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

15 ignificant differences between wild type and NEB KO.

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

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

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

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

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

21 Sensitivity to nocodazole also increased at NEB.

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

23 versus incomplete spindle pole separation at NEB.

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

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

26 ubunits, which are mostly cytoplasmic before NEB.

27 cytoplasm in a CRM1-dependent manner before NEB.

28 d for separating the centrosome pairs before NEB.

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

30 s that complete centrosome separation before NEB.

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

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

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

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

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

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

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

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

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

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

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

42 cortex prior to nuclear envelope breakdown (NEB).

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

44 ule targets upon nuclear envelope breakdown (NEB).

45 Continued repair was accompanied by NEB hyperplasia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 60% reduced force generating capacity of NM-NEB muscle and a leftward-shift of the force-sarcomere l

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

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

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

69 ressing stem cells function independently of NEB microenvironments.

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

71 <1 microM), CK-2066260 increased tension of NEB KO fibers to beyond that of WT fibers.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 67A also becomes kinetochore associated upon NEB, but the majority of the population relocalizes to t

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

101 n MT dynamics occurs tightly correlated with NEB.

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

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