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1 P)-related domain is required for node-based ring formation.
2  mutations that cause defects in contractile ring formation.
3 rongly inhibited at or before the level of Z-ring formation.
4 dies suggesting a role for Rng2p in node and ring formation.
5  quantum-chemical method) of the model epoxy ring formation.
6 ch serves as a key control point in aromatic ring formation.
7 om aggregating into clumps and allows normal ring formation.
8  repositions Ect2 to induce local actomyosin ring formation.
9 son did not induce xylem initiation or false ring formation.
10  the zigzag edge clearly favors six-membered ring formation.
11 ction of SpoIIIAH with SpoIIQ would preclude ring formation.
12 GFP constructs in different stages of septin ring formation.
13 ore passive role for the microtubule in Dam1 ring formation.
14 rations including fusion, fragmentation, and ring formation.
15 ant for intersubunit interactions and stable ring formation.
16 athway to regulate chloroplast size and FtsZ ring formation.
17 FtsZ-FtsZ, both of which are essential for Z ring formation.
18 k between L-plastin and cortactin in sealing ring formation.
19 naling proteins in the regulation of sealing ring formation.
20 in, a key scaffold also required for midbody ring formation.
21 lp bridge two existing models of cytokinetic ring formation.
22 rotein/RNA interaction relies on pRNA static ring formation.
23  of substrate adenylation and intramolecular ring formation.
24 TPase RhoA is a key regulator of contractile-ring formation.
25 to suppress cytoskeletal remodeling or actin ring formation.
26 ting in a densely functionalized cyclohexene ring formation.
27  expression in strains defective in P- and l-ring formation.
28 nation is a cryptic strategy for cyclopropyl ring formation.
29  interactions are not dependent on correct Z-ring formation.
30  that active Rho is required for contractile ring formation.
31 ssary for specifying the site of contractile ring formation.
32 ent of Rho-mediated signaling in contractile ring formation.
33  to prevent polymerization and aberrant FtsZ ring formation.
34 torial region of the cell to permit cleavage ring formation.
35 er the growth rate regulation of medial FtsZ ring formation.
36 usly shown to be important for normal septin-ring formation.
37  by deacetylation of muramic acid and lactam ring formation.
38 erstable monomer that is defective in portal ring formation.
39 nvestigated further the mechanisms of septin-ring formation.
40 gation, E-double bond formation and thiazole ring formation.
41 and thus represent attractive substrates for ring formation.
42 achinery of the cell and acts by promoting Z-ring formation.
43 ogical regulation of MinC, an inhibitor of Z-ring formation.
44  the cyclooctane stereogenic center prior to ring formation.
45  lead to models for MinE activation and MinE ring formation.
46 ook formation, is not essential for rod or P ring formation.
47 ity of the newly formed 2'-oxyanion during C-ring formation.
48 hibiting chaining, nuclear division and FtsZ-ring formation.
49 ion, chromosome segregation, and contractile ring formation.
50 ed during [PSI(+)] curing seem to facilitate ring formation.
51 in Escherichia coli occurs at the stage of Z ring formation.
52 ing reduction, lactamization and carbocyclic ring formation.
53 tinucleated TRAP(+) cells capable of F-actin ring formation.
54 ation and polymerization to ensure correct Z ring formation.
55 tative level that compression by flow drives ring formation.
56 e alignment enhances but is not required for ring formation.
57 more prone to racemization at C-5 during the ring formation.
58  by several cross-cutting faults during peak-ring formation.
59 th necessary and sufficient to promote actin ring formation.
60 inhibition of Cdc14 function prevented actin ring formation.
61 he resulting aminoallene adduct for bicyclic ring formation.
62 division site is predominant for contractile ring formation.
63 involve powerful dearomatizations and medium ring formations.
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 to a reduction of the deformation radius for ring formation, allowing unstable meanders to shed more
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 ed TRAP(+) cell numbers, it suppressed actin-ring formation and bone resorption in these assays.
74              WT VCL completely rescues actin ring formation and bone resorption, as does VCL(P878A),
75 irmed the involvement of PTP-PEST in sealing 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  ARP2/3 complex inhibitor delays contractile ring formation and constriction.
83 y SpAin1 is important for proper contractile ring formation and constriction.
