ライフサイエンスコーパス: RBD

1 RBD (Refined, Bleached and Deodorized) canola oil and vi

2 RBD and cholinergic system degeneration are identified i

3 RBD can precede the onset of PD by decades, suggesting a

4 RBD mutants were used to develop vaccines and monoclonal

5 RBD-like regions are conserved in all other clostridial

6 ted five vaccine candidates, designated 2012-RBD, 2013-RBD, 2014-RBD, 2015-RBD, and Camel-RBD, contai

7 accine candidates, designated 2012-RBD, 2013-RBD, 2014-RBD, 2015-RBD, and Camel-RBD, containing singl

8 didates, designated 2012-RBD, 2013-RBD, 2014-RBD, 2015-RBD, and Camel-RBD, containing single or multi

9 esignated 2012-RBD, 2013-RBD, 2014-RBD, 2015-RBD, and Camel-RBD, containing single or multiple mutati

10 teral beta-helix that associates with BoNT/A-RBD mainly through backbone-to-backbone interactions at

11 f the BoNT/A receptor-binding domain (BoNT/A-RBD) in complex with the SV2C luminal domain (SV2C-LD).

12 tivation events: movement of the ABD and ABD-RBD linker relative to the rest of the catalytic subunit

13 nuation, suggesting that immunoevasion after RBD immunization is accompanied by loss of viral fitness

14 are also comparably upregulated by alpha2M*, RBD, or mutant K1370A.

15 Pharmacological manipulations which alter RBD frequency and severity are reviewed, and the data fr

16 teine flanking the RNA-binding surface in an RBD, were constructed and used in directed hydroxyl radi

17 isms underlying REM sleep without atonia and RBD based on data in cat and rat are presented.

18 as well as Rap1, were observed when CRN and RBD sequences were linked.

19 ive impairment, orthostatic hypotension, and RBD at baseline, and at prospective follow-up, they show

20 ive impairment, orthostatic hypotension, and RBD even at baseline visits.

21 eptide that contains the flexible linker and RBD of Mre11 acts as an inhibitor of Mre11 nuclease acti

22 montage) during sleep in humans with PD and RBD.

23 5.7 to 7.0 causes production of free RBD and RBD-containing fragments.

24 th anti-RBD antibodies (blood and stool) and RBD-specific antibody-secreting cells.

25 h titers of antibody recognizing the anthrax RBD and LEF domains, as well as the full-length PA prote

26 tion induced significant levels of both anti-RBD antibodies (blood and stool) and RBD-specific antibo

27 usion of subjects with medication-associated RBD.

28 bust immunogenicity and efficacy of a TcdA/B RBD-based DNA vaccine in preclinical models of acute tox

29 A comparison with the plexin B1 RBD/Rnd1 complex structure suggests that Rnd1 binding al

30 Because RBD is a prodromal syndrome of Parkinson disease (or rel

31 Because RBD-mediated interactions are essential for RAS signalin

32 hly acidic flexible linker that lies between RBD and the main body of Mre11 increases the nuclease ac

33 icity and functionality, the ability to bind RBD-specific neutralizing monoclonal antibodies (MAbs) a

34 ns are essential for RAS signaling, blocking RBD association with small molecules constitutes an attr

35 The antibody-bound RBD structure is completely defined, revealing two previ

36 tralization of divergent MERS-CoV strains by RBD-induced antibodies remains unknown.

