ライフサイエンスコーパス: gliogenesis

1 quiescent progenitor cells in posttraumatic gliogenesis.

2 h the induction of GLAST, an early marker of gliogenesis.

3 tate gyrus neurogenesis as well as forebrain gliogenesis.

4 nto post-mitotic neurons before the onset of gliogenesis.

5 nstructive role for Notch-Delta signaling in gliogenesis.

6 ating, undergoing neurogenesis or undergoing gliogenesis.

7 g1 regulates the switch from neurogenesis to gliogenesis.

8 cells remained high through the beginning of gliogenesis.

9 dition to its established role in peripheral gliogenesis.

10 hout SVZ formation and the postnatal peak of gliogenesis.

11 transcription factors that are necessary for gliogenesis.

12 during CNS development, particularly during gliogenesis.

13 d in vivo to prevent premature and excessive gliogenesis.

14 f neuronal migration, neurite outgrowth, and gliogenesis.

15 al zones of p27Kip1(-/-) mice at the peak of gliogenesis.

16 differentiated OLs during postnatal cortical gliogenesis.

17 reaches maximal levels during the period of gliogenesis.

18 ages of neurogenesis and the early stages of gliogenesis.

19 s and reduces neurogenesis at the expense of gliogenesis.

20 mounts of neurogenesis coexist with waves of gliogenesis.

21 target of mTORC1 and has been implicated in gliogenesis.

22 the neural tube during neurogenesis but not gliogenesis.

23 this relationship mediates the initiation of gliogenesis.

24 rol the temporal switch from neurogenesis to gliogenesis.

25 pression coordinates neurogenesis and cortex gliogenesis.

26 providing a powerful model for understanding gliogenesis.

27 -X3 and STAT3, which are known regulators of gliogenesis.

28 riod of neurogenesis followed by a period of gliogenesis.

29 umulation was still able to completely block gliogenesis.

30 g that yet-unidentified factors regulate gut gliogenesis.

31 ense of proliferation, function similarly in gliogenesis.

32 r the induction of neurogenesis, but not for gliogenesis.

33 of neural fate to cortical neurogenesis and gliogenesis.

34 therefore may play a role in injury-induced gliogenesis.

35 pment as a regulatory target for REPO during gliogenesis.

36 fects in neurogenesis, but severe defects in gliogenesis.

37 Later, during gliogenesis, activated Notch1 triggers a rapid cellular

38 underlie axonal sprouting, neurogenesis, and gliogenesis after stroke have recently been identified.

39 the greatest potential for neurogenesis and gliogenesis among all taxa, partly due to their indeterm

40 ypotheses that BMPs are required for enteric gliogenesis and act by promoting responsiveness of ENCDC

41 LIN28 expression caused a complete block of gliogenesis and an increase in neurogenesis.

42 However, the molecular cues that instruct gliogenesis and determine glial cell type are poorly und

43 itor character, and in some contexts promote gliogenesis and drive binary fate choices.

44 scade that operates during the initiation of gliogenesis and identifies a unique set of genes that re

45 Noggin, by suppressing subependymal gliogenesis and increasing progenitor availability, pote

46 te throughout the RMS and contribute to both gliogenesis and neurogenesis in the postnatal OB.

47 fic (anti-Hu) antigens, indicating that both gliogenesis and neurogenesis occurred after spinal cord

48 or the transcription factor Ascl1 in enteric gliogenesis and neurogenesis.

49 GGF2 stimulated gliogenesis and proliferation and inhibited glial cell d

50 ; overexpression of either factor suppresses gliogenesis and promotes neurogenesis; each can substitu

51 t affecting proliferation in early phases of gliogenesis, and a p27Kip1-independent event leading to

52 f prenatal nicotine on neurogenesis, but not gliogenesis, and also on the number of newly generated n

53 ic Lhx2 overexpression and suppress baseline gliogenesis, and also to compensate for loss of Lhx2 and

54 scribed is implicated in adult neurogenesis, gliogenesis, and angiogenesis.

