ライフサイエンスコーパス: peptide complex

1 tation is shorter in the ClfB.Fg alpha-chain peptide complex.

2 d structural model for the Act-EF34/palladin peptide complex.

3 served for the clumping factor A.gamma-chain peptide complex.

4 ster of an intermolecular beta-sheet protein-peptide complex.

5 nt on expression of the cognate MHC-molecule/peptide complex.

6 ional outcome of TCR ligation by a given MHC-peptide complex.

7 llagen recognition is limited to an integrin-peptide complex.

8 s of CaM in stabilizing the structure of the peptide complex.

9 ptide and CaM following formation of the CaM-peptide complex.

10 teractions drive formation of the AtOASS.C10 peptide complex.

11 aracterized using a synthesized cross-linked peptide complex.

12 now determined the structure of the K42-41L-peptide complex.

13 lid-state NMR distance measurement in an RNA-peptide complex.

14 ized through protein modeling of the KSHV Pr-peptide complex.

15 contributing to binding of the class II HLA-peptide complex.

16 urfaces (FES), were performed on the protein-peptide complex.

17 confirmed by a crystal structure of the MDM2-peptide complex.

18 d the structure of the Hat1p/Hat2p/CoA/H4/H3 peptide complex.

19 in equilibrium between a 1:1 and 2:1 alpha1I-peptide complex.

20 epresentative structure of an organometallic-peptide complex.

21 +) T cells that can bind to the MHC class II-peptide complex.

22 ydrogen bonds that would stabilize the metal-peptide complex.

23 ducts is rate limiting in generating class I peptide complexes.

24 we generated in silico models of IgFLNa.CFTR peptide complexes.

25 contribute disproportionately in stabilizing peptide complexes.

26 f the conserved hydrogen bond network in MHC-peptide complexes.

27 nology and gentle and rapid isolation of HSP peptide complexes.

28 sional structures of two distinct HePTP-Erk2 peptide complexes.

29 ceptors identified here to internalize Hsp70-peptide complexes.

30 ogenous Ag for the generation of MHC class I/peptide complexes.

31 ural differences between the individual B*57-peptide complexes.

32 ffer from those of other processivity factor-peptide complexes.

33 y IL-2 production in response to agonist MHC-peptide complexes.

34 structures of FvTox1 and FvTox1-interacting peptide complexes.

35 rmation on the structures of different Hsp70-peptide complexes.

36 wn that it differs from typical Src-like SH3/peptide complexes.

37 reases the conformational stability of MHC I/peptide complexes.

38 rising more steeply than those of DMPC/DMPG-peptide complexes.

39 in human, mouse, and P. falciparum profilin.peptide complexes.

40 ceptor-mediated endocytosis of the chaperone/peptide complexes.

41 neously' proliferate in response to self-MHC-peptide complexes.

42 ilondeltagamma complex after ligation by MHC:peptide complexes.

43 c adoptive transfer systems and soluble gp96-peptide complexes.

44 for localized concentration of MHC class II-peptide complexes.

45 th a mAb to folded B27-beta(2)-microglobulin-peptide complexes.

46 d to a low availability of MHC class II-self peptide complexes.

47 olecule that is unable to form highly stable peptide complexes.

48 nts in DCs and regulates formation of MHC II-peptide complexes.

49 into the context of five related PDZ domain-peptide complexes.

50 ctions distinct from those reported for GNAT-peptide complexes.

51 nitrite reductase activities of these copper-peptide complexes.

52 D8 T cells to soluble activating class I MHC-peptide complexes, a complicating phenomenon had been ob

53 rous reports of crystal structures for MHCII-peptide complexes, a detailed analysis comparing all the

54 Ag has now emerged, the issue of whether HSP-peptide complexes act as physiological sources of Ag in

55 The results demonstrate that the RNA-peptide complexes adopt essentially two dynamical confor

56 and over 50% of zinc remained bound in both peptide complexes after peptic-pancreatic digestion.

