ライフサイエンスコーパス: S100B

1 ), and increased to 1.00 at day 12 (0.65 for S100B).

2 rillar acidic and neurofilament proteins and S100B.

3 target that binds to the p53-binding site on S100B.

4 improved the Ca(2+) coordination geometry of S100B.

5 ered in future drug design studies involving S100B.

6 inated dynamic properties observed in Ca(2+)-S100B.

7 of p53 decreased the affinity for S100A2 and S100B.

8 cking protein-protein interactions involving S100B.

9 chemokine CX3CL1 while reducing the level of S100B.

10 tors of both Ca(2+)- and Ca(2+),Zn(2+)-bound S100B.

11 ors interact with the Ca(2+) binding protein S100B.

12 loop of the D(3) receptor did not pull down S100B.

13 idues that define the Zn(2+) binding site on S100B.

14 2+),Ca(2+)-S100B when compared to Pnt-Ca(2+)-S100B.

15 etreated with LR-90 and then stimulated with S100b.

16 294002 blocks the neuroprotective effects of S100B.

17 regulation, regional cerebral saturation, or S100B.

18 erved with the binding of target proteins to S100B.

19 such as the TRTK peptide versus Ca(2+)-bound S100B.

20 of NF-L with the established blood biomarker S100B.

21 bindin complex with the crystal structure of S100B.

22 d serum surges of the potential auto-antigen S100B.

23 The structures of Ca(2+)-S100B (1.5-A resolution) and S100B-Ca(2)(+)-TRTK-12 (2.0

24 phosphorylated NF heavy chain (pNF-H), tau, S100B, 14-3-3) and prion conversion assay (real-time qua

25 The (Ca)S100B.17 structure illustrates, for the first time, a pe

26 for an asymmetric pentamidine analogue ((Ca)S100B.17), this same channel was open.

27 For symmetric pentamidine analogues ((Ca)S100B.5a, (Ca)S100B.6b) a channel between sites 1 and 2

28 ric pentamidine analogues ((Ca)S100B.5a, (Ca)S100B.6b) a channel between sites 1 and 2 on S100B was o

29 s assessed using daily measurements of serum S100B, a biomarker for cerebral ischemia, and computed t

30 ents, atorvastatin decreases serum levels of S100B, a biomarker of brain ischemia.

31 o model, we investigated the hypothesis that S100B, a protein which is released from astrocytes follo

32 Previous studies showed that AGEs and S100b, a specific RAGE ligand, could augment monocyte in

33 smic-reticulum localization and secretion of S100b-a protein that lacks a signal peptide-from brown a

34 There is increasing evidence that S100B acts as a cytokine or damage-associated molecular

35 or complexes revealed that the C-terminus of S100B adopts two different conformations, with location

36 rformed to analyze the structural changes of S100B after oxidation of its thiol groups under denaturi

37 The EF-hand calcium-binding protein S100B also binds one zinc ion per subunit with a relativ

38 e from the brain, increased plasma levels of S100B, an astrocytic protein, and down-regulation of tig

39 s study, we observed for the first time that S100b, an inflammatory protein as well as a specific RAG

40 We simultaneously detect S100B and C-reactive protein, suspected biomarkers for t

41 s evaluated by stimulating chondrocytes with S100B and HMGB-1 and analyzing for activation of the ERK

42 ffect in SK-MEL-28 cells containing elevated S100B and inactive p53 (p53R145L mutant).

43 icted poor outcome and performed better than S100B and MBP.

44 d data on two well-studied blood biomarkers, S100B and MBP.

45 nslated protein, including binding sites for S100B and Mob proteins, part of the protein kinase domai

46 Using best specificity, serum S100b and neuron-specific enolase had optimal positive a

47 Receiver operator curves for serum S100b and neuron-specific enolase to classify favorable

48 tial and highest concentrations in week 1 of S100B and NSE were associated with poor outcome, as were

49 At 48 h after stroke, S100B and RAGE expression was increased in stroke-affect

50 We found that both S100B and S100A4 bind to the tetramerization domain of p

51 n its oligomerization state, we suggest that S100B and S100A4 could regulate the subcellular localiza

52 have identified a novel interaction between S100B and the dopamine D(2) receptor.