37 RBD, 2013-RBD, 2014-RBD, 2015-RBD, and Camel-RBD, containing single or multiple mutations in the RBD

38 The most commonly cited RBD treatments include low-dose clonazepam or high-dose

39 Among group I coronaviruses, RBD cores are conserved but RBMs are variable, explainin

40 he conformation and antigenicity of MERS-CoV RBD and thus will guide rational design of MERS-CoV subu

41 Furthermore, we found that MERS-CoV RBD functions as an effective entry inhibitor of MERS-Co

42 Modeling of the DPP4 and MERS-CoV RBD interaction predicted the ability of MERS-CoV to bin

43 efore, this study demonstrates that MERS-CoV RBD is an important vaccine target able to induce highly

44 The identified MERS-CoV RBD may also serve as a potential candidate for MERS-CoV

45 presents a structural comparison of MERS-CoV RBD with other coronavirus RBDs, successfully positionin

46 NL63-CoV RBD has a novel beta-sandwich core structure consisting

47 Furthermore, NL63-CoV RBD inhibits hACE2-dependent transduction by SARS-CoV sp

48 eptor-binding domain (RBD) with the SARS-CoV RBD (Bat-SRBD).

49 r dual nAb combinations to target a SARS-CoV RBD epitope that shows plasticity may have limitations f

50 ructural constraint rather than the SARS-CoV RBD-like region(s) should have broader utility for antib

51 Adult male rainbow darter (RBD) (Etheostoma caeruleum) were collected from nine sit

52 e rat cathelicidin rCRAMP, and beta-defensin RBD-1; (iii) the human cathelicidin LL-37 killed KIM6 ce

53 s (GEs) of refined, bleached and deodorized (RBD) palm olein during deep-fat frying (at 160 degrees C

54 ized mice and nonhuman primates could detect RBD protein from transfected cells, as well as neutraliz

55 d using a northeastern Brazil regional diet (RBD) for two weeks, followed by oral gavage with a satur

56 Among patients with Parkinson disease, RBD predicts a non-tremor-predominant subtype, gait free

57 eye movement (REM) sleep behavior disorder (RBD) is a failure of the circuitry regulating motor aton

58 Rapid eye movement sleep behavior disorder (RBD) is associated with neurodegenerative disease and pa

59 Rapid eye movement sleep behavior disorder (RBD) is common in Parkinson disease (PD), but its relati

60 rapid eye movement sleep behavior disorder (RBD) is often the first indication of an impending alpha

61 isease (PD) and REM sleep behavior disorder (RBD) show mostly unimpaired motor behavior during REM sl

62 rapid eye movement sleep behavior disorder (RBD), depression, anxiety, and Unified Parkinson's Disea

63 pnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy.

64 REM sleep behaviour disorder (RBD) is a parasomnia characterized by the loss of normal

65 eye movement (REM) sleep behaviour disorder (RBD) is characterised by complex motor enactment of drea

66 Concomitant REM sleep behaviour disorder (RBD) is commonly observed in patients with Parkinson's d

67 tment behavior (REM sleep behavior disorder [RBD]) are common features of sleep in the alpha-synuclei

68 ith four civet S genes, each with a distinct RBD, infected cells expressing human receptor angiotensi

69 VV constructs, the receptor binding domain (RBD or domain 4) or the lethal and edema factor binding

70 ing domain (ABD) and the Ras-binding domain (RBD) (G106V and G118D).

71 distinctive domains, an RNA-binding domain (RBD) and an effector domain (ED) separated by a linker r

72 pes close to the HA receptor binding domain (RBD) and neuraminidase (NA) catalytic site were identifi

73 ferent domains, the receptor binding domain (RBD) and the F activation domain (FAD).

74 eractions between DRaf's Ras binding domain (RBD) and the small GTPase Ras1, as well as Rap1, were ob

75 Ras-Binding domain (RBD) at three concentrations (25, 37.5, 50 mug/mL) showe

76 S)-the question of which RNA-binding domain (RBD) binds to which sites on the IRES.

77 3-CoV spike protein receptor-binding domain (RBD) complexed with human ACE2.

78 -glycine motifs, and one Ran-binding domain (RBD) corrected all transport defects and restored viabil

79 U and that the PERV receptor binding domain (RBD) extends beyond the variable regions A and B (VRA an

80 , namely residues in the RNA-binding domain (RBD) from one chain, and residues in the linker between

81 have identified the receptor-binding domain (RBD) from the MERS-CoV spike protein and determined its

82 of the 138-residue receptor binding domain (RBD) in binding to LRP.