57 here structures of FEN-1:DNA and PCNA:FEN-1-peptide complexes, along with fluorescence resonance ene

58 r observation that a Ib beta-Ibalpha-Ib beta peptide complex (alphabeta(2)) linked through native jux

59 observed between donor-labeled alphabeta(2) peptide complex and acceptor-conjugated IX TM peptide in

60 solved the structure of the Nbp2p SH3-Ste20 peptide complex and compared it with the previously dete

61 on crystal structure of a Hat1p/Hat2p/CoA/H4 peptide complex and found that the H4 tail interacts wit

62 t chemical speciation of the Zn(II)-(S.Cys)4 peptide complex and its effects on modulating the dehydr

63 determined the structure of the PIX-SH3/PAK peptide complex and shown that it differs from typical S

64 Each compound disrupts ExoI/SSB-Ct peptide complexes and abrogates SSB stimulation of ExoI

65 SCTs have been made with many different MHC-peptide complexes and are used as novel diagnostic and t

66 tructural characterization of several HLA-A2/peptide complexes and assessed in parallel their antigen

67 ly bound to A2, 10 of which formed stable A2-peptide complexes and induced CD8(+) T cells in A2-trans

68 endothelial cells-1) are able to bind Hsp70-peptide complexes and mediate its efficient internalizat

69 oliferation depends on low-affinity MHC/self-peptide complexes and on IL-7.

70 ligand for major histocompatibility complex-peptide complexes and perhaps other receptors on the par

71 terizing the interaction interface of domain-peptide complexes and predicting binding specificity for

72 es required for the presentation of class II-peptide complexes and T cell engagement.

73 tal results are 0.73 for 82 protein-protein (peptide) complexes and 0.83 for 45 protein-DNA complexes

74 presenting major histocompatibility complex-peptide complexes, and different forms of CD48 demonstra

75 onist major histocompatibility complex (MHC)-peptide complexes, and elevation of cytoplasmic Ca2+ is

76 es, eliciting responses to pre-assembled MHC-peptide complexes, and unique probes of lymphocyte devel

77 n binding energies for a large number of MHC-peptide complexes; and (3) an even larger binary dataset

78 MHC-viral peptide complexes are also represented by strings and a

79 ation studies showed that G9a-AdoMet and G9a-peptide complexes are catalytically active.

80 The naturally formed immunogenic alpha(2)M-peptide complexes are effective in prophylaxis and thera

81 Furthermore, the acquired MHC class I:peptide complexes are functional in that they induced Ag

82 or tumor cells, structurally unstable MHC I peptide complexes are generated, which are prone to disi

83 We propose that the context in which CII-peptide complexes are present in the membrane following

84 Exogenous heat shock protein (HSP):peptide complexes are processed for cross-presentation o

85 MHC class I-peptide complexes are then expressed on the cell surface

86 , rather than peptides or heat shock protein/peptide complexes, are the major source of antigen that

87 oduct release leading to an inhibitory FTase-peptide complex as a natural consequence of catalysis to

88 interact with many of the side chains of MHC-peptide complexes as 'hot spots' for TCR binding.

89 Instead, these cells recognized foreign MHC-peptide complexes as often as nonregulatory T cells.

90 ctivation is dependent on the density of MHC peptide complexes as well as the duration of interaction

91 a cocrystal structure of a core MOBKL1B-NS5A peptide complex at 1.95 A, NS5A binds to a hydrophobic p

92 termined by mechanically dissociating the Fn.peptide complex at loading rates relevant to the cardiov

93 se inhibitor resulted in expression of MHCII/peptide complexes at the cell surface.

94 n influences the quantity and quality of MHC/peptide complexes at the cell surface; however, little i

95 ass I major histocompatibility complex (MHC) peptide complexes at the surface of infected cells as a

96 and non-covalent peptide-peptide and protein-peptide complexes (ATT).

