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1 f cone proteins, and decreased activation of Muller glial cells.
2 tion of rod photoreceptors at the expense of Muller glial cells.
3 er modified LDL induces apoptosis in retinal Muller glial cells.
4 differentiation and/or survival of postnatal Muller glial cells.
5 ordinately switched from horizontal cells to Muller glial cells.
6 ted locus of Chx10 expression in a subset of Muller glial cells.
7 progenitor cells or partially differentiated Muller glial cells.
8 tor cells at the expense of interneurons and Muller glial cells.
9 as by coculturing with either astrocytes or Muller glial cells.
10 ipal K(+) channel subunit expressed in mouse Muller glial cells.
11 sed in the retinal pigment epithelium and in Muller glial cells.
12 clones containing amacrine interneurons and Muller glial cells.
13 the receptor in the horizontal, bipolar and Muller glial cells.
14 tinal pigment epithelium and for neighboring Muller glial cells.
15 ence some properties of rods or the adjacent Muller glial cells.
16 hes off the expression of genes critical for Muller glial cells.
17 n and colocalized with endothelial cells and Muller glial cells.
18 zed cycle, which appears to involve adjacent Muller (glial) cells.
19 na regeneration in zebrafish and mice is the Muller glial cell, a malleable cell type that is amenabl
20 the retinal pigment epithelium and rlbp1b in Muller glial cells allowed us to create intrinsically ce
21 n central carbon metabolism in primary mouse Muller glial cells and a human Muller glia cell line (M1
22 uggest that a Cx43 isoform may be present in Muller glial cells and neurons of the distal catfish ret
25 , has been linked to a loss in the retina of Muller glial cells and the amino acid serine, synthesize
27 poproteins might allow communication between Muller glial cells and the neurons that they support, in
29 , appearance of prominent GFAP expression in Muller glial cells, and a fourfold increase in the numbe
30 inwardly rectifying K+ (KIR) channels of the Muller (glial) cells are pathways for the redistribution
38 r cells significantly increases the ratio of Muller glial cells as observed by modulation of NM23 act
39 laminin beta2 is present before the birth of Muller glial cells; at this stage of development, lamini
42 B2 in adult mouse photoreceptors, but not in Muller glial cells, causes sporadic loss of adhesion bet
44 reservation of the inner retinal lamination, Muller glial cell disorganization, and increased number
45 ng injury-induced Muller glia, and that each Muller glial cell divides asymmetrically only once to pr
46 produces rod photoreceptors from infrequent Muller glial cell division, yielding neuronal progenitor
47 In this report, we examine the genesis of Muller glial cells during zebrafish (Danio rerio) eye de
48 and glial cell fate and develop a mixed rod/Muller glial cells electrophysiological fingerprint, rev
50 predominantly localized in nuclei of retinal Muller (glial) cells, ganglion cells, and astrocytes, bu
52 dentify the molecular machinery that defines Muller glial cell identity and function, single cell gen
53 tion of the Notch signaling pathway restores Muller glial cell identity to Sox2 mutant cells, but doe
54 brillary acidic protein) was observed within Muller glial cells in areas of retina overlying drusen.
55 e receptor-inducing activity) is produced by Muller glial cells in culture, because significant activ
57 rtially rescue the production of bipolar and Muller glial cells in the absence of Notch1 in mitotic a
60 Barhl2 inhibits the formation of bipolar and Muller glial cells, indicating that Barhl2 is able to fu
61 ree cultures of Muller glia, as well as by a Muller glial cell line but not several neuroblastoma cel
62 line is a novel, conditionally immortalized Muller glial cell line isolated from the P10 mouse retin
63 study was to generate and characterize novel Muller glial cell lines from the postnatal mouse retina.
64 y immortalized (C57M10 [C57BL/6 Muller P10]) Muller glial cell lines were selected by differential ad
70 ors, a subtype of amacrine interneurons, and Muller glial cells (MGs) exhibited rapid responses to di
71 ersely, overexpression of sEH in the retinal Muller glial cells of non-diabetic mice resulted in simi
73 ents via an elegant biochemical mechanism in Muller glial cells of the neural retina that can contrib
74 We tested if CRB expression restricted to Muller glial cells or photoreceptors or co-expression in
75 t increased proliferation and apoptosis, and Muller glial cell overproduction in the developing retin
76 ing the early stage of retinal degeneration, Muller glial cells participated in the phagocytosis of d
82 the subapical regions of photoreceptors and Muller glial cells; rather, it localizes to a small regi
83 regeneration response that is marked by the Muller glial cells reentering the cell cycle to produce
84 a, neuronal alterations, and loss of retinal Muller glial cells resembling human macular telangiectas
85 structural markers of disease may represent Muller glial cell response to photoreceptor stress and a
87 nd in rod photoreceptors, amacrine cells and Muller glial cells, suggesting that Sonic hedgehog promo
88 g either Rbpj or Notch1/2, we induced mature Muller glial cells to reprogram into bipolar- and amacri
92 abnormalities observed in photoreceptors and Muller glial cells were confined to retinal regions dire
93 he subretinal space and weaker activation of Muller glial cells were exhibited by Tlr3(-/-)Rdh8(-/-)
95 ose silent/accessible gene promoters were in Muller glial cells, which function to maintain retinal h
96 ping retina, CRB2 has redundant functions in Muller glial cells, while CRB2 has essential functions i