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1 arlier and was more significant than that in cone cells.
2 which leads to reduction or complete loss of 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 lectroretinogram (ERG) responses and loss 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 lls is early onset, followed by the death of cone cells.
10  and delayed differentiation of non-neuronal cone cells.
11 cells, as well as the outer segments (OS) of cone cells.
12 they displayed a significant preservation of cone cells.
13 ction in photopic ERG amplitudes and loss of cone cells.
14 egeneration that first involved rod and then cone cells.
15 s used to measure ZBED4 mRNA levels in these cone cells.
16  of late-born RGC, amacrine, horizontal, and cone cells.
17 cribed specifically in R7 photoreceptors and cone cells.
18 of generating RGC, amacrine, horizontal, and cone cells.
19 he structural plasticity observed in rod and cone cells.
20  spatiotemporal expression of Delta in pupal cone cells.
21 roughout the subcellular compartments of the cone cells.
22 the organization and survival of pigment and cone cells.
23 translocation of cone arrestin in transduced cone cells.
24  show an early loss of rod cells followed by cone cells.
25 etinal analogue requires delineation also in cone cells.
26 ight-driven protein translocation in rod and cone cells.
27  in neuritic growth of isolated rod, but not cone, cells.
28                        Connecting with these cone cells, a multilayer neuro-network in the retina pro
29 ation-induced optical phase changes occur in cone cells and carry substantial information about spect
30 nal bifurcation of uncommitted ectoplacental cone cells and chorion progenitors.
31 gene is initially expressed in ectoplacental cone cells and chorionic plate, and later in the labyrin
32 age analysis approach to identify individual cone cells and evaluate their opsin expression from immu
33 differentiation of uncommitted ectoplacental cone cells and later for their specification towards tro
34 morphological and functional preservation of cone cells and maintenance of the retinal pigment epithe
35  proximal extensions of the four crystalline cone cells and of distal extensions of retinular cells R
36  resulting in abnormal patterns of bristles, cone cells and photoreceptors.
37                                              Cone cells and primary pigment cells oppose this signal
38  primary disease-causing molecular defect in cone cells and suggest that RDS-associated disease in pa
39 lts in the overproduction of photoreceptors, cone cells, and pigment cells and a corresponding reduct
40                                The number of cone cells appeared normal throughout the superior and i
41               By 2 years, almost all rod and cone cells are gone, and the residual neural retina is i
42                              Retinal rod and cone cells are not required for photoentrainment.
43                                     Although cone cells are resistant to cell damage induced by acute
44 nels in rod cells and cGMP-gated channels in cone cells are the primary calcium channels required for
45 olocalization of NSE with SV2 indicated that cone cells began to make synaptic contacts with horizont
46 mical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; these ON and OFF cone bipol
47 loped with a full complement of SDOCT bands; cone cell bodies >10 deep have thin, elongated, and tigh
48 , and synaptic pedicles and heavily staining cone cell bodies and pedicles.
49                         By 13 months, foveal cone cell bodies stack >6 deep, Henle fiber layer (HFL)
50  up Ca(2+) when it accumulates either in the cone cell body or outer segment.
51 iption repressor Tramtrack (TTK) is found in cone cells but not photoreceptor cells of the Drosophila
52 adherin within a sub-group of retinal cells (cone cells) causes them to form an overall shape that mi
53 that rd7 retinas have an increased number of cone cells compared to wild-type retinas.
54 l cells and a failure to consistently switch cone cell contacts from an anterior-posterior to an equa
55 e photooxidative stress, progressive loss of cone cells continued for up to 3 months after light expo
56           In addition, rod PDE6 expressed in cone cells couples to the light signaling pathway to pro
57 ese data support the hypothesis that gradual cone cell death after rod cell death in RP is due to oxi
58    Intravitreal 7m8-RdCVF slowed the rate of cone cell death and increased the amplitude of the photo
59 a remarkable effect both on the reduction of cone cell death and the maintenance of the overall struc
60 e and white light selectively induce rod and cone cell death in an in vitro model.
61 chanisms involving RIP kinase are crucial in cone cell death in inherited retinal degeneration, sugge
62 cting protein (RIP) kinase mediates necrotic cone cell death in rd10 mice, a mouse model of retinitis
63                             The mechanism of cone cell death is uncertain.
64                In retinitis pigmentosa (RP), cone cell death precedes rod cell death.
65 sms and features of subsequent nonautonomous cone cell death remain largely unknown.