97 ulfide trap created remarkably tenacious MHC/peptide complexes because the peptide moiety of the dtSC

98 g that the transfer of preformed MHC class I:peptide complexes between a virus-infected cell and an u

99 The sharing of Ag as preformed MHC class I:peptide complexes between infected and uninfected DCs wi

100 etermine whether the transfer of MHC class I:peptide complexes between infected and uninfected murine

101 HLA-DR and HLA-DM, and high-affinity HLA-DR-peptide complexes bound HLA-DM only very slowly.

102 Hsp90-OVA peptide complexes bound to scavenger receptor expressed

103 CD8(+) T cell recognition of the HSP/peptide complex, but not the peptide alone, was inhibite

104 evidence that immunization with an AMA1-RON2 peptide complex, but not with AMA1 alone, provided compl

105 soluble oligomers of activating class II MHC-peptide complexes, but not to soluble monomers.

106 proach to increase the affinity of a protein-peptide complex by designing N or C-terminal extensions

107 n cells, and particularly the capture of MHC:peptide complexes by dendritic cells (DCs), led us to pr

108 The high affinity of the GlcNAcyl-peptide complex can be explained by extra-cavity interac

109 is the recent demonstration that MHC class I/peptide complexes can be expressed as single chain trime

110 GRP94 (gp96)-peptide complexes can be internalized by APCs and their

111 Here, we show that immunogenic alpha(2)M-peptide complexes can be isolated from the blood of tumo

112 nown that the formation of DNA-antimicrobial peptide complexes can lead to autoimmune diseases via am

113 ides and the assembly of iron-sulfur cluster-peptide complexes can take place within model protocells

114 decreasing the kinetic stability of class II-peptide complexes causes a corresponding alteration in D

115 40) B cells the biological properties of CII-peptide complexes (CII-peptide) generated by either the

116 g antagonists of protein-protein and protein-peptide complexes circumventing protein purification bot

117 Capture of the GFP-tagged MHC:peptide complexes correlates with an activated phenotype

118 microarrays of immobilized, recombinant MHC-peptide complexes, costimulatory molecules, and cytokine

119 ncludes surface expression of functional MHC-peptide complexes, costimulatory molecules, and other co

120 ll proliferation, nor initial density of CII-peptide complexes could explain the T cell-induced B cel

121 ggesting that the Ab-binding site on the MHC/peptide complex determines cytotoxicity.

122 Thus, nonclassical Qa-1(b)-peptide complexes direct cytotoxic T cells to targets wi

123 usly dissociating from APC often capture MHC:peptide complexes directly from the immunological synaps

124 otes narrowing of the repertoire of class II:peptide complexes displayed by APC, leading to a corresp

125 and subsequent optimization of cross-linked peptide complex dissociation, our reagents were applied

126 PCs and the immunodominance of that class II-peptide complex during an immune response.

127 tyrosinase-related protein 2 (TRP2(175-192)) peptide complexes effectively primed CD8(+) T cells reac

128 dulation: it targets newly synthesized MHC-I/peptide complexes en route to the cell surface.

129 they make the transition state of the DM:DR/peptide complex energetically more favorable.

130 ch sequence in a similar way to standard SH3/peptide complexes, even though the Pro residue positions

131 ructure-based model of the Act-EF34/palladin peptide complex expands our understanding of binding spe

132 The structure of the enzyme-peptide complex explains the marked substrate preference

133 the affinity and avidity of the TCR for MHC-peptide complexes expressed in the thymus.

134 Very small amounts of MHC class II-peptide complexes expressed on the surface of antigen-pr

135 es to measure HLA class I allospecificity-TA peptide complex expression in malignant cells.

136 omplex and the formation of an FTase-product-peptide complex followed by product release leading to a

137 led to reduced generation of MHC class I-Ag peptide complexes, followed by attenuated cross-priming

138 HLA-DM to efficiently target unstable MHCII-peptide complexes for editing and exchange those for mor

139 tructural modifications when designing metal-peptide complexes for somatostatin receptor targeting.

