ライフサイエンスコーパス: nucleotide binding

1 in release from the activated receptor after nucleotide binding.

2 nd Mcm5 that opens and closes in response to nucleotide binding.

3 rotein of 70 kDa (Hsp70) chaperone DnaK upon nucleotide binding.

4 n this conformation may deleteriously affect nucleotide binding.

5 d that their main molecular functions are in nucleotide binding (20.9%), hydrolase activities (10.6%)

6 The nucleotide-binding ability of PCBP1 was impaired by zinc

7 ogy analysis all strongly support defects in nucleotide-binding activity.

8 nd their homologs that represent the NB-ARC (nucleotide-binding adaptor shared by APAF-1, certain R g

9 site rearrangements that lead to a decreased nucleotide binding affinity and incorporation rate.

10 ative variant of Ras that displays decreased nucleotide binding affinity.

11 nd ribonucleotides primarily through reduced nucleotide binding affinity.

12 ction; this rate balance ensures that, after nucleotide binding and fingers-closing, nucleotide incor

13 Proteins with cyclic nucleotide binding and GAF domains can be identified in

14 mediate allosteric regulation in response to nucleotide binding and hydrolysis in MeaB.

15 Using nucleotide binding and hydrolysis mutants, we show that,

16 f enzyme conformational changes that monitor nucleotide binding and incorporation.

17 It is shown how missed events of nucleotide binding and release in these experiments can

18 supports the mechanism involving concurrent nucleotide binding and release.

19 nuclear proteins, like proteins involved in nucleotide binding and RNA splicing.

20 of transposable elements in the expansion of nucleotide-binding and leucine-rich-repeat proteins (NLR

21 Sse1sbd retains nucleotide-binding and nucleotide exchange activities wh

22 Nucleotide-binding and oligomerization domain (NOD)-like

23 te metabolic and inflammatory processes, the nucleotide-binding and oligomerization domain-like recep

24 o alter TCL plasma membrane localization and nucleotide binding, and additional truncation and point

25 of the RecA fold of DnaB that is involved in nucleotide binding, and of the AAA+ domain of DnaC.

26 This was supported by the use of nucleotide-binding assays that revealed an increase in t

27 Nucleotide binding at the degenerate ATP site prevents c

28 We report on nucleotide binding between the separate N- and C-lobes o

29 t capping and stabilization are dependent on nucleotide binding, but not hydrolysis by RFS-1/RIP-1.

30 nes with recessive variants were enriched in nucleotide binding capacity, ATPase activity, and the dy

31 structural plasticity within and around the nucleotide-binding cavity, and the switch I and switch I

32 ed of two largely alpha-helical lobes with a nucleotide binding cleft.

33 -actin contacts and restricts opening of the nucleotide-binding cleft in actin subunits.

34 e PEAK1 kinase-like domain contains a closed nucleotide-binding cleft that in this conformation may d

35 ne binding required the high-affinity cyclic nucleotide-binding (CNB) and Ras association domains, bu

36 ve to 8-oxoG bypass is due to an alternative nucleotide binding conformation in the precatalytic tern

37 We also found that upon nucleotide binding, CrSEPT formed dimers that were stabi

38 We show that a variant of MutS with a nucleotide binding defect is no longer capable of dynami

39 First, we demonstrate that a nucleotide binding-defective form of tTG, which has prev

40 hanical changes within the subdomains of the nucleotide binding domain (NBD) of the heat shock protei

41 deletion of F508 (DeltaF508) from the first nucleotide binding domain (NBD1) of CFTR, results in mis

42 ulator (CFTR) first cytosolic loop (CL1) and nucleotide binding domain 1 (NBD1) that allows ion trans

43 coupling helices predicted to interact with nucleotide binding domain 1 at the interface.

44 Nucleotide binding domain and leucine-rich repeat protei

45 ranslocated bacterial products are sensed by nucleotide binding domain and leucine-rich repeat-contai

46 g that phosphorylation requires a functional nucleotide binding domain and occurs in the post-hydroly

47 different conformational states of the HSP70 nucleotide binding domain highlighted the challenges of

48 of the SUR1-ABC core connected to the first nucleotide binding domain near the inner leaflet of the

49 g domain (CaMBD) overlapping with the cyclic nucleotide binding domain of plant CNGCs.

