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1 ia on astrocytes was also assessed with anti-S100beta.
2 s glial fibrillary acidic protein (GFAP) and S100beta.
3 the rod outer segments and its modulator is S100beta.
4 s at micromolar concentrations of Ca(2+) via S100beta.
5 into a form that only marginally responds to S100beta.
6 is less sensitive to activation by GCAP2 and S100beta.
7 th glial fibrillary acidic protein (GFAP) or S100beta.
10 ually called S100b (S100betabeta or dimer of S100beta), also activates ROS-GC but that the Vmax of ac
17 ed to show that these sites are specific for S100beta and not for another regulator of ROS-GC1, guany
18 ally regulates GFAP expression, as levels of S100beta and vimentin were not altered in the female amy
22 ally displayed high immunostaining for GFAP, S100beta, and CD44, but low immunostaining for glutamine
23 port activity and immunoreactivity for GFAP, S100beta, and glutamate transporter GLT-1 within a few h
24 tudies revealed that CD-GCAP is identical to S100beta, another low-molecular-weight calcium-binding p
25 express markers, including Sox17, Sox10 and S100beta, are cloneable, have telomerase activity, and c
28 nt protein in primary olfactory neurons, and S100beta-DsRed mice which express red fluorescent protei
29 limitans astrocytes, Iba-1(+) microglia and S100beta(+) ependymal cells expressed PLIN in the aging
30 and tyrosine hydroxylase to quantify nerves, S100beta for glia, Kit for interstitial cells of Cajal (
32 neurites), anti-HuC/HuD (neurons), and anti-S100beta (glia) in an allelic series of mice with mutati
33 labeling in white matter was associated with S100beta+/glial fibrillary acidic protein negative macro
34 f ROS-GC1 and on its activation by GCAP1 and S100beta; however, the mutated cyclase becomes more acti
37 Confocal mapping of calcium-binding protein S100beta immunoreactivity (S100beta-ir) and of the inter
41 rn cells colabeled with the astrocyte marker S100beta in higher numbers than when cells were generate
42 eas of tissue expression of RAGE, HMGB1, and S100beta in specific organs of mouse fetuses on E16.
44 ain blood vessels, it was possible to detect S100beta-ir and vimentin-ir cell processes that cross th
46 is suggested the probable means by which the S100beta-ir cells of the extraparenchymal tissues anatom
47 m-binding protein S100beta immunoreactivity (S100beta-ir) and of the intermediate filament vimentin-i
48 hotoreceptor guanylate cyclase activation by S100beta is validated by the identification of two S100b
49 erves, but not of degenerating nerves, while S100beta labeling was observed in the Schwann cells of a
52 al ganglia satellite cells, peripheral nerve S100beta+ myelinating Schwann cells, and peripheral nerv
56 type I nor 3alpha-HSD mRNAs are expressed in S100beta- or glial fibrillary acidic protein-positive gl
64 eatment of astrocytes with ACT, IL-1beta, or S100beta resulted in glial activation, as assessed by re
65 he DRG and sciatic nerve, ATF3 expression in S100beta(+) Schwann cells and increased expression of th
68 ) impulse and inhibits the catalytic module; S100beta senses the impulse and stimulates the catalytic
69 mbryos at E12.5, suggesting that the lack of S100beta staining and Schwann cell coverage in the p75 m
72 53+/- or ink4a/arf+/- animals transgenic for S100beta-v-erbB) showed a similar tumor-specific down-re
75 Privileged anatomical relationships of the S100beta/vimentin network with the glial fibrillary acid
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