140 ssociation (ETD) products and CID of a metal-peptide complex formed from ion/ion reactions.

141 for the unliganded UL44 structure, the UL44-peptide complex forms a head-to-head dimer that could po

142 nstrate the use of a reconstituted manganous peptide complex from the radiation-resistant bacterium D

143 ss-dressing, DC directly acquire MHC class I-peptide complexes from dead, but not live, donor cells b

144 rnative mechanisms for generation of class I peptide complexes from endogenous and exogenous Ags and

145 ism entails the transfer of surface MHC-self peptide complexes from medullary thymic epithelial cells

146 We show that MHC class I:peptide complexes from peptide-pulsed or virus-infected

147 ment and the cell surface delivery of MHC-II-peptide complexes from phagosomes are not known.

148 ell surface molecules, including MHC class I/peptide complexes, from pAPC, Th cells can acquire and p

149 By contrast, K(b)-peptide complexes generated by incubating cells with syn

150 ty complex (MHC) class I:beta2-microglobulin:peptide complexes, generating an assembly with up to 56

151 Although SCTs of HLA class I/peptide complexes have been previously reported, they ha

152 Fluorescently labeled, tetrameric MHC-peptide complexes have been widely used to detect and qu

153 re of the source tissue; thus, purified gp96-peptide complexes have clinical significance as autologo

154 Heat shock protein 70-peptide complexes (Hsp70.PC-F) were extracted from fusio

155 es, we have shown that heat shock protein 70-peptide complexes (HSP70.PCs) derived from the fusion of

156 derived heat-shock protein (glycoprotein 96)-peptide complex (HSPPC-96; vitespen) as adjuvant treatme

157 The crystal structure of an iPGM macrocyclic peptide complex illuminated an allosteric, locked-open i

158 a peptide, forming a stable Al(18)F-chelate-peptide complex in an efficient 1-pot process.

159 cture at 3.5 A resolution of an SRP54-signal peptide complex in the dimer, which reveals how a signal

160 om WT CD8-independent T cells may engage MHC-peptide complexes in a manner unfavorable for efficient

161 bstantial levels of class I and class II MHC:peptide complexes in a temperature- and energy-dependent

162 cations of pH-dependent behavior of class II-peptide complexes in acidic endosomal compartments, wher

163 assing T cell ligands (i.e., appropriate MHC-peptide complexes in association with costimulatory mole

164 Here we report a unique role for MHC II-peptide complexes in controlling immune responses of nai

165 , consequently, a role for native GRP94/gp96-peptide complexes in cross-presentation.

166 ction in their abilities to generate class I peptide complexes in cultured cells or to prime antivira

167 activation by loading specific MHC class II-peptide complexes in discrete lipid raft microdomains.

168 een recently shown that preclustering of MHC-peptide complexes in membrane microdomains on the APC su

169 tion is to concentrate specific MHC class II-peptide complexes in plasma membrane microdomains that c

170 omotes a sustained expression of MHC class I/peptide complexes in the cell surface of DCs.

171 CD4(+) T cell recognition of MHC:peptide complexes in the context of a costimulatory sign

172 Agonist MHC-peptide complexes in the immunological synapse (IS) sign

173 y interactions between TCRs and class II MHC-peptide complexes in thymus "instruct" developing thymoc

174 he discovery that they harbor functional MHC-peptide complexes, in addition to various other immune-s

175 nditions on the conformation of the receptor.peptide complex, including folding dynamics of the pepti

176 lts in an altered repertoire of MHC class II/peptide complexes, indicating that DO modulates DM funct

177 increased the recovery of cell surface MHC I-peptide complexes, indicating that prematurely terminate

178 s that an intrinsic property of the class II:peptide complex is a key determinant that dictates the s