50 cyclic adenosine monophosphate to the cyclic nucleotide binding domain of the bacterial potassium cha

51 tion in the catalytic site of the C-terminal nucleotide binding domain restored proper protein traffi

52 The amino-terminal nucleotide binding domain rotates to close the active si

53 functionally stimulated by the activation of nucleotide binding domain, leucine-rich-containing famil

54 us region of DnaK, involving lobe IIA of the nucleotide binding domain, the inter-domain linker, and

55 the transmembrane domain and the C-terminal nucleotide binding domain.

56 nds that interact with the regulatory cyclic nucleotide-binding domain (CNB) of the cAMP sensor, EPAC

57 y the presence of a carboxyl-terminal cyclic nucleotide-binding domain (CNBD) that connects to the ch

58 eotides to a conserved, intracellular cyclic nucleotide-binding domain (CNBD), which is connected to

59 ls, TRIP8b also binds directly to the cyclic nucleotide-binding domain (CNBD).

60 n two well-structured domains: an N-terminal nucleotide-binding domain (NBD) and a C-terminal substra

61 te-controllable docking and undocking of its nucleotide-binding domain (NBD) and substrate-binding do

62 docked model predicted that a region in the nucleotide-binding domain (NBD) of DnaK interacted with

63 Hsc70 has two major domains: a nucleotide-binding domain (NBD), that hydrolyzes ATP, an

64 of hexameric ClpB/Hsp104 and the DnaK/Hsp70 nucleotide-binding domain (NBD).

65 te the direct binding of VX-809 to the first nucleotide-binding domain (NBD1) of human CFTR.

66 Deletion of Phe-508 (F508del) in the first nucleotide-binding domain (NBD1) of the cystic fibrosis

67 Characterization of the second nucleotide-binding domain (NBD2) of the cystic fibrosis

68 FTR protein lacking the terminal part of the nucleotide-binding domain 1 (NBD1) and thus is likely to

69 ation that disrupts substrate binding to the nucleotide-binding domain 1 (NBD1) pore loop and is abol

70 NLRs (nucleotide-binding domain [NBD] leucine-rich repeat [LRR

71 through key structural motifs in the cyclic nucleotide-binding domain and explore the role of kineti

72 ms a dimer in which each protomer contains a nucleotide-binding domain and four transmembrane helices

73 ATP hydrolysis drives rotation of the nucleotide-binding domain and induces the DNA melting so

74 ic assembly of the channel; ATP binds at the nucleotide-binding domain and inhibits channel activity.

75 Nucleotide-binding domain and leucine-rich repeat (NLR)

76 Nucleotide-binding domain and leucine-rich repeat (NLR)

77 urrently evolved at the DANGEROUS MIX2 (DM2) nucleotide-binding domain and leucine-rich repeat (NLR)-

78 The role of the nucleotide-binding domain and leucine-rich repeat contai

79 d mitochondria are central regulators of the nucleotide-binding domain and leucine-rich repeat pyrin

80 or danger-associated molecular patterns by a nucleotide-binding domain and leucine-rich repeat recept

81 s intracellular immune receptors designated "nucleotide-binding domain and leucine-rich repeat" (NLR)

82 MHC class I transactivator (CITA), NLRC5 [nucleotide-binding domain and leucine-rich repeats conta

83 NLRs (nucleotide-binding domain and leucine-rich repeats) belo

84 the nucleotide-binding domain and substrate-binding domain)

85 In this report, we found that the cyclic nucleotide-binding domain and the C terminus of the HCN

86 The N-terminal nucleotide-binding domain and the C-terminal coiled-coil

87 the extended X loop in the cross-talk of the nucleotide-binding domain and the transmembrane domain.