53 n is based on the following observations: 1) S100B and the third cytoplasmic loop of the dopamine D(2

54 characterize an interaction between Ca(2)(+)-S100B and TRTK-12, a target that binds to the p53-bindin

55 matory molecules (IL-6, HMGB1, HSP70, HSP90, S100B and vWF) were effectively neutralised by the TiO(2

56 the absence of Pnt, including Ca(2+)-loaded S100B and Zn(2+),Ca(2+)-loaded S100B determined here (1.

57 Serum S100 beta (S100B) and neuron-specific enolase concentrations rise a

58 urons (neuron-specific enolase), astrocytes (S100b), and axons (myelin basic protein).

59 to detect TBI versus controls (AUC 0.96 for S100B), and increased to 1.00 at day 12 (0.65 for S100B)

60 S100B (LOX-IM VI) were not affected by siRNA(S100B), and introduction of S100B reduced their UV-induc

61 ds) throughout wild type, (D61N)S100B, (D63N)S100B, and (D65N)S100B were lowered upon binding TRTK-12

62 nclude 14-3-3, tau, neuron-specific enolase, S100B, and alpha-synuclein.

63 EF-hand calcium-binding proteins calmodulin, S100B, and calbindin D9k.

64 ht chain (NF-L), myelin basic protein (MBP), S100B, and heart-type fatty acid binding protein (H-FABP

65 reduction in the astrocyte-derived cytokine, S100B, and in the extent of neuronal Wnt/beta-catenin si

66 We measured serum neuron-specific enolase, S100b, and myelin basic protein on days 1-4 and 7 after

67 istics of enteric glia, including p75, GFAP, S100B, and SOX10 expression.

68 kappaB) activation, as LR-90 suppressed both S100b-and tumor necrosis factor-alpha-induced IkappaB-al

69 n-2 as markers of endothelial activation and S100B as a marker of blood-brain barrier/neurological in

70 4 hrs of admission; 3) serial measurement of S100B as a marker of central nervous system injury; and

71 These authors have proposed S100B as a potential disease activity marker in vitiligo

72 With (D63N)S100B as an exception ((D63N)K(D)=50+/-9 muM), Ca(2+) bi

73 Serum levels of S100B auto-antibodies also predicted persistence of MRI-

74 The correlation of serum S100B, auto-antibodies and DTI changes support a link be

75 inding-induced changes in the line shapes of S100B backbone (1)H and (15)N resonances were monitored

76 termolecular NOEs could suggest that the p53/S100B(betabeta) interface is more dynamic than currently

77 nsights into the structural basis of the p53/S100B(betabeta) recognition but also highlights the impo

78 in complex with various targets, it binds to S100B(betabeta) through formation of nonspecific complex

79 Calcium-dependent binding of dimeric S100B(betabeta) to p53-NRD blocks access to these PTM si

80 ampling) revealed large heterogeneity in the S100B(betabeta)-bound conformation of p53-NRD.

81 lays substantial flexibility in packing with S100B(betabeta).

82 disordered p53 extreme C-terminus to protein S100B(betabeta).

83 RD folds into a stable helix upon binding to S100B(betabeta).

84 expressing the D(2) receptor; 4) a putative S100B binding motif is located at residues 233 to 240 of

85 und that S100A1, S100A2, S100A4, S100A6, and S100B bound to two subdomains of the TAD (TAD1 and TAD2)

86 P1CreER:tdT mice, PLP1 cells that co-express S100b but not RET also give rise to neurons following co

87 SOX10, KROX20 (EGR2), p75NTR (NGFR), MBP and S100B by day 4 in virtually all cells, and maturation wa

88 rate colocalization of the D(2) receptor and S100B by immunostaining.

89 hway, being RAGE up-regulated by hypoxia and S100B by infection by Toll-like receptors.

