbs of wild-type
64 hR density at agrin-induced AChR clusters in cultured myotubes via PI3 kinase acting through GSK3beta
65 ed aggregation of acetylcholine receptors on cultured myotubes was completely blocked by antibodies t
68 so coordinately regulated on the surfaces of cultured myotubes where MuSK and AChRs colocalize both i
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