88 Although the C-terminal cyclic nucleotide-binding domain B of PKG binds cGMP with highe

89 ] increased, reflecting stabilization of the nucleotide-binding domain by ligand binding; (b) a tempe

90 P47 precludes substrate binding and prevents nucleotide-binding domain closure necessary for ATP hydr

91 inding of ATP and thereby impair ATP-induced nucleotide-binding domain dimerization and ABCB4 functio

92 The Q1174E mutation is located in the nucleotide-binding domain in direct proximity of the leu

93 these systems to be recruited as a predicted nucleotide-binding domain in eukaryotic TRPM channels.

94 terminal linker connecting S6 and the cyclic-nucleotide-binding domain interacts directly with both t

95 Nucleotide-binding domain leucine-rich repeat (NLR) prot

96 In this study, we explore the role of the nucleotide-binding domain leucine-rich repeat containing

97 ent of MBD1-3 was found to interact with the nucleotide-binding domain of ATP7B, thus physically coup

98 , we noted a structural homology between the nucleotide-binding domain of NLRs and DNA replication or

99 to the interface between the NTD and the D1 nucleotide-binding domain of the complex.

100 dule (CBM) appended to the C terminus of the nucleotide-binding domain of the transporter.

101 lls overexpressing the E266K mutation in the nucleotide-binding domain or the wild-type NOD1, HCMV wa

102 responding to the N-terminal coiled-coil and nucleotide-binding domain regions of the I-2 NLR of toma

103 We show that TRIP8b binds the HCN cyclic nucleotide-binding domain through a 37-residue domain an

104 upted by mutation within its putative cyclic nucleotide-binding domain within PDZ-GEF1.

105 nd animals use intracellular proteins of the nucleotide-binding domain, leucine-rich repeat (NLR) sup

106 NLRC3 is a recently characterized nucleotide-binding domain, leucine-rich repeat containin

107 e leukocytes to produce MPs and activate the nucleotide-binding domain, leucine-rich repeat pyrin dom

108 l priming and whether HMGB-1 does so via the nucleotide-binding domain, leucine-rich repeat, pyrin do

109 In mice, specific nucleotide-binding domain, leucine-rich repeat-containin

110 sis inhibitory proteins (NAIPs) activate the nucleotide-binding domain, leucine-rich repeat-containin

111 in autolysosomes colocalizes with pyrin and nucleotide-binding domain, leucine-rich repeat/pyrin dom

112 duced FAO resulted in less activation of the nucleotide-binding domain, leucine-rich-repeat-containin

113 role in exchanging ADP for ATP at mtHsp70's nucleotide-binding domain, thereby modulating mtHsp70's

114 rosine residues located in flexible loops in nucleotide-binding domain-1 that extend into the ClpB ce

115 ress immunity; however, the plant can evolve nucleotide-binding domain-leucine-rich repeat domain-con

116 nucleotides binding to a specialized cyclic nucleotide-binding domain.

117 regulated by binding of ATP/ADP to mtHsp70's nucleotide-binding domain.

118 ctivity and binds ATP only in its N-terminal nucleotide-binding domain.

119 NLRX1 is unique among the nucleotide-binding-domain and leucine-rich-repeat (NLR)

120 us contains a region with homology to cyclic nucleotide binding domains (cNBHD), which is directly li

121 composed of transmembrane domains (TMDs) and nucleotide binding domains (NBD).

122 leotides, human P-gp can exist in both open [nucleotide binding domains (NBDs) apart; inward-facing]

123 c gating deficit is not due to dysfunctional nucleotide binding domains (NBDs) as the mutation does n

124 inding-induced dimerization of two cytosolic nucleotide binding domains (NBDs) opens the pore, and di

125 membrane by coupling ATP-driven movements of nucleotide binding domains (NBDs) to the transmembrane d

126 s, is opened by ATP binding to two cytosolic nucleotide binding domains (NBDs), but pore-domain mutat

127 (TMDs) without altering the function of the nucleotide binding domains (NBDs).