90 As with an S100B-Ca(2)(+)-p53 peptide complex, TRTK-12 binding to C

91 tures of Ca(2+)-S100B (1.5-A resolution) and S100B-Ca(2)(+)-TRTK-12 (2.0-A resolution) determined her

92 n the structures of S100B-Ca(2+)-TRTK-12 and S100B-Ca(2+) were compared and calcium ion coordination

93 ibility was ruled out when the structures of S100B-Ca(2+)-TRTK-12 and S100B-Ca(2+) were compared and

94 esolution) determined here indicate that the S100B-Ca(2+)-TRTK-12 complex is dominated by an interact

95 e to the Tc1 include increased levels of the S100B calcium-binding protein, mTOR proteins RAPTOR and

96 ding AGEs, amyloid-beta peptide (Abeta), and S100B/calgranulins, some of which are known components o

97 In contrast, we found that nitrosylation of S100B caused a minor increase in binding to the p53 C-te

98 ell infiltrate as well as increased GFAP and S100B co-expression and decreased HuC/D protein expressi

99 These data suggest that S100B coexpression may serve as an important mediator of

100 markers of enteric glial cells (eg, p75 and S100B), colocalized with gastrin in human duodenal gastr

101 ed the relevance of all three small molecule-S100B complexes in solution.

102 Serum S100b concentrations peaked earliest, followed by neuron

103 Serum neuron-specific enolase and S100b concentrations were increased in the unfavorable v

104 Thus, elevated S100B contributes to abnormal ERK/RSK signaling and incr

105 and SBi523 bind to proximal sites on Ca(2+)-S100B could be useful for the development of a new class

106 to milliseconds) throughout wild type, (D61N)S100B, (D63N)S100B, and (D65N)S100B were lowered upon bi

107 atment of neurons with low concentrations of S100B decreased neuronal death after oxygen-glucose depr

108 on and RNA immunoprecipitation revealed that S100b decreased occupancy of the DNA/RNA-binding protein

109 Lastly, we demonstrate S100B detection (65 nM) in raw human CSF with an estimat

110 Ca(2+)-loaded S100B and Zn(2+),Ca(2+)-loaded S100B determined here (1.88 A; R(free)=0.267).

111 surviving neurons in S100B-treated cultures, S100B did not activate MAPKK.

112 Adjusting for S100B did not alter plasminogen activator inhibitor-1 an

113 D(3)-IC3, which does not bind S100B, does not contain this motif; and 5) coexpression

114 ert et al. explored correlations between the S100B dynamics and vitiligo activity, identifying high c

115 Calbindin D28k (calbindin) and S100B enhance IMPase-1 activity.

116 h showed that that target peptide binding to S100B enhances its calcium-binding affinity.

117 When S100B expression was inhibited in C8146As by siRNA (siRN

118 In summary, reducing S100B expression with siRNA was sufficient to activate p

119 y scattering, and NMR analysis revealed that S100B forms a "fuzzy" complex with RSK1 peptide ligands.

120 of the D(2) receptor also precipitates FLAG-S100B from human embryonic kidney 293 cell homogenates a

121 A changing S100B from low at baseline to high on follow-up seemed t

122 c kidney 293 cell homogenates and endogenous S100B from rat neostriatal homogenates; 3) S100B immunor

123 PA5 hOMCs express glial markers (p75(NTR), S100B, GFAP and oligodendrocyte marker O4), neuronal mar

124 by specifically modulating the expression of S100B, GFAP, inducible nitric oxide synthase, and thromb

125 biomarkers neurofilament light chain (NFL), S100B, glial fibrillary acidic protein (GFAP), amyloid-b

126 r for advanced glycation end products ligand S100B greatly enhanced superoxide generation compared wi

127 Univariate analysis showed that baseline S100B > or = 0.15 microg/L is significantly correlated w

128 Conversely, high concentrations of exogenous S100B had a cytotoxic effect that seems to be RAGE-indep

129 the Fas death receptor (+UV); whereas, siRNA(S100B) had no effect in SK-MEL-28 cells containing eleva

130 the order of magnitude higher affinity that S100B has for calcium in the presence of Zn(2+).