55 ion as a key driver of NSC proliferation and gliogenesis, and identify a unique mechanism for conferr

56 base of neuronal columns at the beginning of gliogenesis, and later within the cortical layers, sugge

57 Neurogenesis, gliogenesis, and neural migration were altered during di

58 pression is both robust and sustained during gliogenesis, and the cis-regulatory region of the dvdup1

59 f these mice, whereas their distribution and gliogenesis appeared normal.

60 The role of Cdk5 in gliogenesis appeared specific to the early postnatal per

61 hat regulate peripheral nervous system (PNS) gliogenesis are incompletely understood.

62 tain neurogenic potential into the period of gliogenesis argues that they do not self-renew.

63 xiety, point to hippocampal neurogenesis and gliogenesis as key in this modulation, and underscore FG

64 identify a new mechanism regulating enteric gliogenesis as well as novel functions for Lgi4 regulati

65 d NFIA are key transcriptional regulators of gliogenesis associated with OL and AS.

66 nate ability of progenitors to switch toward gliogenesis at later passages.

67 amplifying progenitors, leading to increased gliogenesis at the expense of neurogenesis in neonatal a

68 ral crest, neuregulin instructively promotes gliogenesis, but how alternative fates are determined is

69 we demonstrate that oli is not required for gliogenesis, but plays pivotal roles in regulating larva

70 activation of the Notch pathway can promote gliogenesis by peripheral (PNS) and central (CNS) nervou

71 Neurogenesis and gliogenesis continue in discrete regions of the adult ma

72 required to maintain Sox9 expression during gliogenesis, demonstrating that Notch signaling promotes

73 sly been shown to be important for promoting gliogenesis during development, this is the first demons

74 olfactory bulb neurogenesis, or neurogenesis/gliogenesis during development.

75 ration of enteric neurons and for regulating gliogenesis during postnatal development.

76 2 mRNAs were found during the peak period of gliogenesis (E15-E19) in the telencephalic and mesenceph

77 monstrating extensive cell proliferation and gliogenesis following central nervous system (CNS) traum

78 pression enhances it, without any effects on gliogenesis from NPCs in vitro.

79 In examining the early stages of gliogenesis from progenitors in the SVZ, we noted that i

80 urce of Shh throughout both neurogenesis and gliogenesis, has not been clearly defined.

81 However, bHLH factors linked to gliogenesis have not been described.

82 with the ability of BMP signaling to promote gliogenesis, Hipk2(-/-) mutants show a significant incre

83 S development, neurogenesis largely precedes gliogenesis: how is this timing achieved?

84 enesis is delayed and reduced, and posterior gliogenesis impaired.

85 ury at the beginning (E11) and peak (E15) of gliogenesis in an avian tectal model of penetrating embr

86 his review examines the role of Notch during gliogenesis in both fruit flies and vertebrates, as well

87 have defined functions of MEK in regulating gliogenesis in developing cerebral cortex using loss- an

88 ively to instruct a cell-heritable switch to gliogenesis in neighboring stem cells.

89 ndergo primarily neurogenesis in the gut but gliogenesis in nerves.

90 Thus, the primary event controlling gliogenesis in neural progenitors is the transcription o

91 We show that Lhx2 regulates gliogenesis in part by regulating directly the expressio

92 tal alcohol exposure triggers an increase in gliogenesis in the adult motor cortex.

93 oss leads to increased NSC proliferation and gliogenesis in the brainstem, but not in the cortex.

94 o smoke diminishes neurogenesis and promotes gliogenesis in the dentate gyrus of adolescent rats.

95 ors and that levels of MEK activity regulate gliogenesis in the developing cortex.

96 priate amount and timing of neurogenesis and gliogenesis in the developing hippocampus.

97 a inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous

98 ecific temporal sequence of neurogenesis and gliogenesis in the developing spinal cord.

99 n controlling the timing of neurogenesis and gliogenesis in the developing ventral spinal cord.