179 I molecules have bound a peptide, the MHC II-peptide complex is delivered to the cell surface for pre

180 s ~2%, that is, one cell-surface MHC class I-peptide complex is generated for every 50 folded source

181 bound structure of BIV TAR in the chameleon peptide complex is strikingly similar to the bound confo

182 cted cells and suggest that the level of MHC/peptide complex is sufficient to trigger memory but not

183 Gastrointestinal stability of zinc-peptide complexes is essential for zinc delivery.

184 ansfer during dissociation of Co(III)(salen)-peptide complexes is mainly determined by differences in

185 umor immunity elicited by tumor-derived gp96-peptide complexes is shown to be abrogated by anti-CD91

186 ur results suggest the half-life of class II:peptide complexes is the primary parameter that dictates

187 the intrinsic kinetic stability of class II-peptide complexes is tightly correlated with the effects

188 10 helix-turn-310 helix, whereas in the GRK1 peptide complex it forms an alpha-helix.

189 We found that MHC II-peptide complex kinetic stability in the presence of DM

190 eraction of the T cell receptor with the MHC-peptide complex, leading to signaling in the T cells (an

191 ifying the structure of preexisting self MHC-peptide complex, lies on the border between allergic hyp

192 The failure of the cleaved dimers to bind peptide-complexed monomers, together with the relative i

193 the reverse of that previously described for peptide complexes of Escherichia coli DnaK and rat Hsc70

194 TCRs to the same ubiquitously expressed MHC/peptide complex often directs thymocytes to both CD4(+)

195 by MHC-I and hence presentation of the MHC-I-peptide complex on the cell surface.

196 howed that TCR-dependent recognition of Qa-1-peptide complexes on target CD4 cells is essential for s

197 (+) T regulatory (Treg) cells recognize Qa-1/peptide complexes on target T(FH) cells and depend on th

198 multiple T-cell receptors with MHC class II-peptide complexes on the surface of antigen-presenting c

199 jor histocompatibility complex (MHC) class I-peptide complexes on the surface of professional antigen

200 ral CD8(+) T cell recognition of MHC class I-peptide complexes on the surface of professional APCs is

201 ells (EC) basally display class I and II MHC-peptide complexes on their surface and come in regular c

202 these professional APCs to generate class II-peptide complexes on their surface appears to be indisti

203 hat the coexpression of class II autoantigen-peptide complexes on Tregs provides these cells with a d

204 ining intact proteins and heat-shock protein-peptide complexes or with cell lysates depleted of eithe

205 ith previous structural studies on the GroEL-peptide complexes, our work supports the notion that the

206 d ATP independent, suggesting that a Cy3R.Fl-peptide complex passes through the cellular membrane wit

207 TP independent, suggesting that the rotaxane-peptide complex passes through the cellular membrane wit

208 These experiments indicate that HSP70-peptide complexes (PC) derived from DC-tumor fusion cell

209 icating that display of very few class I MHC-peptide complexes per DC can be sufficient for cross-pre

210 on of that observed in the DnaK(SBD)-NRLLLTG peptide complex placing the N and C termini of the pepti

211 The expression and turnover of MHC class II-peptide complexes (pMHC-II) on the surface of dendritic

212 The physiologic significance of MHC-peptide complex presentation by endothelial cells (ECs)

213 at high affinity TCRs bind rare class II MHC/peptide complexes presented in 'thymic niches', which co

214 tions in the nature and affinity of HLA-B*51.peptide complexes probably affect T-cell and natural kil

215 Autologous heat shock protein-peptide complexes produced from each patient's tumor is

216 l pH of the APC cell surface, where class II-peptide complexes promote activation of CD4 T cells.

