ライフサイエンスコーパス: NEB

1 NEB was successfully synthesized, and (18)F labeling inc

2 in is a sarcomeric protein that when absent (NEB KO mouse) or present at low levels (nemaline myopath

3 Accordingly, NEB and LMOD3 were reduced in skeletal muscle of both Kl

4 After NEB, the conserved polarity protein Partner of Inscuteab

5 s required to prevent mitotic collapse after NEB.

6 at the time of NEB or can be completed after NEB.

7 However, prophase cells just after NEB had significantly reduced levels (23%) which recover

8 chanisms driving centrosome separation after NEB are independent of the actin cytoskeleton and compen

9 of living klp61f mutants, reveal that, after NEB, KLP61F drives persistent MT bundling and the outwar

10 ively visualized and quantified by (18)F-AlF-NEB and (64)Cu-NEB PET.

11 ce to evaluate the distribution of (18)F-AlF-NEB, which was compared with in vitro-labeled mouse seru

12 he QM region, free energy estimates along an NEB optimized reaction path, and the inclusion of the in

13 ed, and the underlying mechanisms of AFB and NEB are poorly understood.

14 iquitin and Hsp104 to protein aggregates and NEB events, and the evolution of these structures during

15 on in two keratinocyte cell lines, HaCaT and NEB-1, by transient transfection of each of the four K6a

16 st; ASTA value; surface color intensity; and NEB, which was the lowest.

17 sistant (MHR) waterhemp populations (SIR and NEB) and HPPD inhibitor-sensitive populations (ACR and S

18 ignificant differences between wild type and NEB KO.

19 t submaximal activation in both wildtype and NEB KO fiber bundles and, importantly, that this troponi

20 submaximal activation levels in both WT and NEB KO fiber bundles.

21 neral effect that was present in both WT and NEB KO fiber bundles.

22 As NEB is one component of evolutionary fitness, our identi

23 These studies identify a BADJ-associated, NEB-independent, CCSP-expressing stem cell population in

24 T dynamics showed a similar abrupt change at NEB, basal rates of MT turnover (pre-NEB) increased post

25 Sensitivity to nocodazole also increased at NEB.

26 The abrupt reorganization of MTs at NEB was corroborated by anti-tubulin immunofluorescence

27 versus incomplete spindle pole separation at NEB.

28 Nudged elastic band (NEB) calculations for the nucleation processes toward Ag

29 experiments, along with nudged elastic band (NEB) calculations, suggest that cation motion in these m

30 ional theory (DFT), and Nudged Elastic Band (NEB) calculations, we show that the unique directionalit

31 The nudged elastic band (NEB) technique has been implemented in AMBER to calculat

32 ubunits, which are mostly cytoplasmic before NEB.

33 cytoplasm in a CRM1-dependent manner before NEB.

34 d for separating the centrosome pairs before NEB.

35 f aMTOCs failed to split and separate before NEB, and these entered mitosis with persistent monastral

36 s that complete centrosome separation before NEB.

37 id)-conjugated truncated form of Evans blue (NEB).

38 s that localize to the neuroepithelial body (NEB) and contribute to renewal of the proximal bronchiol

39 ed with either number of children ever born (NEB) or childlessness.

40 irth (AFB) and number of children ever born (NEB)-has a strong relationship with fitness, human devel

41 pathology) and 19 with normal elderly brain (NEB).

42 the time between nuclear envelope breakdown (NEB) and re-formation using parallel total internal refl

43 although mitotic nuclear envelope breakdown (NEB) appears important.

44 c collapse after nuclear envelope breakdown (NEB) characterized by defective chromosome condensation

45 ase cells before nuclear envelope breakdown (NEB) had high levels of MT polymer (62%) similar to that

46 ward flux before nuclear envelope breakdown (NEB) has not been examined.

47 te that prior to nuclear envelope breakdown (NEB) in Drosophila embryos, proper centrosome separation

48 e separation and nuclear-envelope breakdown (NEB) in HeLa cells.

49 ously shown that nuclear envelope breakdown (NEB) is not coordinated with centrosome separation and t

50 cortex prior to nuclear envelope breakdown (NEB).

51 TOC) well before nuclear envelope breakdown (NEB).

52 ule targets upon nuclear envelope breakdown (NEB).