84 isorganized ring material and delays in both ring formation and constriction.
85 ssion through mitosis are required for actin ring formation and contraction.
86 nd tropomyosin are essential for contractile ring formation and cytokinesis in fission yeast.
87 ation and stabilization of F-actin inhibited ring formation and disassembly of the AJC, suggesting a
88 tor Gic1 are involved in septin recruitment, ring formation and dissociation.
89 ated forms of MapZ are required for proper Z-ring formation and dynamics.
90 These metabolites are in accord with the THP ring formation and elaboration in thiomarinol following
91 erizes the physical mechanisms of actomyosin ring formation and highlights the role of flow as a cent
92 otein Iqg1 (Cyk1) promotes cytokinetic actin ring formation and is required for cytokinesis and viabi
93 apB provide additional positional cues for Z-ring formation and may help coordinate its assembly with
94 F-actin and Mid1, a key regulator of F-actin ring formation and positioning, are mispositioned and fr
95     The laws of fluid dynamics govern vortex ring formation and precede cardiac development by billio
96  eyefield in vivo, led to disorganized nerve ring formation and premature cornea innervation.
97 ort which indicated that MinCD acted after Z-ring formation and prevented the recruitment of FtsA to
98 ivision plane by regulating the site of FtsZ-ring formation and represents one of the best-understood
99 ly carries out both deacetylation and lactam ring formation and requires the product of CwlD activity
100                          These approaches to ring formation and retrosynthetic disconnection offer op
101  Myo1p, Iqg1p, and Myo2p to coordinate actin ring formation and targeted membrane deposition during c
102 the normal mid-cell division site inhibits Z-ring formation and that the SOS system, SlmA, and MinC a
103 beta-ol, resulting in spontaneous hemiacetal ring formation and the production of the protolimonoid m
104 ples, debate surrounds the mechanics of peak-ring formation and their depth of origin.
105 ression of M. tuberculosis genes affecting Z-ring formation and thereby cell division.
106 at the similar PhzA and -B proteins catalyze ring formation and thus may be more than noncatalytic ac
107 h was earlier shown to be essential for FlaX ring formation and to mediate interaction with FlaI.
108  initiated very early on, shortly after FtsZ ring formation and well before cell constriction starts.
109 y molecule in this complex disrupts podosome ring formation and/or decreases osteoclast migration.
110 ulfide bond formation is required for portal ring formation and/or stability and for the production o
111  monomeric subunits and contribute to portal ring formation and/or stability.
112 uclear envelope structure, contractile actin ring formation, and cytokinesis were also disrupted.
113 ne eight-electron oxidation, fused five-five ring formation, and decarboxylation.
114 s are detailed: hydroxylation, halogenation, ring formation, and desaturation.
115 before spindle pole body duplication, chitin ring formation, and DNA replication.
116 on of Rac effector cortactin, cortical actin ring formation, and EC barrier enhancement.
117 translocation of FA proteins, cortical actin ring formation, and FAK [Y576] phosphorylation.
118  explain the nucleotide dependence of mHsp60 ring formation, and reveal an inter-ring nucleotide symm
119 ng the link between growth rate, medial FtsZ ring formation, and the intracellular concentration of F
120 teracts with the membrane and is involved in ring formation, and the other C2 domain points radially
121            One example involved cyclopropane ring formation, and the other carbon-carbon bond activat
122 1, followed by endoperoxide and cyclopentane ring formation, and then a second reaction with molecula
123 on of the cell is genetically separable from ring formation, and whereas it is normally restricted to
124 ther proteins known to promote normal septin-ring formation appear to function in a partially redunda
125        In particular, the rates of thioether ring formation are drastically reduced in ProcM, likely
126 disturb interaction with FtsZ or that impair ring formation are no longer able to align FtsZ filament
127 gs, suggesting that the mechanisms governing ring formation are refractile to increases in FtsZ conce
128  organisms, and the mechanisms of actomyosin ring formation are well studied in fission and budding y
129                                          The ring formation arises from the hydrogenation-induced edg
130 ssion yeast has enough Dam1-DASH complex for ring formation around attached MTs.
131                                  While ether ring formation as a result of dehydrogenation of a secon
132 vities in vivo: (i) preventing aberrant FtsZ ring formation at cell poles through inhibition of de no
133  in broth were comparable, suggesting that Z-ring formation at midcell sites was compromised during i
134 icting it to the cell poles, thus allowing Z ring formation at midcell.
