ライフサイエンスコーパス: oligodendroglia

1 only along regions of the axon invested with oligodendroglia.

2 to initiate radial expansion, astrocytes, or oligodendroglia.

3 esting the functional importance of MAP1B in oligodendroglia.

4 ons, MAP1B recently was found in myelinating oligodendroglia.

5 ng a dominant-negative IFN-gamma receptor on oligodendroglia.

6 by the selective RNA-binding protein QKI in oligodendroglia.

7 to be a common mechanism in both neurons and oligodendroglia.

8 tical for the control of JHMV replication in oligodendroglia.

9 pressed the infection of astrocytes, but not oligodendroglia.

10 nd therein, is abundant in both neurones and oligodendroglia.

11 te electron dense cytoplasm derived from the oligodendroglia.

12 ise to cortical interneurons, astroglia, and oligodendroglia.

13 xons is controlled regionally along axons by oligodendroglia.

14 critical for control of viral replication in oligodendroglia.

15 ive astrocytes but had morphology typical of oligodendroglia.

16 -immunopositive inclusions in neurons and in oligodendroglia.

17 and blood-derived immune cells destroy brain oligodendroglia.

18 3'-phosphodiesterase, a specific marker for oligodendroglia.

19 ase labeled astrocytes, but not microglia or oligodendroglia.

20 d lesions, preferential differentiation into oligodendroglia accompanied by axonal preservation, and

21 n the injury site and hours to days later in oligodendroglia adjacent to and distant from the injury

22 Numerous PDGF-alphaR-positive oligodendroglia also colabel heavily with the nuclear ce

23 xons of retinal ganglion cells interact with oligodendroglia and become myelinated during normal mous

24 n (BMP) signaling inhibits the generation of oligodendroglia and enhances generation of astrocytes by

25 bit cortices almost devoid of astrocytes and oligodendroglia and exhibit neurodegeneration.

26 ese two genes sheds light on the ontogeny of oligodendroglia and genetic requirements for their devel

27 This finding contrasts with the loss of oligodendroglia and hypomyelination seen with Tsc1 or Ts

28 Oligodendroglia and microglia up-regulated B7-H1 followi

29 arge numbers of astrocytes, and in scattered oligodendroglia and monocytes/macrophages in both the in

30 lines of evidence now converge to implicate oligodendroglia and myelin in schizophrenia.

31 axons and axon terminals in association with oligodendroglia and neuron loss and slowly progressive m

32 of affected cell types, including astroglia, oligodendroglia and neurons.

33 known as SLC16A1), is highly enriched within oligodendroglia and that disruption of this transporter

34 of IFN-gamma localized almost exclusively to oligodendroglia and was associated with increased CD8+ T

35 minar disruption, astrogliosis, a paucity of oligodendroglia, and myelination defects.

36 ding ependymal cells, astrocytes, microglia, oligodendroglia, and rarely in neurons.

37 uced viral antigen in most cell types except oligodendroglia, and was associated with reduced demyeli

38 We also identified that oligodendroglia are the primary source of brain-derived

39 affect myelination, such as the function of oligodendroglia, are critical processes that could profo

40 mino-terminal region of Nogo-A, expressed by oligodendroglia, as necessary and sufficient to inhibit

41 sed approximately 2-fold each in endothelia, oligodendroglia, astrocytes, and axons of the optic nerv

42 funiculi, and there was a pronounced loss of oligodendroglia at 96 hours following treatment.

43 uced cell death, and increased the number of oligodendroglia at the site of injury.

44 cytolytic activity inhibited replication in oligodendroglia, but not astrocytes.

45 t MAP1B mRNA is markedly up-regulated in the oligodendroglia cell line CG4 upon induced differentiati

46 cells (OPCs), immature oligodendrocytes and oligodendroglia cell lines, where it interacts with a su

47 perimental downregulation of EXOSC8 in human oligodendroglia cells and in zebrafish induce a specific

48 characteristic for mature astroglia (GFAP), oligodendroglia (CNPase), or neurons (MAP2).