53 ace color parameters, nonenzymatic browning (NEB), and the DPPH free radical-scavenging capacity of f

54 Nuclear envelope budding (NEB) is a recently discovered alternative pathway for nu

55 Continued repair was accompanied by NEB hyperplasia.

56 The set of low-energy paths found by NEB show that each G flips independently around the glyc

57 t range of species and that in S. cerevisiae NEB comprises a stress response aiding the transport of

58 In the yeast Saccharomyces cerevisiae, NEB events occur with higher frequency during heat shock

59 g the climbing image nudged elastic band (CI-NEB) method.

60 , 95% confidence interval [CI] 0.49-0.86; CR-NEB HR 0.69, 95% CI 0.50-0.96).

61 her incidence of vascular resection among CR-NEB and IR patients, no demographic, pathologic (eg, tum

62 and treatment characteristics, CR-EB and CR-NEB margin status were found to be independent predictor

63 patients with CR-EB (28 mo, P = 0.01) and CR-NEB resections (24 mo, P = 0.02) as compared with patien

64 complete resection achieved non-en-bloc (CR-NEB), and IR.

65 R-EB cohort comprised 749 (76%) patients, CR-NEB 159 patients (16%), and IR 78 patients (8%).

66 UM-22B tumor uptake of (64)Cu-NEB gradually increased with time (5.73 +/- 1.11 %ID/g a

67 namic and late-point static PET using (64)Cu-NEB in a UM-22B xenograft model.

68 d and quantified by (18)F-AlF-NEB and (64)Cu-NEB PET.

69 ells, LHK15 did not react with K15 deficient NEB-1, KEB-11, MCF-7 and SW13 cells expressing only exog

70 rs from wildtype (WT) and nebulin deficient (NEB KO) mice.

71 knocking down both cyclins A2 and B1 delayed NEB further.

72 er, knocking down cyclin A2 markedly delayed NEB, and knocking down both cyclins A2 and B1 delayed NE

73 exome sequencing revealed mutations in FMN2, NEB, and SYNE1 and a nonsense mutation in KMT2D, all sha

74 r therapy identification and development for NEB-related NM.

75 ividuals for AFB and 343,072 individuals for NEB.

76 hlight the importance of using GC-DFT and GC-NEB to accurately model electrocatalytic reactions.

77 transition states as a function of bias (GC-NEB) and applied it to produce a microkinetic model for

78 imarily caused by mutations in the NEB gene (NEB-NM) and with muscle myosin dysfunction as a major mo

79 -heterozygous mutations in the nebulin gene (NEB) cause typical nemaline myopathy (NM), a muscle diso

80 ants in ARHGAP27 were associated with higher NEB but shorter reproductive lifespan, suggesting a trad

81 icroscopy and tomography, we demonstrate how NEB is evolutionarily conserved from early protists to h

82 ial genotype-phenotype correlations in human NEB patients.

83 -relaxed state was significantly impaired in NEB-NM, inducing an aberrant increase in ATP consumption

84 lding, display the most dramatic increase in NEB, suggesting a causal link to protein quality control

85 lor quality, causing the maximum increase in NEB.

86 a subset of patients who harbor mutations in NEB and ACTA1, the lower force was associated with downw

87 hin filament myopathy caused by mutations in NEB, ACTA1, TPM2, TPM3, TNNT1, KBTBD13, KLHL40, and KLHL

88 ort machinery plays an unanticipated role in NEB-dependent nuclear entry.

89 Maximal active tension in NEB KO tibialis cranialis fibers in the absence of CK-20

90 Recessive mutations in nebulin (NEB) are the most common cause of NM affecting about 50%

91 Mutations in Nebulin (NEB), a giant filamentous protein localized in the sarco

92 ze a 2502 base pair deletion in the Nebulin (NEB) gene that results in Nemaline Myopathy, a 308,769 b

93 mere I band and A band and binds to nebulin (NEB), a protein frequently implicated in NM, as well as

94 nebulin-deficient mouse muscle and human NM-NEB muscle was observed, indicating that the nebulin kno

95 and non-uniform thin filament lengths in NM-NEB muscle compared with control muscle.

96 of the force-sarcomere length relation in NM-NEB muscle fibers.

97 ol muscle to approximately 0.75 microm in NM-NEB muscle.

