ライフサイエンスコーパス: ring formation

1 ing reduction, lactamization and carbocyclic ring formation.

2 ch serves as a key control point in aromatic ring formation.

3 om aggregating into clumps and allows normal ring formation.

4 repositions Ect2 to induce local actomyosin ring formation.

5 son did not induce xylem initiation or false ring formation.

6 ction of SpoIIIAH with SpoIIQ would preclude ring formation.

7 GFP constructs in different stages of septin ring formation.

8 ore passive role for the microtubule in Dam1 ring formation.

9 rations including fusion, fragmentation, and ring formation.

10 ant for intersubunit interactions and stable ring formation.

11 athway to regulate chloroplast size and FtsZ ring formation.

12 FtsZ-FtsZ, both of which are essential for Z ring formation.

13 k between L-plastin and cortactin in sealing ring formation.

14 naling proteins in the regulation of sealing ring formation.

15 tinucleated TRAP(+) cells capable of F-actin ring formation.

16 lp bridge two existing models of cytokinetic ring formation.

17 rotein/RNA interaction relies on pRNA static ring formation.

18 of substrate adenylation and intramolecular ring formation.

19 TPase RhoA is a key regulator of contractile-ring formation.

20 to suppress cytoskeletal remodeling or actin ring formation.

21 ation and polymerization to ensure correct Z ring formation.

22 expression in strains defective in P- and l-ring formation.

23 nation is a cryptic strategy for cyclopropyl ring formation.

24 interactions are not dependent on correct Z-ring formation.

25 that active Rho is required for contractile ring formation.

26 ssary for specifying the site of contractile ring formation.

27 ent of Rho-mediated signaling in contractile ring formation.

28 to prevent polymerization and aberrant FtsZ ring formation.

29 torial region of the cell to permit cleavage ring formation.

30 er the growth rate regulation of medial FtsZ ring formation.

31 usly shown to be important for normal septin-ring formation.

32 by deacetylation of muramic acid and lactam ring formation.

33 erstable monomer that is defective in portal ring formation.

34 nvestigated further the mechanisms of septin-ring formation.

35 gation, E-double bond formation and thiazole ring formation.

36 and thus represent attractive substrates for ring formation.

37 achinery of the cell and acts by promoting Z-ring formation.

38 ogical regulation of MinC, an inhibitor of Z-ring formation.

39 the cyclooctane stereogenic center prior to ring formation.

40 ook formation, is not essential for rod or P ring formation.

41 ity of the newly formed 2'-oxyanion during C-ring formation.

42 hibiting chaining, nuclear division and FtsZ-ring formation.

43 ion, chromosome segregation, and contractile ring formation.

44 ed during [PSI(+)] curing seem to facilitate ring formation.

45 c parameters that are important for aromatic ring formation.

46 modulates the frequency and position of FtsZ ring formation.

47 t the OPGL receptor, RANK, also induce actin ring formation.

48 tative level that compression by flow drives ring formation.

49 e alignment enhances but is not required for ring formation.

50 more prone to racemization at C-5 during the ring formation.

51 by several cross-cutting faults during peak-ring formation.

52 th necessary and sufficient to promote actin ring formation.

53 inhibition of Cdc14 function prevented actin ring formation.

54 he resulting aminoallene adduct for bicyclic ring formation.

55 lead to models for MinE activation and MinE ring formation.

56 division site is predominant for contractile ring formation.

57 P)-related domain is required for node-based ring formation.

58 mutations that cause defects in contractile ring formation.

59 rongly inhibited at or before the level of Z-ring formation.

60 in Escherichia coli occurs at the stage of Z ring formation.

61 dies suggesting a role for Rng2p in node and ring formation.

62 quantum-chemical method) of the model epoxy ring formation.