100 and suppress the resulting enhanced level of gliogenesis in the hippocampus.

101 onmental factors can affect neurogenesis and gliogenesis in the hippocampus.

102 pathways that control perineural and cortex gliogenesis in the post-embryonic brain and have shown t

103 try, a reduction in striatal neuroglia, with gliogenesis in the subventricular zone and the somatosen

104 trolling the transition from neurogenesis to gliogenesis in the vertebrate CNS are incompletely under

105 hysiological Notch signaling is required for gliogenesis in vivo, independent of the role of Notch in

106 s hastened cell cycle withdrawal and blocked gliogenesis in vivo.

107 ther physiological Notch signaling regulates gliogenesis in vivo.

108 Plagl1 and Sox9 did not induce gliogenesis in wildtype animals, but nonetheless activat

109 induced by N1ICD electroporation, inhibited gliogenesis in wildtype animals, but rescued MG developm

110 tion of neurogenesis to a generic program of gliogenesis, in both astrocyte and oligodendrocyte VZ pr

111 We further demonstrate that Muller gliogenesis induced by misexpression of the potently gli

112 the mechanism by which Lgi4 promotes enteric gliogenesis involves binding the ADAM22 receptor.

113 The mechanism underlying the later onset of gliogenesis is poorly understood, although the cytokine-

114 Our findings demonstrate that mPFC gliogenesis is vulnerable to psychostimulant abuse and p

115 or proliferation rate, along with a delay in gliogenesis, is also observed in Gdf11(-/-) spinal cord

116 rmalization of drug-impaired neurogenesis or gliogenesis may help reverse neuroplasticity during abst

117 the molecular regulation of early postnatal gliogenesis may provide clues to normal and pathological

118 at long-term alterations in neurogenesis and gliogenesis might contribute to the observed hippocampal

119 y CNS; (2) during most of the year, baseline gliogenesis occurs mainly in the ependyma with substanti

120 ressed at early developmental stages, before gliogenesis or angiogenesis take place in the neural ret

121 ated by Lhx2: loss of either factor promotes gliogenesis; overexpression of either factor suppresses

122 during the wave of cortical and hippocampal gliogenesis (P2-P4), significantly fewer YFP+ cells were

123 he impact of Abeta pathology on neurogenesis/gliogenesis remains unclear.

124 Gliogenesis requires the careful orchestration of migrat

125 y migratory and metabolic roles during astro-gliogenesis, respectively.

126 n-specific increase in NSC proliferation and gliogenesis results from selective Akt hyperactivation.

127 electrophysiological changes observed during gliogenesis, suggesting that astrocytes undergoing secon

128 receptors can regulate both neurogenesis and gliogenesis that may be developmentally dependent.

129 tenuates self-renewal and induces precocious gliogenesis through modulation of the responsiveness to

130 ggest that Xenopus prune may regulate Muller gliogenesis through phosphodiesterase-mediated regulatio

131 The susceptibility of mPFC gliogenesis to even modest doses of methamphetamine coul

132 will peer through the lens of developmental gliogenesis to gain a clearer understanding of the proce

133 nvolved in cell adhesion, axon guidance, and gliogenesis upon silencing of FoxO6 We then show that Fo

134 This effect on cortical gliogenesis was accompanied by a decrease in YFP+ prolif

135 Enteric gliogenesis was analyzed in mice that overexpress the BM

136 In contrast, ENS gliogenesis was readily observed under steady-state cond

137 Neurogenesis, but not gliogenesis, was affected in HAP1-null neurospheres and

138 or that plays a crucial role in the onset of gliogenesis; we found that its induction is regulated by

139 ression promotes neurogenesis and suppresses gliogenesis, whereas loss of Lhx2 has the opposite effec

140 l densities peak during the latter stages of gliogenesis, which occurs in the SVZ of the lateral vent

141 A (NFIA) as a key regulator of developmental gliogenesis, while miR-223 has been shown to repress NFI

142 d voluntary exercise had profound effects on gliogenesis with differential regulation of oligodendroc