98 nts with a well-defined nebulin mutation (NM-NEB), using a multidisciplinary approach to study thin f

99 60% reduced force generating capacity of NM-NEB muscle and a leftward-shift of the force-sarcomere l

100 uced nebulin levels in skeletal muscle of NM-NEB patients, with the most prominent reduction at nebul

101 but not wild-type cyclin B1, restored normal NEB timing in cyclin A2 knockdown cells.

102 However, activation of NEB-associated stem cells is unlikely to contribute to r

103 These mutants recapitulate most aspects of NEB-based NM, showing drastically reduced survival, defe

104 and, we tested its potency in the context of NEB-NM.

105 ense mutation p.Ser6366Ile and a deletion of NEB exon 55, the Compound-Het model that resembles typic

106 ressing stem cells function independently of NEB microenvironments.

107 e characterized five new zebrafish models of NEB-related NM.

108 , we found that KLHL40 promotes stability of NEB and LMOD3 and blocks LMOD3 ubiquitination.

109 <1 microM), CK-2066260 increased tension of NEB KO fibers to beyond that of WT fibers.

110 ration can be either complete at the time of NEB or can be completed after NEB.

111 We found that the timing of NEB was affected very little by knocking down cyclins B1

112 SNPicker uses the online NEB REBASE to automatically scan for all possible design

113 are significantly associated with AFB and/or NEB in a SNP-based genome-wide association study and 4 a

114 scle fiber bundles from a nebulin knock-out (NEB KO) mouse model.

115 ates of MT turnover (pre-NEB) increased post-NEB and then became slower later in mitosis.

116 ange at NEB, basal rates of MT turnover (pre-NEB) increased post-NEB and then became slower later in

117 Genetic ablation of Ascl1 prevented NEB formation and selectively interfered with the format

118 ; therefore, our data that KLHL40 stabilizes NEB and LMOD3 provide a potential basis for the developm

119 pendent fashion and is capable of supporting NEB if rendered constitutively nuclear.

120 daily, either nebulized and then swallowed (NEB) or as an oral viscous slurry (OVB), for 8 weeks.

121 OVB was more effective than NEB in reducing numbers of esophageal eosinophils in pat

122 conformational change also demonstrates that NEB can be used to discover non-trivial paths for macrom

123 We hypothesize that NEB is part of normal cellular physiology in a vast rang

124 Our mechanical studies revealed that NEB KO fibers had increased tension cost (5.9 versus 4.4

125 lonal analysis, and live imaging showed that NEB progenitors, initially distributed randomly, downreg

126 munopositive cells are proliferative; 3) the NEB microenvironment of both the steady-state and repair

127 -localization studies involving CCSP and the NEB-specific marker calcitonin gene-related peptide indi

128 Baseline eosinophil counts for the NEB and OVB groups were 101 and 83 (P = .62).

129 isease, primarily caused by mutations in the NEB gene (NEB-NM) and with muscle myosin dysfunction as

130 microm and 2.6 microm) and found that in the NEB KO fibers, CK-2066260 had a larger effect on calcium

131 Because of the large size of the NEB gene and lack of mutational hot spots, developing th

132 raphy, was higher for the OVB group than the NEB group (P < .005) and was inversely correlated with e

133 ram of gene expression, and reveals that the NEB microenvironment in the developing airways is a nich

134 These data suggest that the NEB microenvironment is a reservoir of pollutant-resista

135 now provide the following evidence that the NEB microenvironment serves as a source of airway progen

136 ivial paths for macromolecules and therefore NEB can be used as an exploratory method for predicting

137 s show that cyclin A2 is required for timely NEB, whereas cyclins B1 and B2 are not.

138 B1 translocates to the nucleus just prior to NEB in a cyclin A2-dependent fashion and is capable of s

139 acentriolar MTOC reassembled, and, prior to NEB, a functional amphiastral spindle formed.

140 67A also becomes kinetochore associated upon NEB, but the majority of the population relocalizes to t

141 alizes to centromeres and spindle poles upon NEB and remains at these sites throughout anaphase.

142 and MyBP-C1 were upregulated (x > 1) whereas NEB, gamma-ENO and EPSF were downregulated (x < 1) in wi

143 e remains a lack of understanding of whether NEB genotype influences nebulin function and NM-patient

144 n MT dynamics occurs tightly correlated with NEB.

145 levels (nemaline myopathy (NM) patients with NEB mutations) causes muscle weakness.

146 calize to the same spatial domain; 2) within NEB, both Clara cell secretory protein- and calcitonin g