66                                              Cone cell death was analyzed by double labeling with TdT
67  models of retinitis pigmentosa is linked to cone cell death, which can be delayed by systemic admini
68  but later declined, consistent with delayed cone cell death.
69 loped a quantitative, probabilistic model of cone cell decisions in the retinal tissue based on thyro
70 how that loss of Dicer1 leads to early-onset cone cell degeneration and suggest that Dicer1 is essent
71                        With time this causes cone cell degeneration.
72              Immunohistochemical staining of cone cells demonstrates that rd7 retinas have an increas
73 this was accompanied by a 2-fold increase in cone cell density and a 50% increase in medium-wavelengt
74 pography of residual cone function parallels cone cell density.
75 hich may be relevant to their function or to cone cell development, and that differences in this post
76 pe due to a disorganized retina and aberrant cone cell differentiation, which leads to reduction or c
77 g that was required for R7 specification and cone cell differentiation.
78                                           In cone cells, either GRK1, GRK7, or both, depending on the
79 s this issue, we used the fly eye, where the cone cells exchange neighbors over ~10 h to shape the le
80 cone spectral sensitivities and activating M cone cells exclusively.
81 d cone, as revealed by expression of the red cone cell fate determinants thyroid hormone receptor bet
82 r sensitivity in ESCS may be due to abnormal cone cell fate determination during retinal development.
83 ptional regulators in determining rod versus cone cell fate in photoreceptor precursors during the de
84 Notch, which is important in determining the cone cell fate in the Drosophila eye.
85 les but is not required for induction of the cone cell fate.
86 ombinatorial, manner in the specification of cone-cell fate.
87 sed them to adopt R7 fates or, occasionally, cone cell fates.
88           The types of cues used by maturing cone cells for their eventual sclerad location remain to
89 hat GC1-GCAP1 interactions are essential for cone cell function in mice and that GC2 and GCAP2 activi
90 psin coding sequence, suggesting the loss of cone cell function, but maintenance of non-photosensitiv
91                           The shaping of the cone cell group and packing of its components precisely
92 eptor, Notch, and intact primary pigment and cone cells have been implicated in survival or death sig
93 aining protein 1 (GTF2IRD1) in maintaining M cone cell identity and function as well as rod function.
94 ceptor cells, and TTK does not accumulate in cone cells if both PHYL and SINA are present.
95          In this study we use the developing cone cell in the Drosophila visual system to elucidate t
96 ated expression of GC1 in a subpopulation of cone cells in postnatal GC1 knockout retina restores lig
97 ctors required for terminal determination of cone cells in the eye.
98 the first demonstration of a requirement for cone cells in the ommatidial rotation aspect of PCP.
99  of mid-wavelength opsin and the presence of cone cells in the ONL and the choroidal circulation were
100                                              Cone cells in the periphery had remnants of inner segmen
101 of cone arrestin is one of the phenotypes of cone cells in this retina: the cone arrestin in these ce
102 maging methods permit visualization of human cone cells in vivo but have only recently achieved suffi
103 ncreased the number of varicosities, whereas cone cells increased process growth.
104 irless and the Enhancer of split-Complex for cone cell induction.
105 ions of P21 mouse retina were used to assess cone cell integrity by visualizing opsin localization.
106                        Second, we found that cone cell intercalation is regulated by the Notch pathwa
107 EGF receptor, Notch, and primary pigment and cone cells into a single pathway that affected caspase a
108             The rod PDE6 enzyme expressed in cone cells is active and contributes to the hydrolysis o
109                                           In cone cells, L-type channel antagonists caused only modes
110 d how the absorption of a photon in a rod or cone cell leads to the generation of the amplified neura
111 a demonstrated that loss of Tmem30a in mouse cone cells leads to mislocalization of cone opsin, loss
112 ism for supporting cone function in the 661W cone cell line.
113 tinoblastoma cells to differentiate toward a cone cell lineage while selectively leading other cells
114 inner and outer segments of remaining cones; cone cell loss also was dramatic in young mice lacking R
115  results of this study show that the rate of cone cell loss in the GC1 KO mouse is comparable to that
116                                              Cone cell loss was exacerbated in the inferior retinal r
117 rm cone outer segment shortening rather than cone cell loss.
