ライフサイエンスコーパス: peptide complex

1 epresentative structure of an organometallic-peptide complex.

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

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

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

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

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

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

8 scribes an exploration of the dynamic kinase:peptide complex.

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

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

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

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

13 romote the formation of a ternary ERAP1/MHCI/peptide complex.

14 bly affects the internal dynamics of the CaM-peptide complex.

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

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

17 reated by the protein to predict the protein-peptide complex.

18 aracterized using a synthesized cross-linked peptide complex.

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

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

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

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

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

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

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

26 delling and dynamic analysis of the protease-peptide complexes.

27 ilar protein-peptide interactions of smaller peptide complexes.

28 oaffinity capture of naturally processed MHC-peptide complexes.

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

30 contribute disproportionately in stabilizing peptide complexes.

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

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

33 and determined cryo-EM structures of cyclic peptide complexes.

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

35 ceptors identified here to internalize Hsp70-peptide complexes.

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

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

38 cell receptors (TCR) that recognize self MHC/peptide complexes.

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

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

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

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

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

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

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

46 ilondeltagamma complex after ligation by MHC:peptide complexes.

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

48 esent alloantigens is via acquisition of MHC-peptide complexes.

49 structures of FvTox1 and FvTox1-interacting peptide complexes.

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

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

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

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

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

55 nitrite reductase activities of these copper-peptide complexes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 murine fibroblasts expressing antigenic MHC:peptide complexes as APC, we show that trogocytosis-posi

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

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

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

95 A cryo-EM structure of the spastin-peptide complex at 4.2 angstrom resolution revealed an a

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

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

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

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

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

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

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

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

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

105 Hsp90-OVA peptide complexes bound to scavenger receptor expressed

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

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

108 rsors both in solution and in preformed MHCI-peptide complexes, but which mode is more relevant to it

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

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

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

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

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

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

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

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

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

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

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

120 asets, ADCP reliably docked a set of protein-peptide complexes containing peptides ranging in lengths

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 ility of DCs to generate MHC class I (MHC I) peptide complexes for cross-presented Ags.

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

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

143 pplication, we modelled a subset of protease-peptide complexes for which experimental cleavage data a

144 s not only the key residues for the receptor-peptide complex formation but also which positions shoul

145 utes toward inhibition of MHC class I:beta2M:peptide complex formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 allows cross-presentation to generate MHC-I-peptide complexes identical to those produced by convent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 10 helix-turn-310 helix, whereas in the GRK1 peptide complex it forms an alpha-helix.

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

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

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

195 r factors, conformational sampling of enzyme:peptide complexes likely plays a critical role in defini

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

211 Data demonstrated that all six peptides complexed pDNA to produce cationic nanoparticle

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

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

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

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

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

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

218 nd electrostatic properties of the HLA-DQ2.5-peptide complex, providing the fine specificity underlyi

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

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

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

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

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

224 Furthermore, a crystal structure of a USP11-peptide complex revealed a previously unknown binding si

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 ynamic allostery-based perspective to kinase:peptide complexes that have previously been explored onl

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

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

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

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

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

247 In the Fab6E2-peptide complexes, the structured region features a cent

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

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

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

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

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

253 cts) with HLA proteins that present the drug-peptide complex to T cells.

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

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

256 e (NP) platform featuring a cell penetrating peptide complexed to NF-kappaB p65 siRNA.

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

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

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

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

261 Presentation of these HLA-abacavir-peptide complexes to T-cells is hypothesized to trigger

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 sity at the major histocompatibility complex-peptide complex, which dictates ICI efficacy.

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