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1 the importance of MRTFs in actin cycling and myofibrillogenesis.
2 triated muscle potentially playing a role in myofibrillogenesis.
3 ted in an inhibition of costamerogenesis and myofibrillogenesis.
4 1, and FMNL2 are required nonredundantly for myofibrillogenesis.
5 localized to the subsarcolemmal space during myofibrillogenesis.
6 keletal myotubes revealed its involvement in myofibrillogenesis.
7 ress a controversy about different models of myofibrillogenesis.
8 ing involvement of the Rho GTPase in cardiac myofibrillogenesis.
9 myocytes (NRC) under conditions that promote myofibrillogenesis.
10 y a role in cytoskeletal organization during myofibrillogenesis.
11 owth of muscle fibers is largely mediated by myofibrillogenesis.
12  to impaired myosin replacement during early myofibrillogenesis.
13 t by driving cardiomyocyte proliferation and myofibrillogenesis.
14 ugh membraneless compartmentalization during myofibrillogenesis.
15 rcomeric genes, enhanced fusion and improved myofibrillogenesis.
16 scent myofibril-like structures and impaired myofibrillogenesis.
17  proteins are crucial at different stages of myofibrillogenesis, accounting for sarcomeric structural
18 est that LDTs have at least two roles during myofibrillogenesis-activation of sarcoplasmic regulatory
19  Tmod1 nulls results from defects in cardiac myofibrillogenesis and development or from erythroid cel
20 of regenerated myofibers are associated with myofibrillogenesis and endure months post injury.
21 hanically stabilize cells and tissues during myofibrillogenesis and intercalated disc assembly.
22 oduced TTN truncation peptides that impaired myofibrillogenesis and sarcomere function.
23       These studies suggest a role for C3 in myofibrillogenesis and sarcomere remodeling.
24 e a valuable in vivo model for studying both myofibrillogenesis and sarcomere-based cardiac diseases.
25 cyte and matrix fiber alignment and enhances myofibrillogenesis and sarcomeric banding.
26 es of skeletal myotubes to study its role in myofibrillogenesis and the organization of the sarcoplas
27 ick filaments, causing disruption in ordered myofibrillogenesis and/or myofibrillar integrity, and th
28 d1 functions are critical for late stages of myofibrillogenesis, and for the maturation of myofibrils
29  and the role of this pool of the protein in myofibrillogenesis, and implicate the Ozz-E3 ligase in t
30 icular myocytes increase in profile, exhibit myofibrillogenesis, and re-express genes whose expressio
31 f appearance of sarcomeres and MyBP-C during myofibrillogenesis, and the defective formation of sarco
32                                     Although myofibrillogenesis appeared normal, in knockdown hearts
33  thick filament assembly and many aspects of myofibrillogenesis are independent of the myosin head an
34       We show that both costamerogenesis and myofibrillogenesis are initiated at sites of membrane co
35 t replace nonmuscle myosin MYH10, leading to myofibrillogenesis arrest at the early premyofibril stag
36  myosin head in thick filament formation and myofibrillogenesis by generating transgenic Drosophila l
37 ypothesis that C3 mediates remodeling during myofibrillogenesis, C3 knockout (C3KO) mice were generat
38 5-kDa) proteins that play important roles in myofibrillogenesis, cytoskeletal organization, and cell
39 in leads to Mb-beta-catenin accumulation and myofibrillogenesis defects similar to those observed in
40 vian heart suggesting that the mechanism for myofibrillogenesis differs in cultured and uncultured ce
41  the assembly of sarcomeres, suggesting that myofibrillogenesis does not depend on strong myosin-acti
42 derstanding of the role that MyBP-C plays in myofibrillogenesis during cardiac development and indica
43 earance, srcF527 did not detectably increase myofibrillogenesis either alone or in combination with H
44                                              Myofibrillogenesis followed, both spatially and temporal
45 or to modulate the temporal dynamics of core myofibrillogenesis genes and thereby orchestrates sarcom
46                                     Although myofibrillogenesis had occurred, skeletal muscle thin fi
47 ate model for this purpose, we characterized myofibrillogenesis in a developing zebrafish heart and w
48 ping hearts supporting a three-step model of myofibrillogenesis in cardiomyocytes, whether they are p
49 icipating in control of myoblast fusion, and myofibrillogenesis in developing myotubes.
50 n of glycogen in all cell types and abnormal myofibrillogenesis in striated muscle.
51 eveloping muscle cells supports the model of myofibrillogenesis in which assembly begins with premyof
52       Immunofluorescence localization during myofibrillogenesis indicated that the Rho-GEF domain ass
53 n of Golgi components in myogenic cells, and myofibrillogenesis is normal.
54 rophy) and/or the number of myofibrils (i.e. myofibrillogenesis) is not known.
55                 Although CapZ is crucial for myofibrillogenesis, its role in muscle function and intr
56      While both LDTs and SDTs occur prior to myofibrillogenesis, LDT production ceases and only SDTs
57 itical for nascent myosin folding, promoting myofibrillogenesis, maintaining cytoskeletal integrity a
58 nd extend the tension-driven self-organizing myofibrillogenesis model.
59 umber of proteins involved in signalling and myofibrillogenesis; mutations in these proteins lead to
60                             Among them, core myofibrillogenesis proteins (eg, ACTN2 [a-actinin 2], TT
61                             Among them, core myofibrillogenesis proteins (eg, ACTN2 [alpha-actinin 2]
62                   We report mutations in the myofibrillogenesis regulator 1 (MR-1) gene causing PNKD
63                                              Myofibrillogenesis requires proper folding and assembly
64                                              Myofibrillogenesis, the precise assembly of sarcomeric p
65 ease from intracellular stores occurs during myofibrillogenesis, the process of sarcomeric protein as
66 ral aspects of muscle development, including myofibrillogenesis-the terminal differentiation of the s
67  has been proposed to play critical roles in myofibrillogenesis, thin filament length regulation, and
68                                 In addition, myofibrillogenesis was increased by PGF2 alpha as assess
69   alpha1-Adrenergic receptor agonist-induced myofibrillogenesis was inhibited by some but not all of
70          To address this question of in situ myofibrillogenesis, we applied non-enzymatic procedures
71 gnificance of Tmod1 functions during de novo myofibrillogenesis, we generated Tmod1 null embryonic st
72  to differentiate, both costamerogenesis and myofibrillogenesis were disrupted although the expressio
73 ents, such as beta1D integrin expression and myofibrillogenesis, were suppressed in C3KO myotubes.
74          Q529X-MYPN causes RCM via disturbed myofibrillogenesis, whereas Y20C-MYPN perturbs MYPN nucl
75  for both normal costamerogenesis and normal myofibrillogenesis which are tightly coupled during skel
76                                    Disturbed myofibrillogenesis with disruption of alpha-actinin2, de
77 yte hypertrophy (ie, increased cell size and myofibrillogenesis, with concurrent transcriptional chan