131 ncrease in affinity that Zn(2+)-Ca(2+)-bound S100B has for peptide targets such as the TRTK peptide v

132 Although calbindin and S100B have a low sequence homology, they seem to activat

133 nding; the S100A7, S100A9(C3S), S100A12, and S100B homodimers do not exhibit such Mn(II)-binding capa

134 ary aims (PTX3, CLEC7a, CD209, CXCL10, TLR6, S100B, IFNG, PLG, TNFR1), with hazard ratios ranging fro

135 s S100B from rat neostriatal homogenates; 3) S100B immunoreactivity was detected in cultured neostria

136 2, and HDM4 have been shown to interact with S100B in a calcium-dependent manner.

137 accompanying surge of the astrocytic protein S100B in blood may cause an immune response associated w

138 calsyntenin 3beta, and forced expression of S100b in brown adipocytes rescues the defective sympathe

139 t contain this motif; and 5) coexpression of S100B in D(2) receptor-expressing 293 cells selectively

140 define the prognostic significance of serum S100B in patients with high-risk resected melanoma.

141 studies evaluating the diagnostic utility of S100B in patients with TBI have shown that it may be a u

142 ic residues contribute to calcium binding in S100B in the absence and presence of the p53 peptide.

143 ukin-1beta, tumor necrosis factor-alpha, and S100B in the hippocampus.

144 Our results demonstrate a role of S100B in the pathophysiology of Parkinson's disease.

145 play a key role in the activation of RAGE by S100B in VSMCs.

146 This was further confirmed by showing that S100b increased stability of luciferase-COX-2 3'-UTR mRN

147 S100B increased the activation of Src kinase and tyrosin

148 Moreover, S100B increases the formation of pAkt and the up-regulat

149 as does the modulation by the Ca(2+) sensor S100B, increasing [Ca(2+)](i) from 100 to 1000 nM.

150 or of Src kinase, PP2, significantly blocked S100B-induced activation of Src kinase, mitogen-activate

151 This appeared to be mediated by S100b-induced binding of specific RNA-binding protein(s)

152 ediated specific knockdown of hnRNPK blocked S100b-induced COX-2 mRNA stability, whereas on the other

153 her hand, overexpression of hnRNPK increased S100b-induced COX-2 mRNA stability.

154 nslocation-deficient hnRNPK mutant inhibited S100b-induced COX-2 mRNA stability.

155 Cholesterol depletion also inhibited S100B-induced effects indicating the requirement for int

156 as demonstrated by its inhibitory effects on S100b-induced expression of NADPH oxidase and intracellu

157 LR-90 significantly inhibited S100b-induced expression of RAGE and other proinflammato

158 av-1 short hairpin RNA significantly reduced S100B-induced inflammatory gene expression in VSMCs.

159 In addition, LR-90 blocked S100b-induced monocyte adhesion to human umbilical vein

160 g small interfering RNA completely inhibited S100B-induced NF-kappaB activation in RAGE(-/-), but not

161 lecular mechanisms by which the RAGE ligand, S100b, induces COX-2 in monocytes.

162 e was unexpected and provides a new mode for S100B inhibition by this drug.

163 appaB-dependent manner, since pentamidine, a S100B inhibitor, prevented 5-FU-induced neuronal loss, e

164 idine analogues, and X-ray structures of (Ca)S100B.inhibitor complexes revealed that the C-terminus o

165 tivity by 7-fold, further demonstrating that S100B inhibits apoptosis activities in p53-containing ce

166 -C motif) ligand 2, neuron-specific enolase, S100b, intercellular adhesion molecule-5, and brain-deri

167 hydrophobic binding pocket exposed on Ca(2+)-S100B involving residues in helices 2 and 3 and loop 2.