217 ciation with IMPs; resulting IMP-beta-strand peptide complexes resisted aggregation when diluted in d

218 llographic and NMR analyses of smaller Bbk32 peptides complexed, respectively, with (2-3)FNI and (8-9

219 ther with structural features of the TCR-HLA/peptide complex result in this promiscuous HLA class II

220 ational modifications in preexisting HLA-DP2-peptide complexes, resulting in the creation of neoantig

221 induced dissociation (CID) of singly charged peptide complexes results in selective elimination of H2

222 The crystal structure of the USP7-NTD.vIRF1 peptide complex revealed an identical mode of binding as

223 fic TCR interacting with a Be-loaded HLA-DP2-peptide complex revealed that Be is coordinated by amino

224 The NMR structure of an OCRE-SmN peptide complex reveals a specific recognition of poly-p

225 The 2.2-A structure of a LIR-1/UL18/peptide complex reveals increased contacts and optimal s

226 tal structure of an alfalfa mosaic virus RNA-peptide complex reveals that conserved AUGC repeats and

227 ll as direct interaction with several HLA-DR/peptide complexes, reveals an attenuated catalytic activ

228 -glycero-3-[phospho-rac-(1-glycerol)] (DLPG)-peptide complexes rising more steeply than those of DMPC

229 gous tumor-derived heat shock protein (gp96)-peptide complexes show promise in enhancing survival of

230 es of both enzymes, including an O-GlcNAcase.peptide complex, showing conservation of active sites wi

231 In addition, acquired MHC-class I:peptide complexes stimulate T cell responses in vivo, fu

232 The 5G6 Fab-KL10 peptide complex structure confirmed the direct associati

233 Crystallographic analyses of H-2K(b)-peptide complexes suggest that a conformational adaptati

234 osphorylation and crystal structures of PAK4-peptide complexes suggested that phosphoacceptor residue

235 The fact that exosomes express surface MHC-peptide complexes suggests that they could function as A

236 d thermodynamic analyses of Scp1-phospho-CTD peptide complexes support the structures determined.

237 short as 2 cm allow formation of copper(II)-peptide complexes that are detected electrochemically at

238 because it limits the number of MHC class II-peptide complexes that can be recruited into the synapse

239 rding the biochemical attributes of class II-peptide complexes that govern their susceptibility to DM

240 known 3D structures of a small number of MHC-peptide complexes that were used in the original threadi

241 In the Ca(2+)/NCS-1.D2R peptide complex, the C-terminal region adopts a 310 heli

242 n cells and can be purified as an intact HSP-peptide complex, the peptides have had to be complexed a

243 selectively edit the repertoire of class II:peptide complexes, the consequence of DM expression in v

244 the interaction of T cell receptors with MHC/peptide complexes, the development of T cells in the thy

245 reports of the strong immunogenicity of HSP/peptide complexes, the present data suggest that HSP-com

246 Re-presentation requires the uptake of HSP-peptide complexes through a receptor, suggested to be th

247 s as well as to present self and foreign MHC-peptide complexes through formation of an immunological

248 blocking T-cell recognition of HLA class II-peptide complexes through steric hindrance.

249 inding of the fusion proteins to the HLA/HBV peptide complexes through the TCR-like variable regions

250 Despite similar capacities to acquire MHC-peptide complexes, thymic CD8alpha(+) cDC elicited incre

251 ed out molecular modeling of the FXIII-A(2)*/peptide complex to identify contact site(s) involved.

252 ortant contribution of a single class II MHC-peptide complex to the immune response against HIV-1 inf

253 ly the contribution of a single class II MHC-peptide complex to the immune response against HIV-1 inf

254 rom the same extracellularly added precursor peptide complexed to HSP.

255 t depends on the MHC alleles, but not on the peptide complexed to the MHC and whether CD8 is an alpha

256 ulfed cells and then transferred MHC class I/peptide complexes to confer cross-priming capacity to MH

257 tic cells expressing small amounts of MHC-II-peptide complexes to cross-link and stimulate CD4 T cell

258 nal major histocompatibility complex (MHC)-I/peptide complexes to dendritic cells (DCs) for CD8(+) T-

259 The ability of endogenous HSP-peptide complexes to elicit antigen-specific T cells req

260 s process mammalian heat shock protein (HSP):peptide complexes to present HSP-chaperoned peptides on

261 APCs process heat shock protein (HSP):peptide complexes to present HSP-chaperoned peptides on

262 apoptosis, and present immunogenic MHC/tumor peptide complexes to T cells after intratumoral injectio

263 MHC I with peptides, and transport of MHC I-peptide complexes to the cell surface.

264 ial for delivery of phagosome-derived MHC-II-peptide complexes to the plasma membrane.

