ライフサイエンスコーパス: axoplasm

1 ed anterograde transport when added to squid axoplasm.

2 located within juxtaparanodal and internodal axoplasm.

3 d in nodal axoplasm compared with internodal axoplasm.

4 hondrial stationary sites in nodal/paranodal axoplasm.

5 re of PAD inhibited anterograde FAT in squid axoplasm.

6 hondrial distribution and transport in nodal axoplasm.

7 /internodal axoplasm than in nodal/paranodal axoplasm.

8 ced by 86% in 1-mo-old P0-CNS juxtaparanodal axoplasm.

9 ected a single approximately 220 kDa band in axoplasm.

10 liposomes and soluble components from squid axoplasm.

11 u hybridization and microaspiration of their axoplasm.

12 posomes, isolated axonal vesicles, and whole axoplasm.

13 ntibodies on organelle transport in extruded axoplasm.

14 er mg of protein 40-fold higher than that of axoplasm.

15 nse core vesicles along the perimeter of the axoplasm.

16 patial distribution of puncta in subcortical axoplasm.

17 Of the total nonmuscle myosin II in axoplasm, 43.2% copurified with organelles in the 15% su

18 er (M) axon was evaluated in isolated M-cell axoplasm after (1) staining with YOYO-1 and (2) inspecti

19 Our method for isolating CNS axoplasm also represents a new tool to study axon biolog

20 is approximately 235-kDa protein (p235) from axoplasm and demonstrate that it is a myosin, because it

21 entially at the surface boundary of isolated axoplasm and distributed longitudinally at random interv

22 hibit both fast axonal transport in isolated axoplasm and elongation of neuritic processes in intact

23 the 72-kDa radiolabeled band in heat-shocked axoplasm and glial sheath samples comigrated with a band

24 recovery of normal elemental composition in axoplasm and mitochondria of small, medium and large dia

25 utant FUS-induced impairment of FAT in squid axoplasm and of axonal outgrowth in mammalian primary mo

26 lass of unconventional myosins is present in axoplasm and optic lobes.

27 idence, we conclude that the p196 present in axoplasm and purified from optic lobes is a squid homolo

28 rade, but not retrograde, transport in squid axoplasm and reduced the amount of kinesin bound to MBOs

29 After crush injury, LRP-1 is lost from the axoplasm and substantially upregulated in Schwann cells.

30 kDa, 84 kDa, and 87 kDa appeared in both the axoplasm and the sheath.

31 In extruded axoplasm, antibody disruption of kinesin or the dynactin

32 that neurofilament-dependent structuring of axoplasm arises through an "outside-in" signaling cascad

33 This myosin is also present in axoplasm, as determined by two independent criteria.

34 egeneration were prominent in juxtaparanodal axoplasm at 1 mo of age.

35 The herniated axoplasm became directed back towards the internode, for

36 signals were also distributed in peripheral axoplasm below the matrix.

37 inhibited fast axonal transport in isolated axoplasm by decreasing both the number and velocity of v

38 ions are swept out of the membrane into the axoplasm by hyperpolarization.

39 ort speed was significantly reduced in nodal axoplasm compared with internodal axoplasm.

40 ow-contrast background, showed that isolated axoplasm contained characteristic 25 nm P signals, which

41 These data indicate that MGA axoplasm contains relatively high levels of constitutive

42 anges included a significant decrease in the axoplasm diameter of myelinated neurons and an increase

43 tation of RhoA and phosphorylated cofilin in axoplasm-enriched samples from injured optic nerve.

44 We have used iTRAQ to compare axoplasm-enriched samples from naive vs injured optic ne

45 Furthermore, axoplasm ensheathed by 65% of the CNS incisures examined

46 have developed a novel method to enrich for axoplasm from rodent optic nerve and characterised the e

47 fast axonal transport along microtubules in axoplasm from squid giant axons.

48 directly inhibit fast axonal transport using axoplasm from the squid giant axon and suggest that axon

49 Organelles in the axoplasm from the squid giant axon move along exogenous

50 In vitro motility assays performed with axoplasm from the squid giant axon showed a requirement

51 Vesicle motility assays in isolated squid axoplasm further demonstrated that both mutant merlin an

52 Axoplasm, however, contained the constitutively active f

53 otubule packing density), fractional area of axoplasm in the nerve fiber bundle (f), mitochondrial fr

54 atrix, and a confluent volume of subcortical axoplasm integrated through an actin cytoskeleton.

55 Our detergent-free method draws axoplasm into a dehydrated hydrogel of the polymer poly(

56 indings were derived from examination of the axoplasm isolated from myelinated fibers as axoplasmic w

57 th in transgenic mice and, more recently, in axoplasm isolated from squid giant axons.

58 sufficient for activation of this pathway in axoplasms isolated from squid giant axons.

59 Both oAbeta and CK2 treatment of axoplasm led to increased phosphorylation of kinesin-1 l

60 l spacing of plaques around the periphery of axoplasm near the axon-myelin border are likely reasons

61 tive HSP 70s and that, after heat shock, MGA axoplasm obtains inducible HSPs of 72 kDa, 84 kDa, and 8

62 perisynaptic/extrasynaptic membranes and the axoplasm of 13% of excitatory-like, presumably glutamate

63 s, the mutant virus failed to enter into the axoplasm of ganglionic neurons.

64 proximately 1-3% of the total protein in the axoplasm of MGAs.

65 resulting in accumulation of free NE in the axoplasm of sympathetic nerves.

66 without affecting the rate of production of axoplasm or microtubule polymer, and without decreasing

67 Despite the extensive pruning, total axoplasm per neuron increases as axons elongate, thicken

68 ime analysis of vesicle mobility in isolated axoplasms perfused with oAbeta showed bidirectional axon

69 Western blots of axoplasm probed with an affinity purified antibody to ch

70 t axon extension but does not interfere with axoplasm production.

71 eriments presented here using isolated squid axoplasm reveal inhibition of FAT as a common toxic effe

72 The amount of heat-induced proteins in axoplasm samples was greater after a 2-hour heat shock t

73 re also distributed in a delimited volume of axoplasm, subjacent to the plaque.

74 ficantly larger in juxtaparanodal/internodal axoplasm than in nodal/paranodal axoplasm.

75 In squid axoplasm, the M1 peptide dramatically inhibits fast axon

76 hibits FAT in a human cell line and in squid axoplasm through a pathway that involves activation of c

77 e for neurofilament-dependent structuring of axoplasm through intra-axonal crossbridging between adja

78 ning physiological saline; (2) we exposed GA axoplasm to Ca2+-containing salines and observed that me

79 gh spectrin and ank2-L, extend deep into the axoplasm to promote microtubule organization.

80 To deliver HSV into the axoplasm, viral particles stripped of their envelopes by

81 ffusion coefficient of the moving tubulin in axoplasm was 8.6 micrometer(2)/s compared with only 0.43

82 Axoplasm was fractionated through a four-step sucrose gr

83 did form in severed GAs after >99% of their axoplasm was removed by internal perfusion; (3) we exami

84 Using isolated squid axoplasm, we show that MPP+ produces significant alterat

85 and minus-end vesicle populations from squid axoplasm were isolated from each other by selective extr

86 ired anterograde and retrograde FAT in squid axoplasm, whereas FUS WT had no effect.

87 Treatment of axoplasm with antibodies to the p150(Glued) subunit of d

88 Furthermore, perfusion of axoplasms with active CK2 mimics the inhibitory effects