49 nding EGF immediately after injury decreases oligodendroglia death, enhances generation of new oligod

50 Myelin basic protein expression and CC1(+) oligodendroglia decreased after hyperoxia at P8, but ret

51 myelinating coronavirus, B7-H1 expression on oligodendroglia delays virus control, but also dampens c

52 lities, and morphologic abnormalities in the oligodendroglia demonstrated in schizophrenic brains are

53 strain of mouse hepatitis virus persists in oligodendroglia despite the presence of virus-specific C

54 Surprisingly, increased viral load in oligodendroglia did not affect the extent of myelin loss

55 Oligodendroglia did not reveal ERG immunoreactivity.

56 tes, we reveal that deletion of Tsc1 affects oligodendroglia differently depending on the stage of th

57 r advancing MAP1B expression specifically in oligodendroglia during brain development.

58 regulating translation of its bound mRNAs in oligodendroglia during early brain development.

59 our data demonstrate that TrkB expression in oligodendroglia exerts a direct effect on oligodendrocyt

60 s myelin protein zero and is up-regulated in oligodendroglia following axonal injury.

61 The role of oligodendroglia in axon function and neuron survival has

62 erging virus localized almost exclusively to oligodendroglia in B cell+ Ab-deficient mice, whereas it

63 ur finding of large numbers of proliferating oligodendroglia in MS brains expressing up-regulated PDG

64 part to widespread apoptosis of neurons and oligodendroglia in regions distant from and relatively u

65 ferate and differentiate into astrocytes and oligodendroglia in situ.

66 tion was observed in a significant number of oligodendroglia in the dorsal and ventral funiculi, and

67 Ab blockade of B7-H1 on oligodendroglia in vitro enhanced IFN-gamma secretion by

68 ve control levels during EAE, and numbers of oligodendroglia increased as well, but astrogenesis from

69 intercellular interactions between competing oligodendroglia influence the number and length of myeli

70 ceptor demonstrated that B7-H1 expression on oligodendroglia is predominantly regulated by IFN-gamma.

71 biology of myelin loss in which infection of oligodendroglia is required but not sufficient.

72 tion, although the cause of these changes in oligodendroglia is unknown.

73 zil also did not up-regulate myelin genes in oligodendroglia isolated from PPAR-beta(-/-) mice.

74 ompact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to

75 that express Flag-QKI-6 specifically in the oligodendroglia lineage, driven by the proteolipid prote

76 Oligodendroglia, microglia, and the majority of astrocyt

77 heir 3D relationships with other astrocytes, oligodendroglia, neurons, and vasculature of the brain s

78 However, inhibition of viral replication in oligodendroglia occurs via a perforin-independent mechan

79 lateral ventricles and many interfascicular oligodendroglia of forebrain fiber tracts.

80 nt at moderate to high levels in neurons and oligodendroglia of the adult human brain, at a level clo

81 ggests the functional requirement of Cdk5 in oligodendroglia (OL) and CNS myelin development.

82 lthough studies suggest a role for CXCL12 in oligodendroglia ontogeny in vitro, no studies have inves

83 at non-neuronal cells (microglia, astroglia, oligodendroglia) participate in the degenerative process

84 ly QKI-5, QKI-6, and QKI-7, are expressed in oligodendroglia progenitor cells (OPCs) prior to the ini

85 l expression, FMRP expression is detected in oligodendroglia progenitor cells (OPCs), immature oligod

86 se data indicate that IFN-gamma signaling by oligodendroglia reduces viral replication but affects bo

87 brain-derived Hp among brain cells and that oligodendroglia-released Hp plays protective roles again

88 mechanisms that control MAP1B expression in oligodendroglia remain elusive.

89 Knockdown of Scribble expression in cultured oligodendroglia results in disrupted morphology and myel

90 3'UTR of MAP1B mRNA interacts with QKI, and oligodendroglia-specific QKI-deficiency in the quakingvi

91 Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and

92 Oligodendroglia support axon survival and function throu

93 defines a new fundamental mechanism by which oligodendroglia support neurons and axons.

94 ck of functional ASPA, an enzyme enriched in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA)

95 nitor compartment produces new astroglia and oligodendroglia; the latter expand 10- to 18-fold postna

96 he many donor cells that differentiated into oligodendroglia-there appeared to be a shift in the fate

97 The functional consequence of excess MSP on oligodendroglia was determined in vitro by evaluating th

98 as mediator controlling JHMV replication in oligodendroglia was examined in mice deficient in IFN-ga

99 ction; however, although B7-H1 expression on oligodendroglia was prominent and sustained, it was sign

100 Oligodendroglia were immunolabeled with anti CA-II or an

101 GFP-expressing oligodendroglia were significantly more abundant in the

102 s more frequently observed in astrocytes and oligodendroglia, whereas NFIB expression was predominant