128 a C-terminal domain with homology to cyclic nucleotide binding domains (referred to as the CNBh doma

129 The interface between its two cytosolic nucleotide binding domains and coupling helices conferre

130 d in conserved residues of either of the two nucleotide binding domains and determined the effect on

131 l inward-facing conformation whereby the two nucleotide binding domains are misaligned along a two-fo

132 the first structural insights into two novel nucleotide binding domains associated with bacterial vir

133 s reveals how reversible dimerization of the nucleotide binding domains drives opening and closing of

134 Here we show that DNA bricks with longer, 13-nucleotide binding domains make it possible to self-asse

135 P to conserved and well characterized cyclic nucleotide binding domains or structurally distinct cGMP

136 es to the ATP occupancies of their cytosolic nucleotide binding domains.

137 2 nucleotides long, consisting of four eight-nucleotide binding domains.

138 irectly observe binding at individual cyclic nucleotide-binding domains (CNBDs) from human pacemaker

139 A consists of several domains, including two nucleotide-binding domains (NBD1 and NBD2), a polypeptid

140 disengaged from its inhibitory position; the nucleotide-binding domains (NBDs) form a "head-to-tail"

141 pe ATP-binding cassette transporter with two nucleotide-binding domains (NBDs) that bind and hydrolyz

142 oupling of ATP binding and hydrolysis in the nucleotide-binding domains (NBDs) to conformational chan

143 harness the energy of ATP hydrolysis in the nucleotide-binding domains (NBDs) to power the energetic

144 in the intracellular opening between the two nucleotide-binding domains (NBDs), preventing NBD dimeri

145 significantly smaller separation between the nucleotide-binding domains and a larger fraction of mole

146 larger fraction of molecules with associated nucleotide-binding domains in the nucleotide-free apo st

147 fluorescent protein (GFP) and TagRFP to MRP1 nucleotide-binding domains NBD1 and NBD2, respectively.

148 The nucleotide-binding domains of SUR1 are dimerized with Mg

149 the 12 transmembrane helices and 2 cytosolic nucleotide-binding domains of the transporter adopt an i

150 t an inward-facing conformation with the two nucleotide-binding domains separated.

151 s that form a translocation pathway, and two nucleotide-binding domains that hydrolyse ATP.

152 eins bearing leucine-rich repeats (LRRs) and nucleotide-binding domains.

153 e to engagement and hydrolysis of ATP at the nucleotide-binding domains.

154 ral groove between two ATPgammaS-bound Rad50 nucleotide-binding domains.

155 in part, at ATP-binding site 1 formed by the nucleotide-binding domains.

156 sed from ATP binding and hydrolysis at their nucleotide-binding domains.

157 ding helices in the transmembrane domain and nucleotide-binding domains.

158 Based on the correlation between nucleotide binding, effector interaction, and immune sig

159 itation studies revealed that STIM1 binds to nucleotide binding fold-1 (NBF1) of the sulfonylurea rec

160 We previously showed that guanine nucleotide-binding (G) protein alpha subunit (Galpha)-in

161 Although cyclic nucleotide binding has been shown to promote CNG and HCN

162 conserved Higher Eukaryotes and Prokaryotes Nucleotide-binding (HEPN) domains, mutations of which ge

163 and two in the adjacent region of the cyclic nucleotide-binding homology domain, can fully account fo

164 fer activity, leaving the functional role of nucleotide binding in most cases unknown.

165 nly the D2 ATPase ring hydrolyzes ATP, while nucleotide binding in the D1 ring promotes complex assem

166 eport results from assays for solution-based nucleotide binding, intrinsic and GTPase-activating prot

167 and from the replisome, showing that proper nucleotide binding is critical for MutS to localize to t

168 esponse to ADP binding, and the affinity for nucleotide binding is strongly enhanced by the presence

169 alysis afforded thermodynamic parameters for nucleotide binding (Kd , DeltaG, DeltaH, and DeltaS at 3

170 logous to barley Mla, encoding a coiled-coil nucleotide-binding leucine-rich repeat (CC-NB-LRR) prote

171 Nucleotide-binding leucine-rich repeat (NB-LRR, or NLR)

172 to identify Recognition of XopQ 1 (Roq1), a nucleotide-binding leucine-rich repeat (NLR) protein wit

173 ACQOS is identical to VICTR, encoding a nucleotide-binding leucine-rich repeat (NLR) protein(3).

174 idopsis thaliana named RPS5, which encodes a nucleotide-binding leucine-rich repeat (NLR) protein.

