ライフサイエンスコーパス: cone cell

1 etinal analogue requires delineation also in cone cells.

2 arlier and was more significant than that in cone cells.

3 varicosity formation and synthesis of SV2 in cone cells.

4 uces neighboring cells to become nonneuronal cone cells.

5 on tonic synaptic release of glutamate from cone cells.

6 cells, as well as the outer segments (OS) of cone cells.

7 ells and a second affected the production of cone cells.

8 No expression of the gene was detected in cone cells.

9 they displayed a significant preservation of cone cells.

10 ction in photopic ERG amplitudes and loss of cone cells.

11 lectroretinogram (ERG) responses and loss of cone cells.

12 egeneration that first involved rod and then cone cells.

13 s used to measure ZBED4 mRNA levels in these cone cells.

14 of late-born RGC, amacrine, horizontal, and cone cells.

15 cribed specifically in R7 photoreceptors and cone cells.

16 of generating RGC, amacrine, horizontal, and cone cells.

17 he structural plasticity observed in rod and cone cells.

18 spatiotemporal expression of Delta in pupal cone cells.

19 lls is early onset, followed by the death of cone cells.

20 roughout the subcellular compartments of the cone cells.

21 the organization and survival of pigment and cone cells.

22 translocation of cone arrestin in transduced cone cells.

23 show an early loss of rod cells followed by cone cells.

24 ight-driven protein translocation in rod and cone cells.

25 which leads to reduction or complete loss of cone cells.

26 in neuritic growth of isolated rod, but not cone, cells.

27 gene is initially expressed in ectoplacental cone cells and chorionic plate, and later in the labyrin

28 proximal extensions of the four crystalline cone cells and of distal extensions of retinular cells R

29 resulting in abnormal patterns of bristles, cone cells and photoreceptors.

30 Cone cells and primary pigment cells oppose this signal

31 primary disease-causing molecular defect in cone cells and suggest that RDS-associated disease in pa

32 lts in the overproduction of photoreceptors, cone cells, and pigment cells and a corresponding reduct

33 The number of cone cells appeared normal throughout the superior and i

34 By 2 years, almost all rod and cone cells are gone, and the residual neural retina is i

35 Retinal rod and cone cells are not required for photoentrainment.

36 Although cone cells are resistant to cell damage induced by acute

37 nels in rod cells and cGMP-gated channels in cone cells are the primary calcium channels required for

38 olocalization of NSE with SV2 indicated that cone cells began to make synaptic contacts with horizont

39 mical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; these ON and OFF cone bipol

40 loped with a full complement of SDOCT bands; cone cell bodies >10 deep have thin, elongated, and tigh

41 , and synaptic pedicles and heavily staining cone cell bodies and pedicles.

42 By 13 months, foveal cone cell bodies stack >6 deep, Henle fiber layer (HFL)

43 up Ca(2+) when it accumulates either in the cone cell body or outer segment.

44 iption repressor Tramtrack (TTK) is found in cone cells but not photoreceptor cells of the Drosophila

45 adherin within a sub-group of retinal cells (cone cells) causes them to form an overall shape that mi

46 that rd7 retinas have an increased number of cone cells compared to wild-type retinas.

47 l cells and a failure to consistently switch cone cell contacts from an anterior-posterior to an equa

48 e photooxidative stress, progressive loss of cone cells continued for up to 3 months after light expo

49 In addition, rod PDE6 expressed in cone cells couples to the light signaling pathway to pro

50 ese data support the hypothesis that gradual cone cell death after rod cell death in RP is due to oxi

51 Intravitreal 7m8-RdCVF slowed the rate of cone cell death and increased the amplitude of the photo

52 a remarkable effect both on the reduction of cone cell death and the maintenance of the overall struc

53 e and white light selectively induce rod and cone cell death in an in vitro model.

54 chanisms involving RIP kinase are crucial in cone cell death in inherited retinal degeneration, sugge

55 cting protein (RIP) kinase mediates necrotic cone cell death in rd10 mice, a mouse model of retinitis

56 The mechanism of cone cell death is uncertain.

57 In retinitis pigmentosa (RP), cone cell death precedes rod cell death.

58 sms and features of subsequent nonautonomous cone cell death remain largely unknown.

59 Cone cell death was analyzed by double labeling with TdT

60 models of retinitis pigmentosa is linked to cone cell death, which can be delayed by systemic admini

61 but later declined, consistent with delayed cone cell death.

62 With time this causes cone cell degeneration.

63 Immunohistochemical staining of cone cells demonstrates that rd7 retinas have an increas

64 this was accompanied by a 2-fold increase in cone cell density and a 50% increase in medium-wavelengt

65 pography of residual cone function parallels cone cell density.

66 pe due to a disorganized retina and aberrant cone cell differentiation, which leads to reduction or c

67 In cone cells, either GRK1, GRK7, or both, depending on the

68 r sensitivity in ESCS may be due to abnormal cone cell fate determination during retinal development.

69 ptional regulators in determining rod versus cone cell fate in photoreceptor precursors during the de

70 Notch, which is important in determining the cone cell fate in the Drosophila eye.

71 les but is not required for induction of the cone cell fate.

72 ombinatorial, manner in the specification of cone-cell fate.

73 sed them to adopt R7 fates or, occasionally, cone cell fates.

74 The types of cues used by maturing cone cells for their eventual sclerad location remain to

75 hat GC1-GCAP1 interactions are essential for cone cell function in mice and that GC2 and GCAP2 activi

76 psin coding sequence, suggesting the loss of cone cell function, but maintenance of non-photosensitiv

77 The shaping of the cone cell group and packing of its components precisely

78 eptor, Notch, and intact primary pigment and cone cells have been implicated in survival or death sig

79 aining protein 1 (GTF2IRD1) in maintaining M cone cell identity and function as well as rod function.

