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1 kinase C, a negative regulator of non-muscle myosin IIB.
2 ched in tropomodulin 1 (Tmod1) and nonmuscle myosin IIB.
3 This zone is also enriched for nonmuscle myosin IIB.
4 nd ERK, myosin light chain kinase (MLCK) and Myosin IIB.
5 as distinct from that of a nonmuscle myosin, myosin IIb.
6 cle myosin II, referred to as myosin IIA and myosin IIB.
7 ompensatory mechanism between myosin IIA and myosin IIB.
8 d states, which is in contrast to non-muscle myosin IIB.
9 the nonmuscle isoforms of alpha-actinin and myosin IIB.
10 little effect on the assembly properties of myosin-IIB.
11 However, in this study, we demonstrate that myosin IIB, a cytoplasmic myosin II particularly enriche
15 ults in an isoform switch from myosin IIC to myosin IIB and increased phosphorylation of myosin heavy
16 ntative of skeletal muscle myosin, nonmuscle myosin IIB, and nonmuscle myosin IIA revealed three dist
20 ts in the localized selective aggregation of myosin IIB but not myosin IIA at the region of parasite
22 hese observations indicate that asymmetry of myosin IIB, but not IIA, is regulated by light-chain pho
24 yosin II drives actin flow, and depletion of myosin IIB, but not myosin IIA, showed similar nondirect
26 unction of one of the isoforms of myosin II, myosin IIB, by analyzing the movement and mechanical cha
28 siRNA)-mediated suppression of myosin IIA or myosin IIB causes an increase in mitochondrial length in
30 shwork instability and collapse, followed by myosin IIB concentration at the rear of the cone and nec
32 o develop convergence forces parallel to the myosin IIB-dependent dynamics of the actin cytoskeleton.
34 in IIA forms de novo filaments away from the myosin IIB-enriched center and back to form regions that
37 indicate that transition between myosin IIC/myosin IIB expression is a critical feature of EMT that
38 n IIC is expressed in luminal cells, whereas myosin IIB expression is up-regulated in myoepithelial c
41 onses to Wnt5a involve recruitment of actin, myosin IIB, Frizzled 3, and melanoma cell adhesion molec
42 t did not affect protrusion, suggesting that myosin IIB functions in pulling the rear of the cell for
44 ced lamellar spreading, whereas depletion of myosin IIB impaired not only migration but also impaired
47 have found that MLC-dependent activation of myosin IIB in migrating cells is required to form an ext
50 ion analysis reveals for the first time that myosin IIB is associated with vimentin, linking vimentin
62 mediated traction force in growth cones from myosin IIB knock-out (KO) mice and compared them with ne
67 l family kinase substrates and suggests that myosin IIB may be regulated by tyrosine phosphorylation.
68 that the individual nonprocessive nonmuscle myosin IIB molecules form a highly processive unit when
69 issue-targeting techniques, we show that the myosin IIB motor protein complex is essential for both t
70 power stroke, specifically activating human myosin IIB (MYH10) and human myosin IIC (MYH14), but not
71 2, beta-catenin (CTNNB1), N-cadherin (CDH2), myosin IIB (MYOIIB), aPKCzeta, LGL, PAR3, pericentrin, P
74 ry of a viable therapeutic target, nonmuscle myosin IIB (NMIIB), a molecular motor that supports memo
75 chain IIB (NMHCIIB), a subunit of nonmuscle myosin IIB (NMIIB), as an ER stress-dependent interactin
76 of myo1b and the motor domain from nonmuscle myosin-IIb (nmMIIb) concentrates on actin filaments in r
79 te bending, whereas in the deep neural cells myosin IIB organizes a cortical actin cytoskeleton, whic
80 ic stem and progenitor cells, with polarized myosin-IIB promoting asymmetric self-renewal and constit
82 al for the mechanics of cell migration, with myosin IIB seeming to have a preferential role in the me
85 atin or selective RNA-mediated repression of myosin IIB significantly inhibits (P < 0.05) C. parvum c
88 netic characterization of a human non-muscle myosin IIB subfragment-1 construct produced in the bacul
90 in the offspring and increased the ratio of myosin IIb to other isoforms by 17.6 +/- 4.9% (P < 0.05)
91 hese results show that emerin functions with myosin IIB to polarize actin flow and nuclear movement i
92 e-Rap1 pathway as responsible for recruiting myosin IIB to the ZA and supporting contractile tension.
93 In contrast, genetic ablation of non-muscle myosin IIB was associated with a 60% decrease in mitocho
94 Immunofluorescence staining indicated that myosin IIB was localized preferentially along stress fib
96 s of CARMIL2 also caused decreased levels of myosin-IIB, which may contribute to the polarity phenoty
97 in COS7 cells disrupted the localization of myosin IIB without obviously affecting actin filaments.
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