83 ept in the putative receptor binding domain (RBD) in env, which contained novel sequences related to

84 role of the C-terminal Rad50 binding domain (RBD) in Mre11 activation, we constructed a series of C-t

85 via its N-terminal ribosome-binding domain (RBD) mainly to ribosomal protein uL23 at the tunnel exit

86 n identified in the receptor-binding domain (RBD) of different SARS-CoV strains isolated from humans

87 ta suggest that the receptor-binding domain (RBD) of HKU1 spike protein is located in the C domain, w

88 is mediated by the receptor binding domain (RBD) of its spike, the hemagglutinin (HA).

89 interaction of the receptor-binding domain (RBD) of MERS-CoV spike protein and DPP4 was determined b

90 100A4 interacts with the Rho-binding domain (RBD) of Rhotekin, thus connecting S100A4 to the Rho path

91 Here, we show that the RNA-binding domain (RBD) of SRSF1 optimally binds to decameric purine rich E

92 tation within the S receptor binding domain (RBD) of SZ16, the recombinant virus (icSZ16-S K479N) rep

93 ment of 23S rRNA and the RNA binding domain (RBD) of the Bacillus subtilis DbpA protein YxiN was crys

94 ence and presence of the Ras-binding domain (RBD) of the c-Raf kinase protein (Raf-RBD).

95 ing the receptor (CD26/DPP4) binding domain (RBD) of the MERS-CoV spike glycoprotein from a very larg

96 ically binds to the receptor-binding domain (RBD) of the MERS-CoV spike protein and thereby competiti

97 an nAbs against the receptor-binding domain (RBD) of the MERS-CoV Spike protein.

98 that contained the receptor-binding domain (RBD) of the neurovirulent virus induced neurological dis

99 s indicate that the receptor binding domain (RBD) of the SARS-CoV spike (S) glycoprotein contains maj

100 The receptor binding domain (RBD) of the spike (S) glycoprotein of severe acute respi

101 779) represents the receptor-binding domain (RBD) of the toxin.

102 at targets the host receptor-binding domain (RBD) of the type IV pilus of P. aeruginosa.

103 cused solely on the receptor-binding domain (RBD) of the viral Spike (S) glycoprotein may not optimiz

104 Abs that target the receptor binding domain (RBD) of the virus.

105 s between a defined receptor-binding domain (RBD) on a viral spike protein and its host receptor, ang

106 d expressed alpha2M receptor binding domain (RBD) should trigger comparable signaling events.

107 l genes and the HA1 receptor binding domain (RBD) than for the younger age groups (0 to 69 years).

108 the Bat-SCoV Spike receptor-binding domain (RBD) with the SARS-CoV RBD (Bat-SRBD).

109 udies have identified an RNA binding domain (RBD) within TERT, which includes three evolutionarily co

110 s spike (S) protein receptor-binding domain (RBD), a key vaccine target, have been identified, raisin

111 for binding to the receptor-binding domain (RBD), suggesting a mechanism of neutralization that invo

112 ions of the EBOV GP receptor-binding domain (RBD), thereby blocking epitopes within the RBD, we also

113 region contains the receptor-binding domain (RBD), which has a potential to be developed as a MERS-Co

114 ng via an amino-terminal RAS-binding domain (RBD).

115 nal peptide of THPO receptor binding domain (RBD).

116 LV envelope protein receptor binding domain (RBD).

117 (K41) in the N-terminal RNA-binding domain (RBD).

118 two segments by a Rho GTPase-binding domain (RBD).

119 separated by the Rho GTPase binding domain (RBD).

120 to uPAR mRNA through its RNA binding domain (RBD).

121 e spike (S) protein receptor-binding domain (RBD).

122 eins containing a common RAS-binding domain (RBD).