168 S100B is a calcium-binding protein expressed in, and sec

169 S100B is a calcium-binding protein with both extracellul

170 S100B is a member of the S100 subfamily of EF-hand prote

171 S100B is a prognostic marker for malignant melanoma.

172 Thus, S100B is a proinflammatory cytokine bridging RAGE and CD

173 elanoma, a high baseline or increasing serum S100B is an independent prognostic marker of risk for mo

174 onding Ca(2+) association rate constants for S100B, k(on), for the EF2 domains in the absence and pre

175 Using S100B overexpression and shRNA(S100B) knockdown studies in melanoma cell lines, elevate

176 B testing results showed that the higher the S100B level is, the higher the risk of relapse and death

177 ardia or ventricular fibrillation, and lower S100B level.

178 rs on day 3 were younger age and lower day 3 S100B level.

179 Increasing S100B levels are predictive of advancing disease stage,

180 s with good outcomes had significantly lower S100B levels at all time points and lower neuron-specifi

181 Beginning with reports about increased S100B levels in different inflammatory and tissue damage

182 iligo activity, identifying high circulating S100B levels in patients with active depigmentation whic

183 ght-junction protein, Claudin 5, and reduced S100B levels in periphery).

184 with control tissue, and cerebrospinal fluid S100B levels were higher in a large cohort of patients w

185 S100B levels were significantly lower in statin-treated

186 a well known marker for malignant melanoma, S100B, likely contributes to cancer progression by down-

187 As expected, cells lacking S100B (LOX-IM VI) were not affected by siRNA(S100B), and

188 Targeting S100B may emerge as a potential treatment strategy in th

189 siRNA(S100B)-mediated apoptosis was independent of the mitocho

190 ,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels.

191 otransduction in both rods and cones and the S100B mode in the transmission of neural signals to cone

192 with a progressive increase in RAGE ligands (S100B, N-[carboxymethyl]lysine, HSP70, and HMGB1).

193 r 3 weeks were analyzed for the neuromarkers S100B, neuron-specific enolase (NSE), and glial fibrilla

194 Preliminary data show that serum S100b, neuron-specific enolase, and myelin basic protein

195 erall and an increasing profile over time in S100B, NSE, and GFAP.

196 luated whether the anti-apoptotic effects of S100B on fetal rhombencephalic neurons were linked to th

197 Using S100B overexpression and shRNA(S100B) knockdown studies

198 The SBi279 binding site on Ca(2+)-S100B overlaps the SBi132 and SBi523 sites and contacts

199 or-1 (p = 0.002), E-selectin (p = 0.02), and S100B (p < 0.001) concentrations were associated with fe

200 inogen activator inhibitor-1 (p = 0.007) and S100B (p = 0.01) concentrations were associated with lon

201 0), neuron-specific enolase (p = 0.006), and S100b (p = 0.015) and in patients with versus without ab

202 drug design program aimed at inhibiting the S100B-p53 interaction and restoring wild-type p53 functi

203 based drug design is underway to inhibit the S100B-p53 interaction as a strategy for treating maligna

204 The S100B-p53 protein complex was discovered in C8146A malig

205 S100B, which will impact next generation (Ca)S100B.p53 inhibitor design.

206 um-dependent complex formation with p53 ((Ca)S100B.p53) in malignant melanoma (MM) and restores p53 t

207 Co-staining of BrdU+ cells with NeuN or S100B permitted the parallel study of the ongoing neurog

208 A deficiency of S100b phenocopies deficiency of calsyntenin 3beta, and f

209 S100b promoted the release of entrapped COX-2 mRNA from

210 Furthermore, serum S100B protein has been shown to be superior to lactate d

211 S100B protein is elevated in the brains of patients with

212 In this study, we show that S100B protein levels were higher in post-mortem substant

213 three additional time points were tested for S100B protein using chemiluminescence.

214 ight, we screened these peptides against the S100B protein using isothermal titration calorimetry and

215 rkers, including neuron-specific enolase and S100B protein.