63 e kinetics of posttranslational heterocyclic ring formation (-20 Da per ring) and demonstrated the ac

64 e (TPD) monomers, including Gewald thiophene ring formation, a Sandmeyer-type reaction, and neat cond

65 Concerted A-C ring formation: A concerted, but highly asynchronous, pa

66 Cs and rapidly (within 30 min) induces actin ring formation; a marked cytoskeletal rearrangement that

67 thylations, isomerization, sulfur insertion, ring formation, anaerobic oxidation and protein radical

68 lis FtsZ chimera had a low frequency of FtsZ ring formation and a high degree of filamentation relati

69 ting the peptidase function from thiolactone ring formation and AIP transport.

70 nters of the rings, but are not required for ring formation and are less clearly defined, suggesting

71 h SIN components operate downstream of actin ring formation and are necessary for ring contraction an

72 Furthermore, XN inhibited osteoclast actin-ring formation and bone resorption in a dose-dependent m

73 WT VCL completely rescues actin ring formation and bone resorption, as does VCL(P878A),

74 irmed the involvement of PTP-PEST in sealing ring formation and bone resorption.

75 that OPG blocks OPGL's effects on both actin ring formation and bone resorption.

76 Moderate/severe degrees of Soemmering's ring formation and capsulorhexis phimosis were observed

77 In an effort to understand whether Z-ring formation and cell constriction are driven solely b

78 In Bacillus subtilis, FtsZ ring formation and cell division is favoured at the midc

79 , the effects of inhibiting replication on Z-ring formation and cell division were tested in both syn

80 osome equivalents at mid-cell also blocked Z-ring formation and cell division.

81 /KI) osteoclasts resulted in disrupted actin ring formation and cell fusion.

82 y SpAin1 is important for proper contractile ring formation and constriction.

83 isorganized ring material and delays in both ring formation and constriction.

84 ssion through mitosis are required for actin ring formation and contraction.

85 nd tropomyosin are essential for contractile ring formation and cytokinesis in fission yeast.

86 ation and stabilization of F-actin inhibited ring formation and disassembly of the AJC, suggesting a

87 tor Gic1 are involved in septin recruitment, ring formation and dissociation.

88 ated forms of MapZ are required for proper Z-ring formation and dynamics.

89 These metabolites are in accord with the THP ring formation and elaboration in thiomarinol following

90 erizes the physical mechanisms of actomyosin ring formation and highlights the role of flow as a cent

91 otein Iqg1 (Cyk1) promotes cytokinetic actin ring formation and is required for cytokinesis and viabi

92 apB provide additional positional cues for Z-ring formation and may help coordinate its assembly with

93 F-actin and Mid1, a key regulator of F-actin ring formation and positioning, are mispositioned and fr

94 The laws of fluid dynamics govern vortex ring formation and precede cardiac development by billio

95 eyefield in vivo, led to disorganized nerve ring formation and premature cornea innervation.

96 ort which indicated that MinCD acted after Z-ring formation and prevented the recruitment of FtsA to

97 ivision plane by regulating the site of FtsZ-ring formation and represents one of the best-understood

98 ly carries out both deacetylation and lactam ring formation and requires the product of CwlD activity

99 Myo1p, Iqg1p, and Myo2p to coordinate actin ring formation and targeted membrane deposition during c

100 the normal mid-cell division site inhibits Z-ring formation and that the SOS system, SlmA, and MinC a

101 ples, debate surrounds the mechanics of peak-ring formation and their depth of origin.

102 ression of M. tuberculosis genes affecting Z-ring formation and thereby cell division.

103 at the similar PhzA and -B proteins catalyze ring formation and thus may be more than noncatalytic ac

104 h was earlier shown to be essential for FlaX ring formation and to mediate interaction with FlaI.

105 initiated very early on, shortly after FtsZ ring formation and well before cell constriction starts.

106 y molecule in this complex disrupts podosome ring formation and/or decreases osteoclast migration.

107 ulfide bond formation is required for portal ring formation and/or stability and for the production o

108 monomeric subunits and contribute to portal ring formation and/or stability.

109 uclear envelope structure, contractile actin ring formation, and cytokinesis were also disrupted.

110 ne eight-electron oxidation, fused five-five ring formation, and decarboxylation.

111 s are detailed: hydroxylation, halogenation, ring formation, and desaturation.

112 before spindle pole body duplication, chitin ring formation, and DNA replication.