123 MAbs recognized the receptor-binding domain (RBD; aa 318 to 510), and 6 MAbs reacted with the C-termi

124 rrier site and the LRP-1 recognition domain (RBD) as separate GST fusion proteins (FP3 and FP6, respe

125 TDP-43 possesses two RNA binding domains (RBD) and a glycine-rich C terminus classifying it with o

126 lling in Dp110(RBD) imaginal discs and Dp110(RBD) flies are small.

127 aximally activate PI(3)K signalling in Dp110(RBD) imaginal discs and Dp110(RBD) flies are small.

128 ive amino acid residues involved in the DPP4-RBD interaction.

129 tions for the improved motor function during RBD episodes are evaluated in light of recent publicatio

130 Of note, patients with PD observed during RBD episodes exhibit improved motor function, relative t

131 wn seemingly normal motor performance during RBD in PD patients might be generated by activating alte

132 significantly more susceptible to both EboV RBD binding and GP-pseudotyped virus infection than thei

133 nt Ebola virus receptor binding domain (EboV RBD) and to be infected with Ebola virus glycoprotein (G

134 ore, with 293F cells the acquisition of EboV RBD binding paralleled cell spreading and did not requir

135 their strong cross-reactivity with anti-EMC-RBD antibodies.

136 Like the RBD of prototype EMC2012 (EMC-RBD), all five RBDs maintained good antigenicity and fun

137 The entire RBD, comprised of two RRMs and a glycine-rich linker, is

138 l glycoprotein (G) was used as a carrier for RBD in an inactivated form of the vector.

139 es from 5.7 to 7.0 causes production of free RBD and RBD-containing fragments.

140 ch of the three RBD variants (Tor2-RBD, GD03-RBD, and SZ3-RBD) that differ at several amino acids.

141 ng of a globular receptor-binding domain (HA-RBD) that is inserted into a membrane fusion-mediating s

142 Recombinant HA-RBD is immunogenic and protective in ferrets, and the pr

143 olutionary standpoint, the ability of the HA-RBD to refold spontaneously into its native conformation

144 In the 2.10-A structure of the HA-RBD, the receptor-binding pocket is intact and its confo

145 ography, we show that the influenza virus HA-RBD refolds spontaneously into its native, immunogenic s

146 t at the SARS-CoV/hACE2 interface, and hence RBD/hACE2 binding affinities are decreased either by NL6

147 However, RBD-directed nAbs may be useful for providing broad neut

148 Patients with idiopathic RBD are at very high risk of neurodegenerative synuclein

149 itudinal studies in patients with idiopathic RBD are warranted to characterize the natural history of

150 e samples involving subjects with idiopathic RBD have suggested an increased risk of incident mild co

151 RBD, as well as in patients with idiopathic RBD, to further elucidate the pathophysiology and also c

152 synucleinopathy to patients with idiopathic RBD.

153 suggest that many patients with 'idiopathic' RBD are actually exhibiting an early clinical manifestat

154 In RBD, alpha-synuclein abnormalities in the brainstem disi

155 In RBD, degeneration of this circuitry disinhibits phasic m

156 Simple behaviors in RBD may originate from cortical, brainstem and spinal co

157 and SARS-CoV have no structural homology in RBD cores or RBMs; yet the 2 viruses recognize common AC

158 tion of tyrosine residue 57 (Y57) present in RBD of hnRNPC by uPA is essential for uPAR 3'-UTR mRNA b

159 The transcriptomic response in RBD was independently compared with that of fish from ea

160 Indeed, RBD or its K1370A mutant that binds to GRP78 but cannot

161 er, our simulations suggest that while inter-RBD reorientation may be important, it is not, by itself

162 THPO has 4 conserved cysteines in its RBD that form 2 disulfide bonds.

163 l GTPases bind and activate p110beta via its RBD.

164 g in PC12 cells was reproduced by the 18-kDa RBD, isolated from plasma-purified alpha(2)M by proteoly

165 s of the RBD and a docking model of the m336-RBD complex.

