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1 hing a mechanism by which Mef2A controls the costamere.
2 l proteins and pathways that link Z-disk and costamere.
3 ocalized at the muscle adhesion sites termed costameres.
4 se bodies, structures analogous to mammalian costameres.
5 h beta2 spectrin recruitment of ankyrin-B to costameres.
6 uired to align sarcolemmal microtubules with costameres.
7 rt and is enriched at intercalated discs and costameres.
8 PM-sarcomere attachment sites also known as costameres.
9 s involvement in the establishment of mature costameres.
10 ocal adhesion-like cell-matrix contacts into costameres.
11 l adhesion kinase (FAK), are associated with costameres.
12 ation of dystrophin and beta-dystroglycan at costameres.
13 ate filament protein of muscle in organizing costameres.
14 or the peripheral layer of myofibrils to the costameres.
15 tting sites, the myotendinous junctions, and costameres.
16 omes the main Tln isoform, localizing to the costameres.
17 d we present the initial description for the costamere, a key muscle stability complex, in Drosophila
18 ctrin is normally found at the sarcolemma in costameres, a rectilinear array of longitudinal strands
23 of integrin-containing adhesion complexes at costameres and MTJs advance normally in the mutants.
24 -glycoprotein complex (DGC) are localized at costameres and neuromuscular junctions in the sarcolemma
26 microtubules, localization of dystrophin at costameres, and maintenance of sarcolemmal integrity.
28 cal interactions between desmin and Z-disks, costameres, and nuclei were measured during passive defo
29 by severe disruption of desmosome as well as costamere architecture and composition in the heart, as
32 A central question in muscle biology is how costameres are formed and become aligned with underlying
35 ystrophin, dystroglycan, and microtubules at costameres as well as protection of muscle from exercise
36 n-glycoprotein complex, and by extension the costamere, as harboring signaling components has receive
38 ween dystrophin and MTs has been documented, costamere-associated MTs are disrupted when dystrophin i
39 end on beta2 spectrin and ankyrin-B, whereas costamere association of ankyrin-B required beta2 spectr
41 ing myofilaments to the cell surface through costameres at the sarcolemma and desmosomes at intercala
42 s via interactions with alpha-actinin and to costameres at the sarcolemma via interactions with vincu
44 uscle, focal adhesion-like structures called costameres attach myofibrils at the periphery of muscle
47 selectively stabilizes the Z line domains of costameres, but that cytokeratins associate with all thr
49 ts may also be an important precursor to the costamere disarray observed in dystrophin-deficient musc
50 ptor protein family member ponsin in nascent costameres during muscle differentiation, which is media
52 resent study, we investigated the process of costamere formation ("costamerogenesis") in differentiat
57 unctions directly downstream of MEF2A at the costamere in striated muscle potentially playing a role
64 een these proteins resulted in loss of their costamere-localizing activity and increased muscle fiber
66 skeletal muscle, beta 1D was concentrated in costameres, myotendinous, and neuromuscular junctions.
71 tion factor-binding sites in this network of costamere promoters that may provide insight into the me
72 ype and desmin-null fibers revealed that the costamere protein talin colocalized with the Z-disk prot
75 mma of fast-twitch muscle is organized into "costameres," structures that are oriented transversely,
76 lated in CMs and is specifically detected at costameres, suggesting its importance in the compensator
77 protein talin (Tln) is a component of muscle costameres that links integrins ultimately to the sarcom
78 in skeletal muscle but uniquely localizes to costameres, the cytoskeletal networks that couple periph
79 te at the sarcolemma at all three domains of costameres when the latter are retained in desmin -/- mu
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