113 on of Rac effector cortactin, cortical actin ring formation, and EC barrier enhancement.

114 translocation of FA proteins, cortical actin ring formation, and FAK [Y576] phosphorylation.

115 ng the link between growth rate, medial FtsZ ring formation, and the intracellular concentration of F

116 teracts with the membrane and is involved in ring formation, and the other C2 domain points radially

117 One example involved cyclopropane ring formation, and the other carbon-carbon bond activat

118 1, followed by endoperoxide and cyclopentane ring formation, and then a second reaction with molecula

119 on of the cell is genetically separable from ring formation, and whereas it is normally restricted to

120 ther proteins known to promote normal septin-ring formation appear to function in a partially redunda

121 In particular, the rates of thioether ring formation are drastically reduced in ProcM, likely

122 disturb interaction with FtsZ or that impair ring formation are no longer able to align FtsZ filament

123 gs, suggesting that the mechanisms governing ring formation are refractile to increases in FtsZ conce

124 organisms, and the mechanisms of actomyosin ring formation are well studied in fission and budding y

125 The ring formation arises from the hydrogenation-induced edg

126 ssion yeast has enough Dam1-DASH complex for ring formation around attached MTs.

127 While ether ring formation as a result of dehydrogenation of a secon

128 vities in vivo: (i) preventing aberrant FtsZ ring formation at cell poles through inhibition of de no

129 in broth were comparable, suggesting that Z-ring formation at midcell sites was compromised during i

130 icting it to the cell poles, thus allowing Z ring formation at midcell.

131 le formin, SepA, which is required for actin ring formation at septation sites and also plays a role

132 s Exo70 and Exo84 localize specifically in a ring formation at the appressorium pore.

133 the combined data reveal how SlmA derails Z-ring formation at the correct place and time to effect N

134 oroplast division, but whether this involves ring formation at the division site has not been determi

135 a known clock output pathway to inhibit FtsZ ring formation at the division site.

136 and Bacillus subtilis, FtsZ plays a role in ring formation at the leading edge of the cell division

137 hinery to midcell by preventing FtsZ ring (Z ring) formation at cell poles.

138 ignificant differences in regulation of FtsZ ring formation based on growth medium.

139 The barrier to azametalacyclobutadiene ring formation/breakup is greater than that for the corr

140 The IQ motifs are not required for ring formation but are important for ring constriction a

141 nitial phase of PMC migration (subequatorial ring formation), but also for the second phase (migratio

142 oth require the endocytic protein, Sla2, for ring formation, but not propagation.

143 tion of FtsL has little or no effect on FtsZ ring formation, but the assembly of other division prote

144 inity of the bud site several minutes before ring formation, but the ring itself is the first distinc

145 esents a convergent atom economic method for ring formation by a series of simple additions.

146 ding ability of Nopp140, the inhibition of R-ring formation by calcium chelators, and the concentrati

147 also used to demonstrate that prostaglandin ring formation by cyclooxygenases does not involve carbo

148 Homologation to diester 18 and ring formation by Dieckman cyclization, followed by redu

149 pea and tobacco, suggesting that midplastid ring formation by FtsZ1 and FtsZ2 is universal among flo

150 s that stabilize FtsZ assembly and enhance Z ring formation by increasing lateral assembly of FtsZ pr

151 d proteins, Zaps, which typically modulate Z-ring formation by increasing lateral interactions betwee

152 oteins, MinC is the inhibitor and prevents Z-ring formation by interacting directly with FtsZ.

153 -terminal domain ((Z)MinC) suppresses septal ring formation by interfering with FtsZ polymerization,

154 BPalpha exhibits a dispensable role on actin ring formation by mature OCs but is critically involved

155 oducts compete with intramolecular exocyclic ring formation by meso-phenyl ring addition, which occur

156 esuccinylase (DapE) facilitates functional Z ring formation by strengthening the Ter signal via ZapB.

157 ccurred at or prior to the step of bipolar Z-ring formation by the cell division protein FtsZ.