80 ceptor cells, and TTK does not accumulate in cone cells if both PHYL and SINA are present.

81 In this study we use the developing cone cell in the Drosophila visual system to elucidate t

82 ated expression of GC1 in a subpopulation of cone cells in postnatal GC1 knockout retina restores lig

83 ctors required for terminal determination of cone cells in the eye.

84 the first demonstration of a requirement for cone cells in the ommatidial rotation aspect of PCP.

85 of mid-wavelength opsin and the presence of cone cells in the ONL and the choroidal circulation were

86 Cone cells in the periphery had remnants of inner segmen

87 of cone arrestin is one of the phenotypes of cone cells in this retina: the cone arrestin in these ce

88 ncreased the number of varicosities, whereas cone cells increased process growth.

89 irless and the Enhancer of split-Complex for cone cell induction.

90 ions of P21 mouse retina were used to assess cone cell integrity by visualizing opsin localization.

91 EGF receptor, Notch, and primary pigment and cone cells into a single pathway that affected caspase a

92 The rod PDE6 enzyme expressed in cone cells is active and contributes to the hydrolysis o

93 In cone cells, L-type channel antagonists caused only modes

94 d how the absorption of a photon in a rod or cone cell leads to the generation of the amplified neura

95 a demonstrated that loss of Tmem30a in mouse cone cells leads to mislocalization of cone opsin, loss

96 ism for supporting cone function in the 661W cone cell line.

97 tinoblastoma cells to differentiate toward a cone cell lineage while selectively leading other cells

98 inner and outer segments of remaining cones; cone cell loss also was dramatic in young mice lacking R

99 results of this study show that the rate of cone cell loss in the GC1 KO mouse is comparable to that

100 Cone cell loss was exacerbated in the inferior retinal r

101 Light damage resulted in rod, but not cone, cell loss.

102 delayed, so that, at P12, positioning of the cone cell nuclei within the ONL was still quite irregula

103 the outer border of the ONL, the location of cone cell nuclei, at 1 and 2 days after injection of FeS

104 er and inner segment length was reduced, and cone cell numbers were reduced, as were scotopic and pho

105 calization in the photoreceptors and reduced cone cell numbers, and led to progressive loss of vision

106 restores cone arrestin translocation in the cone cells of postnatal GC1 knockout mouse retina.

107 ed enhancer that activates the dPax2 gene in cone cells of the developing Drosophila eye.

108 ys directly regulate D-Pax2 transcription in cone cells of the Drosophila eye disc.

109 The rod and cone cells of the mammalian retina are the principal pho

110 one cell survival was determined by counting cone cells on flat-mounted retinas.

111 The cone cell phenotype is sensitive to the level of rugose

112 appears to be distinct from that of rod and cone cell photopigments for vision.

113 How rod and cone cells prevent the accumulation of 11-cis-retinal in

114 may function by regulating genes involved in cone cell proliferation, and mutations in this gene lead

115 In cone cells, quantitative analysis showed that NO or cGMP

116 Delayed loss of cone cells, remaining rod cells, and choroidal circulati

117 vector and to localize cone arrestin within cone cells, respectively.

118 idermis, but only a moderate effect on petal cone cell ridges.

119 We show that cone cell shapes depend little on adhesion bonds and mos

120 Finally, whole retinas and isolated cone cells show increased photosensitivity following exp

121 sparkling, a Notch- and EGFR/MAPK-regulated, cone cell-specific enhancer of the Drosophila Pax2 gene,

122 ifferentiation but also promotes nonneuronal cone cell specification in early Drosophila eye developm

123 Detailed analysis of R7 and cone cell specification reveals that extramacrochaetae a

124 l. exploit two different pathways to promote cone cell survival and preserve vision in murine retinal

125 fic for cone transducin were used to examine cone cell survival in the GC1 KO retina at 4, 5, 9, 16,

126 Cone cell survival was determined by counting cone cells

127 Cone cell survival was determined by counting cone opsin

128 6 months of age; however, 40% to 70% of the cone cells survived in the superior region at this age.

129 Cone cell terminals, however, are relatively inactive.

130 ted channels, known to be present on rod and cone cell terminals, respectively, were used to block ca

131 se findings, which show that fully developed cone cells that have developed in the absence of GC1 can

132 The Notch signal from the cone cells then functions in the direct specification of

133 MP causes neuritic sprouting in rod, but not cone, cells through the AC-PKA-CREB pathway known to be

134 es coexpress both S and M opsins in a common cone cell type throughout the retina.

135 w progression, differentiation of R4, R7 and cone cell types, and rotation of ommatidial clusters.

136 ng natural noise stimuli and preservation of cone cells upon spectral domain optical coherence tomogr

137 yramids) was found in layer II/III; another (cone cells) was found in clusters spanning layer VI thro

138 or cone arrestin in transduced and wild-type cone cells were indistinguishable after dark and light a

139 Single rod and cone cells were isolated by micromanipulation, and the a

140 Individual rod and cone cells were lysed for RT-PCR and Southern blot analy

141 Axonal extensions of NSE-labeled cone cells were shown to interact with those of differen

142 A total of 5400 and 7252 margin cones cells were found in each of two monkeys.

143 d LS neurons (stellates, small pyramids, and cone cells) were encountered in layers II/III and VI of

144 th CRX predominantly in the inner segment of cone cells, with additional costaining in the outer nucl