265 Exogenously delivered antigenic peptides complexed to heat shock proteins (HSPs) are abl

266 thousands of diverse endogenous self-derived peptides complexed to MHC (pMHC complexes).

267 from irradiated hosts, including MHC class I-peptide complexes, to donor cells, including dendritic c

268 As with an S100B-Ca(2)(+)-p53 peptide complex, TRTK-12 binding to Ca(2+)-S100B was fou

269 ucture in solution of an RIM/ELKS C-terminal peptide complex using NMR spectroscopy.

270 ermodynamics data we obtained for calmodulin-peptide complexes using our methodology corroborate well

271 Each peptide complex was found to have an integrated Re(V) co

272 The nature of this scFv-peptide complex was further explored in solution by high

273 The structure of the alpha1I-peptide complex was investigated using data from NMR, sm

274 Biophysical characterization of the DNA-PNA-peptide complex was performed using gel electrophoresis

275 lls, that is, of endogenously generated TRiC-peptide complexes, was investigated, and such preparatio

276 ystal structure analysis of receptor-stapled peptide complexes, we describe in detail the molecular i

277 s of the vancomycin, peptide, and vancomycin-peptide complex were carried out to explore the low ener

278 r cytokine staining, and a tetrameric HLA-A2-peptide complex were used to define the T cell populatio

279 Nonbinding covalent HLA-DR-peptide complexes were converted into efficient HLA-DM b

280 y more class II MHC-peptide than class I MHC-peptide complexes were displayed.

281 Several soluble B3-peptide complexes were identified by ESI-MS.

282 ndritic cells that acquired host MHC class I-peptide complexes were potent stimulators of peptide-spe

283 In this study, MHC peptide complexes were purified from NIT-1 beta-cells, i

284 ither soluble tetramers or aAPC in which MHC-peptide complexes were uniformly distributed within arti

285 a Be(2+) cation becomes buried in an HLA-DP2/peptide complex, where it is coordinated by both MHC and

286 ormation of these residues in the calmodulin-peptide complex, where they are nonhelical.

287 mall region of the alpha-helix of the Mn(2+).peptide complex, which displays cation-induced alpha-hel

288 enoted TTP73, forms a dynamic, equimolar RNA.peptide complex with a 13-nucleotide fragment of the ARE

289 ather, the TCR recognizes a modified HLA-DP2-peptide complex with charge and conformational changes.

290 This report describes a novel HLA/peptide complex with potential prognostic and therapeuti

291 pecific comparison to another kinase-derived peptide complex with similar thermodynamic values reveal

292 ucture of a LMW tropomyosin N-terminal model peptide complexed with a smooth/nonmuscle tropomyosin C-

293 The crystal structure of the wild-type peptide complexed with a specific TCR shows that TCR bin

294 On the basis of the NMR structure of a SMAC peptide complexed with the BIR3 domain of X-linked IAP (

295 ) on these cells recognize self-MHC class II-peptide complexes with high or higher affinity and that

296 The structures of these sites as peptide complexes with motavizumab and 101F have been pr

297 gagement of TCRs with a diverse pool of self-peptides complexed with self-MHC molecules.

298 The biological consequences of these Cp*Rh-peptide complexes, with respect to GPCR binding and grow

299 ulates processing of engulfed Ags into MHC I:peptide complexes within hepatocytes.

300 itively selected if they respond to self-MHC-peptide complexes, yet mature T cells are not activated