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

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

4 ered in future drug design studies involving S100B.

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

6 of p53 decreased the affinity for S100A2 and S100B.

7 cking protein-protein interactions involving S100B.

8 chemokine CX3CL1 while reducing the level of S100B.

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

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

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

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

13 2+),Ca(2+)-S100B when compared to Pnt-Ca(2+)-S100B.

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

15 294002 blocks the neuroprotective effects of S100B.

16 regulation, regional cerebral saturation, or S100B.

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

18 erved with the binding of target proteins to S100B.

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

20 (2+)-bound S100B that is not in Ca(2+)-bound 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 Both AGE and S100B activated cultured RPE cells, as revealed by upreg

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 othesis, we analyzed the interaction between S100B and capping protein in solution.

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

43 The ability of S100B and HMGB-1 to stimulate matrix metalloproteinase 1

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

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

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

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

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

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

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

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

52 y these proteins bind to p53 could result in S100B and S1004 having different effects on p53 function

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

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

55 for the interaction between each subunit of S100B and target proteins such as the tumor suppressor p

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

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

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

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

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

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

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

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

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

65 ionally searched for potential inhibitors of S100B, and 60 compounds were selected for testing on the

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

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

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

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

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

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

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

73 4 hrs of admission; 3) serial measurement of S100B as a marker of central nervous system injury; and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 In addition, S100B binds to the negative regulatory and nuclear local

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 Serum S100b concentrations peaked earliest, followed by neuron

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 2, and HDM4 have been shown to interact with S100B in a calcium-dependent manner.

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

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 s of Ca(2+) (k(off)) from the EF2 domains of S100B in the absence and presence of the p53 peptide was

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

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

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

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

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

148 S100B increased the activation of Src kinase and tyrosin

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

150 o test the hypothesis that overexpression of S100B increases vulnerability to cerebral hypoxic-ischem

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 S100B is a calcium-binding protein with both extracellul

171 S100B is a calcium-binding protein, localized to astrogl

172 S100B is a dimeric Ca(2+)-binding protein that undergoes

173 S100B is a glial-derived protein that is a well-establis

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

175 S100B is a prognostic marker for malignant melanoma.

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

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

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

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

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

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

182 ardia or ventricular fibrillation, and lower S100B level.

183 Increasing S100B levels are predictive of advancing disease stage,

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

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

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

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

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

189 S100B levels were significantly lower in statin-treated

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

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

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

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

194 ,2,3,6-tetrahydropyridine showed upregulated S100B messenger RNA and protein levels.

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

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

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

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

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

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

201 Stimulation of chondrocytes with S100B or HMGB-1 increased phosphorylation of the ERK MAP

202 Using S100B overexpression and shRNA(S100B) knockdown studies

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

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

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

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

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

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

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

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

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

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

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

214 S100B protein is elevated in the brains of patients with

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

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

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

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

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

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

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

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

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

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

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

232 S100B serum levels and auto-antibodies against S100B wer

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

234 2+)-bound (2.0A) and TRTK-bound (1.2A) (D63N)S100B showed no change in Ca(2+) coordination; thus, the

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

236 S100b significantly increased COX-2 mRNA accumulation in

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

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

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

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

241 S100B testing requires further investigation, but may se

242 S100B testing results showed that the higher the S100B l

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

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

245 helix 4 was observed in Zn(2+)-Ca(2+)-bound S100B that is not in Ca(2+)-bound S100B.

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

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

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

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

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

251 8146As, the decrease in survival after siRNA(S100B) transfection (+UV) could be reversed by the p53 i

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

253 We used S100B transgenic (Tg) and knockout (KO) mice to test the

254 9 reduced the number of surviving neurons in S100B-treated cultures, S100B did not activate MAPKK.

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

256 S100b treatment promoted the translocation of nuclear hn

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

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

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

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

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

262 Baseline S100B was a significant prognostic factor for survival (

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

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

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

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

267 quaternary structure of Zn(2+)-Ca(2+)-bound S100B was found to be dimeric with helices H1, H1', H4,

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 d in cells pretreated with soluble RAGE, and S100B was shown to bind to chondrocyte RAGE.

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

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

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

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

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

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

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

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

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

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

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

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

290 00B serum levels and auto-antibodies against S100B were measured and correlated by direct and reverse

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

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

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

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

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

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

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

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

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

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