216 ound that S100A1, S100A2, S100A4, S100A6 and S100B proteins bound different p63 and p73 tetramerizati

217 S100B+/PV+ ependymal cells found in younger mice diminis

218 ntributed to the sustained activation of the S100B-RAGE pathway, being RAGE up-regulated by hypoxia a

219 odel to investigate the participation of the S100B/RAGE/NFkappaB pathway in intestinal mucositis and

220 liosis and reduction of enteric neurons in a S100B/RAGE/NFkappaB-dependent manner, since pentamidine,

221 etry (ITC) and deletion experiments indicate S100B recognition by RAGE is an entropically driven proc

222 ffected by siRNA(S100B), and introduction of S100B reduced their UV-induced apoptosis activity by 7-f

223 It, however, partially overlaps with the S100B-regulatory site.

224 A biomarker of cerebral ischemia, S100b, remained unchanged, suggesting preserved cerebral

225 In turn, ablation of S100B resulted in neuroprotection, reduced microgliosis

226 S100B-RSK complex formation was shown to be Ca(2+)-depen

227 Although S100B-RSK1 and the calmodulin-CAMKII system are clearly

228 mical and structural characterization of the S100B-RSK1 interaction.

229 Moreover, we determined whether S100B's pro-survival effects were associated with mitoge

230 Oxidation of S100B's thiol groups resulted in the formation of oligom

231 d SC proliferation and the number of BrdU(+)-S100B(+)-SCs over time.

232 Additionally, the overexpression of S100B sequesters RSK into the cytosol and prevents it fr

233 S100B serum levels and auto-antibodies against S100B wer

234 Serum S100B showed high sensitivity as well (84.2%), but lower

235 2+)-bound (2.0A) and TRTK-bound (1.2A) (D63N)S100B showed no change in Ca(2+) coordination; thus, the

236 Furthermore, S100b significantly down-regulated the expression of a k

237 S100b significantly increased COX-2 mRNA accumulation in

238 On the other hand, S100b significantly increased IP-10 mRNA half-life and s

239 the plasma levels of factors such as TGF-b, S100B, sRAGE and IL-8 as well as with myeloid DC counts.

240 S100b stimulates neurite outgrowth from sympathetic neur

241 As part of an effort to inhibit S100B, structures of pentamidine (Pnt) bound to Ca(2+)-l

242 nation arising from His-15 and His-25 of one S100B subunit and from His-85 and Glu-89 of the other su

243 nsity corresponding to two Pnt molecules per S100B subunit was mapped for both drug-bound structures.

244 S100B testing requires further investigation, but may se

245 S100B testing results showed that the higher the S100B l

246 en with minor TBI, and evaluates the role of S100B testing.

247 (C4a/C4b, Cd74, Ctss, Gfap, Nfe2l2, Phyhd1, S100b, Tf, Tgfbr2, and Vim) was increased in the App (NL

248 mmatory cytokines (IL-1 beta, TNF-alpha, and S100B), the chemokine CCL2, microglial activation, seizu

249 omolog of RAGE, and it shows that binding of S100B to CD166/ALCAM induces dose- and time-dependent ex

250 inding of S100A1, S100A2, S100A4, S100A6 and S100B to homologous domains of p63 and p73 in vitro by f

251 The Ca(2+)-dependent binding of S100B to the calcium/calmodulin-dependent protein kinase

252 Our results also suggest that the binding of S100B to the dopamine D(2) receptor enhances receptor si

253 8146As, the decrease in survival after siRNA(S100B) transfection (+UV) could be reversed by the p53 i

254 siRNA(S100B) transfections also restored p53-dependent apoptos

255 9 reduced the number of surviving neurons in S100B-treated cultures, S100B did not activate MAPKK.

256 ts of these investigations demonstrated that S100B treatment prevented ethanol-associated apoptosis o

257 S100b treatment promoted the translocation of nuclear hn

258 Therefore, a model for how S100B-TRTK-12 complex formation increases Ca(2+) binding

259 ved when the structures of S100A1-TRTK12 and S100B-TRTK12 were compared, providing insights regarding

260 tudy (>/=1 x 10(7) M(-1) s(-1)) suggest that S100B utilizes a "fly casting mechanism" in the recognit

261 Lower S100B values at baseline and during follow-up were assoc

262 S100B values measured at later time points over 1 year w

263 Baseline S100B was a significant prognostic factor for survival (

264 ography on the last available scan and serum S100B was assayed daily for 15 days after admission.