158 ve-stain electron microscopy, whereas portal ring formation cannot be detected for C173S, which forms

159 addition to outer membrane pore formation, L-ring formation catalyzes the removal of the FlgJ rod cap

160 indle formation, activation of Cdc25C, actin ring formation, centrosome maturation, and activation of

161 t the alpha-carbon of MeLan, suggesting that ring formation could be reversible.

162 which the rate-limiting step is beta-lactam ring formation coupled to a protein conformational chang

163 lie between DHHA and PCA, ketone formation, ring formation, decarboxylation, and oxidation, we hypot

164 Myo1p ring formation depends on the septins but not on F-actin

165 division-plane specification and contractile-ring formation during cytokinesis, but how they regulate

166 cortical transport contribute to contractile ring formation during cytokinesis.

167 ibitor of FtsZ that prevents inappropriate Z-ring formation during sporulation.

168 The spoIIE mutation also impaired polar FtsZ ring formation during sporulation.

169 cell bodies, expressed robustly during nerve ring formation (E5-8), then later declining concurrent w

170 igenetically optimized to accommodate vortex ring formation for volume pumping.

171 which focuses distortions at G67 to promote ring formation from amino acids S65, Y66, and G67.

172 ycles, there is an overall directionality of ring formation from N-terminal to C-terminal sites.

173 d for both the normal process of contractile ring formation from precursor nodes and an alternative m

174 n, necessitating the strategic decoupling of ring-formation from the establishment of functionality a

175 Contractile ring formation has been well characterized in Schizosacc

176 her and how the SIN functions in contractile ring formation has remained unclear.

177 We confirmed that ZipA is not required for Z ring formation; however, we found that ZipA, like FtsA,

178 s twofold overexpression of EzrA blocks FtsZ ring formation in a sensitized genetic background, consi

179 or of cellular morphogenesis, inducing actin-ring formation in association with cytokinesis.

180 We have identified a regulator of FtsZ ring formation in Bacillus subtilis.

181 the MipZ gradient that spatially regulates Z ring formation in Caulobacter crescentus.

182 ly is also supported by studies showing that ring formation in cells adapting from fermentative to ae

183 These results suggest a path for aromatic ring formation in cold acetylene-rich environments such

184 ng support for the SCPR model of contractile-ring formation in cytokinesis.

185 ctin and to assemble F-actin for contractile ring formation in dividing cells.

186 f FtsZ bundling and that ultimately affect Z-ring formation in dividing cells.

187 otein, mediates the insertion of ammonia and ring formation in IGP by channeling ammonia from one rem

188 2) inhibition of cell spreading and of actin ring formation in osteoclasts plated on glass or bone an

189 ndered TcREG inefficient in preventing actin ring formation in osteoclasts, a process required for bo

190 SP phosphorylation and the resulting sealing ring formation in osteoclasts.

191 actin polymerization in the process of actin ring formation in osteoclasts.

192 locked actin polymerization as well as actin ring formation in osteoclasts.

193 ions of Kelly's methods to induce thiazoline ring formation in other crucial steps of the apratoxin s

194 hese genes, a possible pathway for aziridine ring formation in the azecimicins can now be proposed.

195 a viable reaction pathway for either C- or D-ring formation in the cyclization reaction.

196 cryptic chlorination leading to cyclopropane ring formation in the synthesis of the natural product c

197 the predicted oligomeric interface disrupted ring formation in vitro and impaired forespore gene expr

198 diolide formation, we sought to reconstitute ring formation in vitro by using a non-natural substrate

199 MalE-SulA10, which does not block Z ring formation in vivo, is unable to inhibit the GTPase

200 ndicate that ClpX but not ClpP inhibits FtsZ-ring formation in vivo.

201 opsonization, agglutination, and phagocytic ring formation in vivo.

202 t this translocation and disrupt contractile ring formation, indicating that active Rho is required f

203 R-ring formation initiates at the nuclear envelope, appare

204 The final ring formation involves a novel visible light-promoted h

205 Actin ring formation is a prerequisite for osteoclast bone res

206 Spatial and temporal control of Z-ring formation is achieved by the Min and nucleoid occlu

207 The enigmatic ring formation is catalyzed by two proteins with homolog

208 nomers, it is still an open question whether ring formation is crucial for membrane interaction.