135 le formin, SepA, which is required for actin ring formation at septation sites and also plays a role
136 s Exo70 and Exo84 localize specifically in a ring formation at the appressorium pore.
137  versus a topologically similar six-membered ring formation at the armchair edge reveals that the bar
138  the combined data reveal how SlmA derails Z-ring formation at the correct place and time to effect N
139 oroplast division, but whether this involves ring formation at the division site has not been determi
140 a known clock output pathway to inhibit FtsZ ring formation at the division site.
141  and Bacillus subtilis, FtsZ plays a role in ring formation at the leading edge of the cell division
142 hinery to midcell by preventing FtsZ ring (Z ring) formation at cell poles.
143       The barrier to azametalacyclobutadiene ring formation/breakup is greater than that for the corr
144           The IQ motifs are not required for ring formation but are important for ring constriction a
145 one important component required for midbody ring formation but its mechanisms of action and relation
146 nitial phase of PMC migration (subequatorial ring formation), but also for the second phase (migratio
147 oth require the endocytic protein, Sla2, for ring formation, but not propagation.
148 inity of the bud site several minutes before ring formation, but the ring itself is the first distinc
149 esents a convergent atom economic method for ring formation by a series of simple additions.
150 ding ability of Nopp140, the inhibition of R-ring formation by calcium chelators, and the concentrati
151  also used to demonstrate that prostaglandin ring formation by cyclooxygenases does not involve carbo
152               Homologation to diester 18 and ring formation by Dieckman cyclization, followed by redu
153  pea and tobacco, suggesting that midplastid ring formation by FtsZ1 and FtsZ2 is universal among flo
154 s that stabilize FtsZ assembly and enhance Z ring formation by increasing lateral assembly of FtsZ pr
155 d proteins, Zaps, which typically modulate Z-ring formation by increasing lateral interactions betwee
156 oteins, MinC is the inhibitor and prevents Z-ring formation by interacting directly with FtsZ.
157 -terminal domain ((Z)MinC) suppresses septal ring formation by interfering with FtsZ polymerization,
158 BPalpha exhibits a dispensable role on actin ring formation by mature OCs but is critically involved
159 oducts compete with intramolecular exocyclic ring formation by meso-phenyl ring addition, which occur
160 esuccinylase (DapE) facilitates functional Z ring formation by strengthening the Ter signal via ZapB.
161 ccurred at or prior to the step of bipolar Z-ring formation by the cell division protein FtsZ.
162 d by loss of 4 carbons with associated furan ring formation, by an as yet unknown mechanism.
163 ve-stain electron microscopy, whereas portal ring formation cannot be detected for C173S, which forms
164 addition to outer membrane pore formation, L-ring formation catalyzes the removal of the FlgJ rod cap
165 indle formation, activation of Cdc25C, actin ring formation, centrosome maturation, and activation of
166 t the alpha-carbon of MeLan, suggesting that ring formation could be reversible.
167  which the rate-limiting step is beta-lactam ring formation coupled to a protein conformational chang
168  lie between DHHA and PCA, ketone formation, ring formation, decarboxylation, and oxidation, we hypot
169 protein EB1/EBP-2 around the wound and actin ring formation, dependent on ARP2/3 branched actin polym
170 division-plane specification and contractile-ring formation during cytokinesis, but how they regulate
171 cortical transport contribute to contractile ring formation during cytokinesis.
172 ibitor of FtsZ that prevents inappropriate Z-ring formation during sporulation.
173 cell bodies, expressed robustly during nerve ring formation (E5-8), then later declining concurrent w
174 igenetically optimized to accommodate vortex ring formation for volume pumping.
175  which focuses distortions at G67 to promote ring formation from amino acids S65, Y66, and G67.
176 d for both the normal process of contractile ring formation from precursor nodes and an alternative m
177 n, necessitating the strategic decoupling of ring-formation from the establishment of functionality a
178  robust deuterated methyl groups, and tandem ring formation, further demonstrate the potential of the
179                                  Contractile ring formation has been well characterized in Schizosacc
180 her and how the SIN functions in contractile ring formation has remained unclear.