175 Plant nucleotide-binding leucine-rich repeat (NLR) proteins en

176 Plant nucleotide-binding leucine-rich repeat (NLR) proteins en

177 plant disease resistance genes encoding for nucleotide-binding leucine-rich repeat (NLR) proteins ha

178 Nucleotide-binding leucine-rich repeat (NLR) proteins se

179 Mi-1.2 encodes a coiled-coil nucleotide-binding leucine-rich repeat protein that in a

180 We show that the rice gene Xa1, encoding a nucleotide-binding leucine-rich repeat protein, confers

181 Nucleotide-binding leucine-rich repeat proteins (NLRs) s

182 luding two linked genes encoding coiled-coil nucleotide-binding leucine-rich repeat proteins designat

183 the Prf recognition complex, composed of the nucleotide-binding leucine-rich repeats protein Prf and

184 Several plant nucleotide-binding, leucine-rich repeat (NB-LRR) immune

185 y should enable de novo assembly of complete nucleotide-binding, leucine-rich repeat receptor (NLR) g

186 onserved cysteines that is positioned at the nucleotide-binding loop of eukaryotic ADPGK.

187 novel signaling hub centering on the NLRX1 (nucleotide-binding, lots of leucine-rich repeats-contain

188 Mutation of the nucleotide-binding motif GxxG to GDDG in all three KH do

189 The MshEN domain contains the longest nucleotide-binding motif reported to date.

190 inating the AMP with its main chain atoms, a nucleotide-binding motif that appears unique to eukaryot

191 Its motor domain contains conserved nucleotide binding motifs, but is divergent in sequence

192 d two polymorphic regions in the TIR and the nucleotide binding (NB) domains that regulate both effec

193 (TIR) or coiled-coil (CC) domain, a central nucleotide-binding (NB) domain, and a C-terminal leucine

194 ffect of the T2S system was not dependent on nucleotide binding oligomerization domain (NOD)-like rec

195 disrupted the ability of TRIM22 to regulate nucleotide binding oligomerization domain containing 2 (

196 TLR, nucleotide binding oligomerization domain-like receptor,

197 of genes encoded for components of the TLR, nucleotide binding oligomerization domain-like receptor,

198 Activation of nucleotide-binding oligomerization domain (NOD) 1 and NO

199 , termed the inflammasome, by members of the nucleotide-binding oligomerization domain (Nod), leucine

200 ation of immune response pathways, including nucleotide-binding oligomerization domain (NOD)-, Toll-,

201 Nucleotide-binding oligomerization domain (Nod)-containi

202 Nucleotide-binding oligomerization domain (NOD)-like rec

203 also promote inflammation by activating the nucleotide-binding oligomerization domain (NOD)-like rec

204 ptors (PRRs), such as Toll-like receptors or nucleotide-binding oligomerization domain (NOD)-like rec

205 yrin domain containing 1 (NLRP1), NLRP3, and nucleotide-binding oligomerization domain (NOD)-like rec

206 We investigated the role of nucleotide-binding oligomerization domain 1 (NOD1), whic

207 Induction of nucleotide-binding oligomerization domain 2 (NOD2) and d

208 immunity, the intracellular pathogen sensor nucleotide-binding oligomerization domain 2 (NOD2) has b

209 at correlate with the expression of CYLD and nucleotide-binding oligomerization domain 2 (NOD2), 2 st

210 Acute stimulation of nucleotide-binding oligomerization domain 2 (NOD2), the

211 ase domain with RIPK4's did not complement a nucleotide-binding oligomerization domain 2 signaling or

212 lasmatic pattern recognition receptor, NOD2 (nucleotide-binding oligomerization domain 2), belongs to

213 enotype showed increased JAK2 expression and nucleotide-binding oligomerization domain 2-induced JAK2