166 hese results support a model where the Mre11 RBD and linker domain act as an autoinhibitory domain wh

167 ted by solving the atomic structure of a NAb-RBD complex, through sequencing of neutralization escape

168 Among viruses carrying the neurovirulent RBD, the severity of the disease was increased when enve

169 at immunization elicits NAbs to RBD and, non-RBD portions of S1 and S2 subunit.

170 onstruct an isolated RNA-binding domain (Nop-RBD) that folds correctly as demonstrated by x-ray cryst

171 These data demonstrate that the Nop-RBD is an autonomously folding and functional module imp

172 of K41 disrupts the association of the NS1A RBD domain with importin-alpha, the protein that mediate

173 he premotor stages of PD, the association of RBD with motor and non-motor features in early PD remain

174 The association of RBD with neurological disease ('secondary RBD') is prese

175 The behaviors of RBD are often theatrical, with complexity, aggression, a

176 he MR complex when combined with deletion of RBD.

177 of the patients had a previous diagnosis of RBD.

178 The effects of RBD and its mutant were similarly blocked by these antib

179 ified, raising concerns over the efficacy of RBD-based MERS vaccines against circulating human and ca

180 ation affects the conformational ensemble of RBD globally, including the RBD-FAD interface, suggestin

181 f 80 subjects (33.8%) indicated a history of RBD symptoms.

182 nism and/or dementia well after the onset of RBD.

183 rk and new schema for the pathophysiology of RBD are proposed based on recent data in rat regarding t

184 The hypothesized pathophysiology of RBD is presented in relation to the Braak staging system

185 INTERPRETATION: The presence of RBD symptoms in PD is associated with relative neocortic

186 The presence of RBD symptoms may signal cholinergic system degeneration.

187 The presence of RBD symptoms was determined using the Mayo Sleep Questio

188 idues in the receptor-binding motif (RBM) of RBD and demonstrated their strong cross-reactivity with

189 clinical and pathophysiological relevance of RBD in neurodegenerative disease.

190 m structures responsible for the symptoms of RBD correspond to the premotor stages of PD, the associa

191 ween cholinergic denervation and symptoms of RBD in PD patients without dementia.

192 Treatment of RBD can prevent injury to patients and bed partners.

193 ycle that contribute to our understanding of RBD.

194 y mimicking immune responses with the use of RBD as an antigen to screen a large human antibody libra

195 c findings supporting the prodromal value of RBD for PD, incorporating clinical and electrophysiologi

196 identified in a PubMed search of articles on RBD from January 1, 1986, through July 31, 2014.

197 condary RBD') is presented, with emphasis on RBD associated with neurodegenerative disease, particula

198 The civet-optimized RBD contains all of the cACE2-adapted residues (Tyr-442,

199 The human-optimized RBD contains all of the hACE2-adapted residues (Phe-442,

200 from mice carrying mutations in the p110beta RBD show reduced PI3K activity and defective chemotaxis,

201 entify the specific elements within the PERV RBD that interact with the C-terminal elements of SU to

202 ropism-determining sequences within the PERV RBD.

203 conserved backbone conformation of the pilin RBD.

204 dementia, and PD among the exposed (probable RBD [pRBD](+)) and unexposed (pRBD(-)) cohorts.

205 of aging who screened positive for probable RBD using the Mayo Sleep Questionnaire were followed at

206 rs of diagnosis for the presence of probable RBD (pRBD) using the REM Sleep Behaviour Disorder Screen

207 e binding energies of MERS-CoV spike protein RBD to DPP4 of human (susceptible) or hamster (nonsuscep

208 omain (RBD) of the c-Raf kinase protein (Raf-RBD).

209 itch I, and switch II, as well as at the Raf-RBD binding pocket.

210 n the Switch I region of Ras, similar to Raf-RBD, and competes with Raf-RBD for binding.

211 s, similar to Raf-RBD, and competes with Raf-RBD for binding.