181 We confirmed that ZipA is not required for Z ring formation; however, we found that ZipA, like FtsA,
182 s twofold overexpression of EzrA blocks FtsZ ring formation in a sensitized genetic background, consi
183 the MipZ gradient that spatially regulates Z ring formation in Caulobacter crescentus.
184 ly is also supported by studies showing that ring formation in cells adapting from fermentative to ae
185    These results suggest a path for aromatic ring formation in cold acetylene-rich environments such
186 ng support for the SCPR model of contractile-ring formation in cytokinesis.
187 ctin and to assemble F-actin for contractile ring formation in dividing cells.
188 f FtsZ bundling and that ultimately affect Z-ring formation in dividing cells.
189 otein, mediates the insertion of ammonia and ring formation in IGP by channeling ammonia from one rem
190 2) inhibition of cell spreading and of actin ring formation in osteoclasts plated on glass or bone an
191 ndered TcREG inefficient in preventing actin ring formation in osteoclasts, a process required for bo
192 SP phosphorylation and the resulting sealing ring formation in osteoclasts.
193 actin polymerization in the process of actin ring formation in osteoclasts.
194 locked actin polymerization as well as actin ring formation in osteoclasts.
195 ions of Kelly's methods to induce thiazoline ring formation in other crucial steps of the apratoxin s
196 synthases, GrsA and GrsB, essential for GDGT ring formation in Sulfolobus acidocaldarius Both protein
197 hese genes, a possible pathway for aziridine ring formation in the azecimicins can now be proposed.
198 a viable reaction pathway for either C- or D-ring formation in the cyclization reaction.
199 sZ movement leading to septal and equatorial ring formation in the ovoid-shaped pathogen, Streptococc
200 cryptic chlorination leading to cyclopropane ring formation in the synthesis of the natural product c
201 the predicted oligomeric interface disrupted ring formation in vitro and impaired forespore gene expr
202 diolide formation, we sought to reconstitute ring formation in vitro by using a non-natural substrate
203 ndicate that ClpX but not ClpP inhibits FtsZ-ring formation in vivo.
204  opsonization, agglutination, and phagocytic ring formation in vivo.
205 t this translocation and disrupt contractile ring formation, indicating that active Rho is required f
206                                            R-ring formation initiates at the nuclear envelope, appare
207                                    The final ring formation involves a novel visible light-promoted h
208                                        Actin ring formation is a prerequisite for osteoclast bone res
209            Spatial and temporal control of Z-ring formation is achieved by the Min and nucleoid occlu
210                                The enigmatic ring formation is catalyzed by two proteins with homolog
211 nomers, it is still an open question whether ring formation is crucial for membrane interaction.
212 ting temperature sensitive mutant Z (FtsZ) Z-ring formation is crucial for proper cell division in ba
213              However, the mechanism of actin ring formation is currently unclear.
214 itment occurs in the absence of F-actin, but ring formation is delayed.
215 s, but the involvement of Rho in contractile ring formation is disputed.
216                                The chain and ring formation is facilitated by conformational switchin
217 s of years, suggesting that diastolic vortex ring formation is instrumental in defining the shape of
218             We propose that lobe contractile ring formation is locally inhibited by the PGC nucleus,
219                                  Contractile ring formation is mediated by RhoA activation at the equ
220 ulsion from the lens and cornea during nerve ring formation is mediated by Robo-Slit signaling.
221                                        Thus, ring formation is not crucial for, and even counteracts,
222           Efficient dot propagation, but not ring formation, is dependent upon the Hsp104 chaperone.
223           EzrA, a negative regulator of FtsZ ring formation, is important for ensuring that the ring
224       cwn-2 is required at the time of nerve ring formation; it is expressed by cells posterior of th
225 often brought to a bioactive conformation by ring formation (macrocyclization).
226                       Our data suggests that ring formation may be triggered at an early step in syna
227 rmore, their careful analysis of contractile ring formation may help bridge two existing models of cy
228 st that this "McClintock mechanism" of small-ring formation might be the predominant mechanism of ori
229 FtsA, as well as the spatial regulators of Z-ring formation, MinC and SlmA, requires the CCTP.
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 apture-pull and release model of contractile ring formation predicted that nodes clump when the relea
243                                Five-membered ring formation proceeds less readily, but the yield of c
244                                              Ring formation promotes microtubule assembly, stabilizes
245 ocation chemistry, including highly specific ring formations, proton and hydride transfers, and methy
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  catalyze C5-hydroxylation and spirobicyclic ring formation, respectively.