214 AA carrier macrophages switched to increased nucleotide-binding oligomerization domain 2-induced proi

215 Recognition of symbiotic bacteria via the nucleotide-binding oligomerization domain containing 2 (

216 during streptozotocin (STZ)-induced T1D, the nucleotide-binding oligomerization domain containing 2 (

217 the Toll-like receptors 1, 2, and 4 and the nucleotide-binding oligomerization domain protein 1 indu

218 We demonstrate that both TNF-R and nucleotide-binding oligomerization domain stimulation pr

219 The inflammasome proteins nucleotide-binding oligomerization domain, leucine rich

220 , including IL-1 receptor (IL-1R) family and nucleotide-binding oligomerization domain, leucine-rich

221 f the Crohn's disease susceptibility protein nucleotide-binding oligomerization domain-containing 2 (

222 ppressor of cytokine signaling-3, rs4969170; nucleotide-binding oligomerization domain-containing pro

223 nic chlamydial species are known to activate nucleotide-binding oligomerization domain-containing pro

224 Nucleotide-binding oligomerization domain-containing pro

225 mal regulation of the innate immune receptor nucleotide-binding oligomerization domain-containing pro

226 nd synergistically enhanced by activation of nucleotide-binding oligomerization domain-containing pro

227 c acid-inducible gene 1-like receptor (RLR), nucleotide-binding oligomerization domain-like receptor

228 including, cytokine and chemokine signaling, nucleotide-binding oligomerization domain-like receptor

229 Excessive nucleotide-binding oligomerization domain-like receptor

230 hisms in genes encoding Toll-like receptors, nucleotide-binding oligomerization domain-like receptor-

231 e intracellular immunity receptors, known as nucleotide-binding oligomerization domain-like receptors

232 lysaccharide of Gram-negative microbes-while nucleotide-binding oligomerization domain-like receptors

233 eceptors (TLRs), cytosolic receptors such as nucleotide-binding oligomerization domain-like receptors

234 bial sensors, recent evidence indicates that nucleotide-binding oligomerization domains (NODs) can al

235 e N terminus and a loop region distal to the nucleotide binding pocket of TCL capable of allosterical

236 is able to adjust the key residues in the 5-nucleotide binding pocket to compensate for the change i

237 anonical RhoGAP domains and inserts into the nucleotide-binding pocket of RhoA, whereas the second ar

238 ligand-binding pocket of the receptor to the nucleotide-binding pocket of the G protein.

239 nhibited state with the ATP lid bound to the nucleotide-binding pocket.

240 ent causes several loops to close around the nucleotide-binding pocket.

241 ly observe the cooperativity between the two nucleotide binding pockets in the protein dimer.

242 s on the allosteric link between ligand- and nucleotide-binding pockets that shed new light on the G-

243 Nucleotide-binding/processing domains include TIR domain

244 To identify any differences in the nucleotide binding properties, as well as in the EF-Ts-m

245 Thus, the NTRs affect the specific nucleotide-binding properties of MYO1C isoforms, adding

246 and short hairpin RNA to knock down guanine nucleotide binding protein (GNB) isoforms (GNB1, GNB2, G

247 ar and right atrial beta2-AR and Gi (guanine nucleotide binding protein inhibitory regulatory) levels

248 Mutations in the MATR3 gene encoding the nucleotide binding protein Matrin 3 have recently been i

249 of left ventricular beta1-AR and Gs (guanine nucleotide binding protein stimulatory) were reduced, wh

250 activity is inhibited by the histidine triad nucleotide-binding protein 1 (HINT1) through direct bind

251 This poses the question of how NBP35 (Nucleotide-Binding Protein 35 kDa), the heteromeric part

252 Immunostaining with guanine nucleotide-binding protein beta 3 (GNB3) and cellular re

253 PilB of the motor complex, and the cytosolic nucleotide-binding protein PilM of the alignment complex

254 of protein kinase A (PRKACA) or the guanine nucleotide-binding protein subunit alpha (GNAS) gene, th

255 we show by microarray and RNAi that guanine nucleotide-binding protein subunit alpha13 (Galpha13) is

256 -region of GNB1, a gene encoding the guanine nucleotide-binding protein subunit beta-1, Gbeta.