118        Light damage resulted in rod, but not cone, cell loss.
119 delayed, so that, at P12, positioning of the cone cell nuclei within the ONL was still quite irregula
120 the outer border of the ONL, the location of cone cell nuclei, at 1 and 2 days after injection of FeS
121 er and inner segment length was reduced, and cone cell numbers were reduced, as were scotopic and pho
122 calization in the photoreceptors and reduced cone cell numbers, and led to progressive loss of vision
123  restores cone arrestin translocation in the cone cells of postnatal GC1 knockout mouse retina.
124 ed enhancer that activates the dPax2 gene in cone cells of the developing Drosophila eye.
125 ys directly regulate D-Pax2 transcription in cone cells of the Drosophila eye disc.
126                                  The rod and cone cells of the mammalian retina are the principal pho
127 one cell survival was determined by counting cone cells on flat-mounted retinas.
128  whereas mouse Ubap1l is highly expressed in cone cells only.
129                                          The cone cell phenotype is sensitive to the level of rugose
130  appears to be distinct from that of rod and cone cell photopigments for vision.
131                                  How rod and cone cells prevent the accumulation of 11-cis-retinal in
132 or pigment granules in the extensions of the cone cell projections are present above the BM in T. eva
133 may function by regulating genes involved in cone cell proliferation, and mutations in this gene lead
134                                           In cone cells, quantitative analysis showed that NO or cGMP
135                              Delayed loss of cone cells, remaining rod cells, and choroidal circulati
136 ization of gene editing in the macula and of cone cell replacement in general.
137  vector and to localize cone arrestin within cone cells, respectively.
138 idermis, but only a moderate effect on petal cone cell ridges.
139                                 We show that cone cell shapes depend little on adhesion bonds and mos
140          Finally, whole retinas and isolated cone cells show increased photosensitivity following exp
141 sparkling, a Notch- and EGFR/MAPK-regulated, cone cell-specific enhancer of the Drosophila Pax2 gene,
142 ifferentiation but also promotes nonneuronal cone cell specification in early Drosophila eye developm
143                  Detailed analysis of R7 and cone cell specification reveals that extramacrochaetae a
144 l. exploit two different pathways to promote cone cell survival and preserve vision in murine retinal
145 fic for cone transducin were used to examine cone cell survival in the GC1 KO retina at 4, 5, 9, 16,
146                                              Cone cell survival was determined by counting cone cells
147                                              Cone cell survival was determined by counting cone opsin
148  6 months of age; however, 40% to 70% of the cone cells survived in the superior region at this age.
149                                              Cone cell terminals, however, are relatively inactive.
150 ted channels, known to be present on rod and cone cell terminals, respectively, were used to block ca
151 se findings, which show that fully developed cone cells that have developed in the absence of GC1 can
152                    The Notch signal from the cone cells then functions in the direct specification of
153 MP causes neuritic sprouting in rod, but not cone, cells through the AC-PKA-CREB pathway known to be
154 al lens with normal refractive power, and in cone cells to enable complete extension of the photorece
155 es coexpress both S and M opsins in a common cone cell type throughout the retina.
156 w progression, differentiation of R4, R7 and cone cell types, and rotation of ommatidial clusters.
157 ng natural noise stimuli and preservation of cone cells upon spectral domain optical coherence tomogr
158 yramids) was found in layer II/III; another (cone cells) was found in clusters spanning layer VI thro
159 kout mouse (Dicer CKO) to delete Dicer1 from cone cells, we show that cone photoreceptor cells degene
160 or cone arrestin in transduced and wild-type cone cells were indistinguishable after dark and light a
161                               Single rod and cone cells were isolated by micromanipulation, and the a
162                           Individual rod and cone cells were lysed for RT-PCR and Southern blot analy
163             Axonal extensions of NSE-labeled cone cells were shown to interact with those of differen
164              A total of 5400 and 7252 margin cones cells were found in each of two monkeys.
165 d LS neurons (stellates, small pyramids, and cone cells) were encountered in layers II/III and VI of
166 s individual cone dysfunction by stimulating cone cells with flashes of light and measuring nanometer
167 th CRX predominantly in the inner segment of cone cells, with additional costaining in the outer nucl
168                          Analysis of rod and cone cells within the photoreceptor layer showed a distu

 
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