250 the initial and maturation phases of sealing 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  involves three Scholl-type cycloheptatriene ring formation steps of the 1,4,8-tris(3',4'-dimethoxyph
254 rbates the phenotypes of cells impaired in Z ring formation such as ftsZ84 or a min mutant.
255 in previously shown to be required for actin ring formation, suggesting that formin-like proteins and
256      The yeast prion [PIN(+)] enhances HET-s ring formation, suggesting that prions with and without
257 ooperate to form an efficient inhibitor of Z-ring formation that is spatially regulated by MinE.
258 f ATP and are associated with an open spiral ring formation that is vital for asymmetric subunit func
259 pic contribution of the concomitant pyrazole ring formation that serves as both a kinetic and thermod
260 f FA proteins associated with cortical actin ring formation, thrombin caused the redistribution of FA
261 ion technique for proteins via a benzoxazine ring formation through a Diels-Alder reaction in water a
262        Our binder-free ink suppresses coffee ring formation through induced recirculating Marangoni f
263 ng protein SlmA binds to FtsZ and prevents Z-ring formation through the nucleoid in a process called
264 rystallization from its origins in Liesegang ring formation to current research in the generation of
265 undergo an unusual tandem Heck-lactamization ring formation to generate 5-chloro-1-aryl-1,6-naphthyri
266 , and the Min system serves to restrict FtsZ ring formation to mid-chloroplast or mid-cell.
267 tsZ polymerization, thereby restricting FtsZ ring formation to midcell, the region of lowest MipZ con
268 ation of MinC that is proposed to force FtsZ ring formation to midcell.
269 v) a radical cyclization for the cyclobutane ring formation to provide the tricyclo[5.2.1.0(1,6)]dece
270 n was not sufficient for Z-ring formation; Z-ring formation took place only in stalked cells.
271 lthough Rho and Cdc42 are required for actin ring formation, transduction of either one of the protei
272 tail to understand the mechanism of pyridine ring formation under the described conditions.
273 eeds via the initial step of a five-membered ring formation upon attack of the hydrazine, followed by
274 ccess to the regioselectivity of lanthionine ring formation using high-resolution tandem mass spectro
275  (Cdk) sites flanking the CHD promotes actin ring formation, using site-specific alanine mutants.
276 tive charge to a remote position and enables ring formation via a Friedel-Crafts-type reaction.
277  a configuration-dependent [6 + 8 + 5] fused ring formation via a tandem cyclic N-acyliminium nucleop
278 ng N-acyliminium cyclization, dihydrofuranyl ring formation via silver-catalyzed intramolecular alcoh
279                                          The ring formation was accompanied by a 1,2-acyloxy migratio
280                                  The ease of ring formation was dependent on its size, while even mil
281                                              Ring formation was facilitated by microtubules but could
282                                              Ring formation was not significantly different from wild
283                                 In contrast, ring formation was reduced in a cox6 mutant, consistent
284 To explore the early stage of intramolecular ring formation, we cloned and expressed the spnJ gene an
285 tes ECT-2 to promote cytokinetic contractile ring formation, we show that the ECT-2 regulator NOP-1,
286     Lacunar resorption and filamentous actin ring formation were measured as indicators of osteoclast
287 nt culture, chromosomal replication and FtsZ-ring formation were no longer blocked, although competen
288 portant for oligomer interactions and stable ring formation, which in turn are required for genome en
289 near dimeric thioester is an intermediate in ring formation, which indicates iterative use of the thi
290 EM analyses showed that it is sufficient for ring formation, which is explained by the filaments in t
291 synthetic pathway that catalyze cyclopropane ring formation, which is followed by thiolester hydrolys
292 onversation there ignited my interest in DNA ring formation, which later led me to study different to
293  the average molecular weight and to enhance ring formation, which otherwise is very limited.
294                       A diastereoselective C-ring formation, which proceeds through a 5-exo-trig cycl
295 nsitional structure and abolishes the double ring formation while causing no obvious defect in actomy
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

 
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