257 dentified biallelic mutations in the guanine nucleotide-binding protein subunit beta-3 gene (GNB3).

258 De novo mutations in the guanine nucleotide-binding protein, beta 1 (GNB1) gene, encoding

259 ptins comprise a conserved family of guanine nucleotide binding proteins that polymerize in the form

260 The guanine nucleotide-binding proteins beta-3 subunit (GNB3) has a

261 rgerat fold resembling that found in certain nucleotide-binding proteins, and a Cys3His zinc finger.

262 arvested proteins, such as glycoproteins and nucleotide-binding proteins.

263 Heterotrimeric guanine-nucleotide-binding regulatory proteins (G-proteins) main

264 er synthesis, and demonstrate equivalence of nucleotide-binding residues in PriX with eukaryotic PriL

265 y approximately 60% while maintaining single-nucleotide binding resolution.

266 Nucleotide binding results in limited changes in the act

267 on genes encoding binding proteins, such as nucleotide-binding, RNA-binding and poly(U)-binding prot

268 ethionine residue M584 (Walker B sequence of nucleotide binding site 1) by glutamate imparted hydroly

269 hen the catalytic glutamate of the canonical nucleotide binding site 2 was mutated to glutamine.

270 is different in shape and location from the nucleotide binding site in the previously determined str

271 acity from the canonical to the noncanonical nucleotide binding site results in loss of active and ad

272 that mechanical energy is transmitted to its nucleotide binding site, thus lowering the affinity for

273 The cytosolic nucleotide binding site-leucine rich repeat (NBS-LRR) re

274 y as a result of divergent residues near the nucleotide binding site.

275 ding cassette proteins with one noncanonical nucleotide binding site.

276 ogens by plants is mediated by intracellular nucleotide-binding site leucine-rich repeat (NLR) recept

277 Nucleotide-binding site leucine-rich repeat resistance g

278 The motion centers on a dynamic hub near the nucleotide-binding site of Galphas, and radiates to heli

279 Here we show that PriX contains a nucleotide-binding site required for primer synthesis, a

280 The AMP-bound ADPGK structure defines the nucleotide-binding site with one of the disulfide bond c

281 alpha Ras-like domain that girds the guanine nucleotide-binding site, and destabilizes the interface

282 on and enable loop restructuring to form the nucleotide-binding site.

283 molecular modelling revealed variability in nucleotide binding sites between flatworm and human RIOK

284 ine and guanine nucleotides to the canonical nucleotide binding sites of the regulatory Bateman domai

285 sp90 in dependence on the number of occupied nucleotide binding sites.

286 the regulatory RCK domains, thus connecting nucleotide-binding sites and ion gates.

287 The transmembrane domains are coupled to the nucleotide-binding sites by networks of interactions tha

288 gh distinctly different from other cyclic-di-nucleotide-binding sites, as the half-binding sites are

289 isentangles the protein conformation and the nucleotide binding state of Hsp90 and extracts the kinet

290 We observed that species and nucleotide-binding state have significant impacts on the

291 ve site in the absence of PPi, suggests that nucleotide binding stimulates PPi dissociation and occur

292 36-amino acid long C-terminal domain in the nucleotide-binding subunit alpha (Mtalpha) of F-ATP synt

293 Specifically, our data suggest that nucleotide binding takes place as a small stretch of ami

294 2beta mutation prevents eIF5 GDI stabilizing nucleotide binding to eIF2, thereby altering the off-rat

295 n in the two-head-bound state does not alter nucleotide binding to the front head.

296 s conformational changes triggered by cyclic nucleotide binding to the gate.

297 ormation of HerA and detail the mechanism of nucleotide binding to the HerA-NurA complex from thermop

298 -independent cell death signaling as well as nucleotide binding to the receptor.

299 gical roles by opening in response to cyclic nucleotides binding to a specialized cyclic nucleotide-b

300 rt a kinetic analysis of fluorescent guanine nucleotides binding to EFL1 alone and in the presence of