209 ting temperature sensitive mutant Z (FtsZ) Z-ring formation is crucial for proper cell division in ba

210 However, the mechanism of actin ring formation is currently unclear.

211 itment occurs in the absence of F-actin, but ring formation is delayed.

212 s, but the involvement of Rho in contractile ring formation is disputed.

213 The chain and ring formation is facilitated by conformational switchin

214 In both cases, ring formation is frequently initiated near the cell pol

215 s of years, suggesting that diastolic vortex ring formation is instrumental in defining the shape of

216 Contractile ring formation is mediated by RhoA activation at the equ

217 ulsion from the lens and cornea during nerve ring formation is mediated by Robo-Slit signaling.

218 Thus, ring formation is not crucial for, and even counteracts,

219 Ring formation is not sensitive to taxol, colchicine, or

220 Efficient dot propagation, but not ring formation, is dependent upon the Hsp104 chaperone.

221 EzrA, a negative regulator of FtsZ ring formation, is important for ensuring that the ring

222 cwn-2 is required at the time of nerve ring formation; it is expressed by cells posterior of th

223 often brought to a bioactive conformation by ring formation (macrocyclization).

224 Our data suggests that ring formation may be triggered at an early step in syna

225 rmore, their careful analysis of contractile ring formation may help bridge two existing models of cy

226 st that this "McClintock mechanism" of small-ring formation might be the predominant mechanism of ori

227 FtsA, as well as the spatial regulators of Z-ring formation, MinC and SlmA, requires the CCTP.

228 By inhibiting FtsZ ring formation near the cell ends, the MinC protein play

229 M, P<0.01), but MK801 had no effect on actin ring formation necessary for osteoclast polarization, at

230 Interestingly, Z-ring formation occurs coincidently with initiation of DN

231 hael cycloreductions, five- and six-membered ring formation occurs in good yield with high levels of

232 ta/alpha)8 barrel cyclase that completes the ring formation of imidizole glycerol phosphate synthase.

233 c nature of the para-substituent on the aryl ring, formation of the regioisomeric tetrahydroquinoline

234 Where six-membered ring formation operates, cyclization can be performed di

235 mimetic mutations in Shs1 can either prevent ring formation or promote formation of a gauzelike meshw

236 ockdown did not affect cell viability, actin ring formation, or apoptosis in mature osteoclasts.

237 main of Rng2p is not required for viability, ring formation, or ring constriction.

238 ed data indicate that SlmA DNA helps block Z-ring formation over chromosomal DNA by forming higher-or

239 To block Z-ring formation over the nucleoid and help coordinate cel

240 agmentation by binding FtsZ and inhibiting Z-ring formation over the nucleoid.

241 ace of its envelope and produced interesting ring formation phenomena due to cell detachment upon inf

242 ults are consistent with ZipA acting after Z ring formation, possibly to link the membrane to FtsZ fi

243 apture-pull and release model of contractile ring formation predicted that nodes clump when the relea

244 Five-membered ring formation proceeds less readily, but the yield of c

245 Ring formation promotes microtubule assembly, stabilizes

246 rates that SpnF specifically accelerates the ring formation reaction with an estimated 500-fold rate

247 Specific mutations affecting ring formation reduce protein stability in vitro.

248 We show that the ring-formation region in parameter space lies close to r

249 the initial and maturation phases of sealing ring formation, respectively.

250 catalyze C5-hydroxylation and spirobicyclic ring formation, respectively.

251 Using computational modeling, we show that Z-ring formation results from the colocalization of FtsZ a

252 cells lacking RefZ are delayed in polar FtsZ ring formation, spending more time in the medial and tra

253 It is suggested that septal ring formation starts by assembly of the FtsZ ring, afte

254 involves three Scholl-type cycloheptatriene ring formation steps of the 1,4,8-tris(3',4'-dimethoxyph

255 rbates the phenotypes of cells impaired in Z ring formation such as ftsZ84 or a min mutant.