212 ntional ELISA format with immobilized RalGDS-RBD as a bait to selectively capture GTP-bound active Ra

213 Here, we constructed four recombinant RBD (rRBD) proteins with single or multiple mutations de

214 specifically and directly binds to Rhotekin RBD, but not the other Rho effector RBDs.

215 of RBD with neurological disease ('secondary RBD') is presented, with emphasis on RBD associated with

216 chanisms of each of these naturally selected RBD mutations.

217 al simulations that ephrin induces a similar RBD-RBD reorientation in a stimulation-deficient G mutan

218 Since RBD mutations occur in different MERS-CoV isolates and a

219 en developed, it remains unclear if a single RBD-targeting nAb or two in combination can prevent neut

220 a safe, highly effective, and broad-spectrum RBD-based subunit vaccine to prevent MERS-CoV infection.

221 proximately 50% of patients with spontaneous RBD will convert to a parkinsonian disorder within a dec

222 ee RBD variants (Tor2-RBD, GD03-RBD, and SZ3-RBD) that differ at several amino acids.

223 reveals the molecular structure of the TcdB RBD for the first time, facilitating the crystallization

224 entify sites of interaction between the TERT RBD and TER, revealing that the CP2 motif is in close pr

225 Based on previous studies suggesting that RBD may be prognostic for the development of later parki

226 The RBD contains critical neutralizing epitopes and serves a

227 The RBD is bound between two RNA strands at a three-way junc

228 The RBD is not dimerized, as observed previously.

229 The RBD is very immunogenic; it is a major SCV neutralizatio

230 The RBD overlaps with the coiled coil and extends through th

231 to compete with dimerization and anchors the RBD to the GAP domain.

232 Both the N-terminal segment and the RBD make extensive interactions with the GAP domain, sug

233 tope that overlaps the interface between the RBD and its receptor, angiotensin-converting enzyme 2 (A

234 hain, and residues in the linker between the RBD and the effector domain from the other chain.

235 Thus, the interactions between the RBD and the rest of the pilin can either be mediated by

236 Likewise, only viruses containing the RBD of the neurovirulent virus exhibited increased bindi

237 ich has generated interest in developing the RBD as a viable vaccine target.

238 nt mutation of the conserved residues in the RBD (e.g., D429A, R441A, or D454A) and the Conf III epit

239 Two putative hot-spot residues in the RBD (Ile-489 and Tyr-491) were identified within the SAR

240 nAbs bind to three different epitopes in the RBD and human dipeptidyl peptidase 4 (hDPP4) interface w

241 bstitutions of non-conserved residues in the RBD are compensated for by complementary changes in the

242 y ACE2-induced conformational changes in the RBD but may involve other conformational changes or/and

243 ntaining single or multiple mutations in the RBD of representative human and camel MERS-CoV strains d

244 ed approximately 30 residue positions in the RBD that present distinct profiles with the receptor ana

245 onal ensemble of RBD globally, including the RBD-FAD interface, suggesting the latter's role in G sti

246 volve at least one of the two interfaces-the RBD-FAD interface and/or the RBD-RBD interface.

247 Like the RBD of prototype EMC2012 (EMC-RBD), all five RBDs mainta

248 upported by site-directed mutagenesis of the RBD and a docking model of the m336-RBD complex.

249 hibition due to the tight association of the RBD and the Rad50 coiled-coil.

250 Furthermore, alanine scanning of the RBD has identified several residues at the DPP4-binding

251 Deletion of the RBD in Mre11 eliminates Rad50 binding but only has moder

252 Binding of the RBD to 23S rRNA in the late stages of ribosome subunit m

253 reby competitively blocks the binding of the RBD to its cellular receptor, dipeptidyl peptidase 4 (DP

254 mains, a conformational rearrangement of the RBD upon ribosome binding, and an increase in rigidity w

255 Mutation of the RBD within this fragment caused lethality and perturbed

256 and determined the crystal structure of the RBD-antibody complex at 2.3-A resolution.