265 game, transient BBB damage measured by serum S100B was detected only in players experiencing the grea

266 or as bait in a bacterial two-hybrid system, S100B was determined to be a potential binding partner.

267 terization of zinc binding to calcium-loaded S100B was examined using high-resolution NMR techniques,

268 cells (i.e. C8146A, UACC-2571, and UACC-62), S100B was found to contribute to cell survival after UV

269 own studies in melanoma cell lines, elevated S100B was found to enhance cell viability and modulate M

270 3 peptide complex, TRTK-12 binding to Ca(2+)-S100B was found to increase the protein's Ca(2)(+)-bindi

271 No elevation in S100B was found.

272 In contrast, S100B was not related to outcome.

273 ssays showed that IP-10 mRNA accumulation by S100b was not via increased transcription.

274 Sustained expression of RAGE and its ligand S100B was observed in murine lung and human epithelial c

275 In addition, a conformational change in S100B was observed upon the addition of Zn(2+) to Ca(2+)

276 S100B.6b) a channel between sites 1 and 2 on S100B was occluded by residue Phe88, but for an asymmetr

277 Cell death and expression of S100B was significantly reduced when AZA was added short

278 A pull-down assay using biotin-labeled S100B was used to demonstrate binding to RAGE.

279 side-chain (15)N resonances of Asn63 ((D63N)S100B), was reduced upon TRTK-12 binding when measured b

280 e interaction with a known RAGE ligand, Ca2+-S100B, was mapped to VC1, with the major contribution fr

281 SBi132, SBi1279, and SBi523) bound to Ca(2+)-S100B were determined by X-ray crystallography at 2.10 A

282 nd to Ca(2+)-loaded and Zn(2+),Ca(2+)-loaded S100B were determined by X-ray crystallography at 2.15 A

283 Elevated levels of auto-antibodies against S100B were elevated only after repeated sub-concussive e

284 EF-hand calcium-binding mutants of S100B were engineered at the -Z position (EF-hand 1, E31

285 cle, the two dots corresponding to Cidea and S100b were erroneously moved to the top left of the volc

286 cle, the two dots corresponding to Cidea and S100b were erroneously moved to the top left of the volc

287 and, B-factors for residues in EF2 of Ca(2+)-S100B were found to be significantly lowered with TRTK-1

288 trophil gelatinase-associated lipocalin, and S100B were higher in nonsurvivors than survivors.

289 contrast, soluble AGE-BSA, fresh Abeta, and S100B were less effective in increasing VEGF secretion.

290 ld type, (D61N)S100B, (D63N)S100B, and (D65N)S100B were lowered upon binding TRTK-12.

291 00B serum levels and auto-antibodies against S100B were measured and correlated by direct and reverse

292 CSF cell count, 14-3-3 protein detection and S100B were of limited value.

293 cond EF-hand (D61N, D63N, D65N, and E72A) of S100B were used to study its Ca(2+) binding and dynamic

294 bound to sites 1 and 2 of Pnt-Zn(2+),Ca(2+)-S100B when compared to Pnt-Ca(2+)-S100B.

295 served upon the addition of Zn(2+) to Ca(2+)-S100B, which changed the conformation and orientation of

296 means to block all three "hot spots" on (Ca)S100B, which will impact next generation (Ca)S100B.p53 i

297 hydrophobic target binding pocket of Ca(2+)-S100B with minimal structural changes observed for the p

298 were then used to show that coexpression of S100B with the D(2) receptor increases the ability of D(

299 any small-molecule inhibitor bound to Ca(2+)-S100B would also have to cause an increase in calcium-io

300 ion was inhibited in C8146As by siRNA (siRNA(S100B)), wt p53 mRNA levels were unchanged, but p53 prot

301 as adjacent to a p53 peptide binding site on S100B (+/-Zn(2+)), and the second Pnt molecule was mappe