256 in previously shown to be required for actin ring formation, suggesting that formin-like proteins and

257 1 overexpression resulted in premature actin-ring formation, suggesting that Iqg1 activity temporally

258 The yeast prion [PIN(+)] enhances HET-s ring formation, suggesting that prions with and without

259 ooperate to form an efficient inhibitor of Z-ring formation that is spatially regulated by MinE.

260 f ATP and are associated with an open spiral ring formation that is vital for asymmetric subunit func

261 pic contribution of the concomitant pyrazole ring formation that serves as both a kinetic and thermod

262 f FA proteins associated with cortical actin ring formation, thrombin caused the redistribution of FA

263 ion technique for proteins via a benzoxazine ring formation through a Diels-Alder reaction in water a

264 Our binder-free ink suppresses coffee ring formation through induced recirculating Marangoni f

265 ng protein SlmA binds to FtsZ and prevents Z-ring formation through the nucleoid in a process called

266 rystallization from its origins in Liesegang ring formation to current research in the generation of

267 undergo an unusual tandem Heck-lactamization ring formation to generate 5-chloro-1-aryl-1,6-naphthyri

268 , and the Min system serves to restrict FtsZ ring formation to mid-chloroplast or mid-cell.

269 tsZ polymerization, thereby restricting FtsZ ring formation to midcell, the region of lowest MipZ con

270 ation of MinC that is proposed to force FtsZ ring formation to midcell.

271 v) a radical cyclization for the cyclobutane ring formation to provide the tricyclo[5.2.1.0(1,6)]dece

272 n was not sufficient for Z-ring formation; Z-ring formation took place only in stalked cells.

273 lthough Rho and Cdc42 are required for actin ring formation, transduction of either one of the protei

274 tail to understand the mechanism of pyridine ring formation under the described conditions.

275 eeds via the initial step of a five-membered ring formation upon attack of the hydrazine, followed by

276 ccess to the regioselectivity of lanthionine ring formation using high-resolution tandem mass spectro

277 (Cdk) sites flanking the CHD promotes actin ring formation, using site-specific alanine mutants.

278 tive charge to a remote position and enables ring formation via a Friedel-Crafts-type reaction.

279 ng N-acyliminium cyclization, dihydrofuranyl ring formation via silver-catalyzed intramolecular alcoh

280 The ring formation was accompanied by a 1,2-acyloxy migratio

281 The ease of ring formation was dependent on its size, while even mil

282 Ring formation was facilitated by microtubules but could

283 critical concentration of FtsZ required for ring formation was lower in ezrA null mutants than in wi

284 Ring formation was not significantly different from wild

285 In contrast, ring formation was reduced in a cox6 mutant, consistent

286 To explore the early stage of intramolecular ring formation, we cloned and expressed the spnJ gene an

287 Lacunar resorption and filamentous actin ring formation were measured as indicators of osteoclast

288 nt culture, chromosomal replication and FtsZ-ring formation were no longer blocked, although competen

289 portant for oligomer interactions and stable ring formation, which in turn are required for genome en

290 near dimeric thioester is an intermediate in ring formation, which indicates iterative use of the thi

291 EM analyses showed that it is sufficient for ring formation, which is explained by the filaments in t

292 synthetic pathway that catalyze cyclopropane ring formation, which is followed by thiolester hydrolys

293 onversation there ignited my interest in DNA ring formation, which later led me to study different to

294 the average molecular weight and to enhance ring formation, which otherwise is very limited.

295 A diastereoselective C-ring formation, which proceeds through a 5-exo-trig cycl

296 Myo2p initiates ring formation while Myp2p acts later to increase the ef

297 ynthesized intramolecularly via six-membered ring formation with high regio- and diastereoselectivity

298 d to account for the selective five-membered-ring formation with the rearrangement of the aryl groups

299 s causally related to polar body contractile ring formation, with anaphase entry and aster disassembl

300 FtsZ concentration was not sufficient for Z-ring formation; Z-ring formation took place only in stal