257 subunit causes substantial protection of the RBD-C2 linker as well as the helical domain of p110gamma

258 Strikingly, all of the RBD-specific MAbs had potent neutralizing activity, 6 of

259 tropositive band generated by lysines of the RBD.

260 ain a conserved backbone conformation of the RBD.

261 of exposed side-chains on the surface of the RBD.

262 hat overlap the receptor binding site on the RBD as suggested by competition experiments and further

263 close proximity of the three epitopes on the RBD interface, escape from one epitope did not have a ma

264 5%]; P = .052), and had higher scores on the RBD questionnaire (mean [SD], 7.8 [2.2] vs 5.1 [3.3]; P

265 le residue positions that are exposed on the RBD surface.

266 toxin B is toxic to cells, depending on the RBD-like region (residues 1349-1811) but does not intera

267 dynamics the effect of ephrin binding on the RBD-RBD interface.

268 interfaces-the RBD-FAD interface and/or the RBD-RBD interface.

269 ces from the neurovirulent virus outside the RBD were also present.

270 ges in individual RBDs, ephrin reorients the RBD-RBD interface extensively, and in a manner that will

271 ed the receptor binding, confirming that the RBD contains the main neutralizing epitopes and that blo

272 Thus, the RBD determined both neurovirulence and folding instabili

273 nd a Rho-family GTPase (Rac1 or Rnd1) to the RBD.

274 lear import of the NS1A protein, whereas the RBD retains its double-stranded RNA-binding activity.

275 d structure of human ACE2 complexed with the RBD from a human SARS-CoV strain, have revealed a struct

276 tranded loop of hairpin 92 interact with the RBD, including the guanosine base of G2553, which forms

277 cell epitopes residing primarily within the RBD of the molecule, using a restricted number of TRBV a

278 (RBD), thereby blocking epitopes within the RBD, we also tested whether VSVDeltaG bearing EBOV GPs t

279 These RBD mutants with diminished DPP4 binding also led to vir

280 These RBD-based vaccine candidates maintained good functionali

281 reacted significantly with each of the three RBD variants (Tor2-RBD, GD03-RBD, and SZ3-RBD) that diff

282 396, which competes with ACE2 for binding to RBD, and determined the crystal structure of the RBD-ant

283 , as measured by Biacore for Fabs binding to RBD.

284 d efferent and afferent pathways) crucial to RBD pathophysiology.

285 s revealed that immunization elicits NAbs to RBD and, non-RBD portions of S1 and S2 subunit.

286 The terminology relating to RBD, and mechanisms underlying REM sleep without atonia

287 on the orientation of the ED with respect to RBD can be summarized as "open," "semi-open," and "close

288 We also demonstrate that the Tor2-RBD induced-Conf I-VI mAbs can potently neutralize both

289 ly with each of the three RBD variants (Tor2-RBD, GD03-RBD, and SZ3-RBD) that differ at several amino

290 idues (residues 31, 35, 38, and 353) and two RBD residues (residues 479 and 487), that early civet SA

291 ped, the orientation of binding (i.e., which RBD binds to which site in the IRES) is unknown.

292 While RBD can occur idiopathically, it is usually comorbid wit

293 data from the few published human cases with RBD associated with structural lesions in the brainstem

294 with early neurodegeneration, patients with RBD demonstrate subtle motor, cognitive, and autonomic i

295 timately, nearly all (81%-90%) patients with RBD develop a neurodegenerative disorder.

296 ng REM sleep in some of the cases of PD with RBD emphasizes the complexity of motor pathway control d

297 Subjects with RBD symptoms, in comparison to those without, exhibited

298 Subjects with and without RBD symptoms showed no significant differences in age, m

299 h dementia or parkinsonism, with and without RBD, as well as in patients with idiopathic RBD, to furt

300 were compared to 20 matched controls without RBD who underwent DAT-SPECT.