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1 ype I), IFN-gamma (type II), and IFN-lambda (type III).
2 avage is required to allow signaling of NRG1 type III.
3 I, 17 (26.2%) as type II, and 21 (32.4%) as type III.
4 st common phenotype was type I (50.3%), with type III (29.6%), type II (14.5%) and type IV (5.7%).
6 rRNA maturation and establish a link between Type III-A CRISPR-Cas immunity and central nucleic acid
7 targeting by the Staphylococcus epidermidis type III-A CRISPR-Cas system does not require PAM or see
10 dition, mutations in the active sites of the type III-A RNases Csm3 and Csm6 lead to the accumulation
11 should be considered as primary therapy for type III achalasia; 4) if the expertise is available, PO
14 egulation (p < 0.01) with increased Collagen type III and increased expression of several apoptosis r
16 saliva formation, mediated by Na/K-ATPase in type III and type II acini, is followed by a dopamine-in
18 rentially expressed during infection and the type III and VI secretion systems were highly expressed
19 hydrocarbon-dominated organic matter types (types III and IV; mainly land plant, metamorphosed or de
20 , acquired angioedema, hereditary angioedema type III, and angiotensin converting enzyme inhibitor-in
34 sinaemia type I into the benign tyrosinaemia type III by deleting Hpd (hydroxyphenylpyruvate dioxigen
35 ic responses could explain why a minority of type III cells (34%) had AI salt responses but lacked an
38 se responses were significantly larger in AI type III cells that did not exhibit the anion effect.
44 opment, establish an in vivo function of CHD Type III chromatin remodeling proteins in this process,
45 ypes of ependymal cilia, type-I, type-II and type-III classified based upon their beating frequency,
47 effect by increasing the amount of refolded type III collagen in vitro and FKBP19 seems to interact
48 agen, the unhydroxylated quarter fragment of type III collagen, and synthetic peptides as substrates.
49 preferences of these PPIases in vitro using type III collagen, the unhydroxylated quarter fragment o
50 icated cracks, a combination of a Type I and Type III cracks, which may or may not be confluent with
53 I and II systems, the relaxed specificity of type III CRISPR-Cas targeting provides robust immune res
55 activating mutation in the fibronectin-like type III domain of the extracellular region of CSF3R (W3
56 -binding proteins based upon the fibronectin type III domain, and we find that variations in sequence
57 F splice variants 1, 2, 4, 6 and fibronectin type III domain-containing protein 5 (FNDC5) mRNA levels
61 EBV infection and suggest that TET2 promotes type III EBV latency in B cells with an ABC or naive phe
62 ed Xam strains in which individual predicted type III effector (T3E) genes were mutated and applied m
64 ttom-up approach, showing that the bacterial type III effector AvrRxo1 of plant pathogens is an authe
70 from an extensive phylogenetic analysis, and type III effector translocation and host cell invasion a
71 viously unstudied Pseudomonas syringae (Psy) type III effector, HopBB1, interacts with TCP14 and targ
73 DC3000 (Pst DC3000), demonstrating that the type-III effector HopG1 is required for pathogen-induced
74 oduce a computational method that identifies type III effectors by combining homology-based inference
77 erstanding of the basis of host specificity, type III effectors, microbe-associated molecular pattern
78 The spike resonance of these phasic-firing (type III excitable) MSO neurons and of the model is of p
79 A marked shift in collagen predominance from type III (fetal/early wound) to type I (adult/mature) wa
80 PavA and PavB target at least 13 out of 15 type III fibronectin domains as demonstrated in ligand o
81 t antigen to be MrkA, a major protein in the type III fimbriae complex, and showed that these serotyp
82 a highly conserved region of the fibronectin type III (FN3) domain of the receptor tyrosine kinase Ep
83 C2 type (IgC2) domains and four fibronectin type III (FnIII) domains that are shared with many other
84 is mediated by membrane-proximal fibronectin type III (FNIII) domains that were omitted in previous s
85 ructural switch within its first fibronectin type III (FnIII-1) domain to control RbmA structural dyn
86 d-optimal temperatures, predators may have a type III functional response, and prey carrying capacity
90 ram-positive group B Streptococcus, capsular type III (GBS-III) bacteria resulted in augmented serum
92 ally (occluso-gingival) oriented cracks; and Type III - hybrid or complicated cracks, a combination o
93 skin, but the mechanisms that regulate this type III hypersensitivity process remain poorly understo
95 ms made with IBPs (both from winter rye, and type III IBP) had aggregates of ice crystals that entrap
96 ound that adding recombinantly produced fish type III IBPs at a concentration 3mg.L(-1) made ice crea
97 pha/beta) controls systemic replication, and type III IFN (IFN-lambda) controls MNV persistence in th
106 se replication-competent HRV antagonizes the type III IFN response at pre- and posttranscriptional le
107 overned by genetic polymorphisms that affect type III IFN signaling and virus-specific cellular immun
108 tion, with type I IFN being more potent than type III IFN, suggesting that extraepithelial sources of
109 In addition, we found that fetuses lacking type III IFN-lambda signaling had increased ZIKV replica
111 alpha/beta) and the more recently identified type III IFNs (IFN-lambda) function as the first line of
113 hoblasts through the constitutive release of type III IFNs (IFNlambda1 and IFNlambda2) and become res
115 ter of pregnancy also constitutively release type III IFNs and use these IFNs in autocrine and paracr
117 ly expressed from TLRs present on endosomes, type III IFNs could be induced by TLRs that reside at th
119 on and new human models to study the role of type III IFNs in the vertical transmission of ZIKV and o
120 hepatocytes (PHHs) treated with recombinant type III IFNs or infected with Sendai virus to model acu
121 ctions in cell-intrinsic antiviral immunity, type III IFNs protect epithelial barrier integrity, an a
127 zontal uptake and maintenance of promiscuous type III interference modules that supplement existing h
128 ay, suppress IFNL2 and IFNL3, members of the type III interferon (IFN) gene family, to support viral
131 L-10R family and highlight the plasticity of type III interferon signaling and its therapeutic potent
139 pe 2-oriented membrane-retained stub of NRG1 type III is further processed by signal peptide peptidas
142 lar resistance, proteolysis, quorum sensing, Type III/IV secretion systems, phages and toxins in the
144 H3 at lysine 4) and H3 acetylation at Cp in type III latency and Qp in type I latency, as well as an
145 e transcripts are regulated similarly to EBV type III latency genes and that TET2 protein is a cofact
146 cofactor of EBNA2 and coregulator of the EBV type III latency program and DNA methylation state.IMPOR
147 n correlate with the highly demethylated EBV type III latency program permissive for expression of EB
148 a germinal center (GC) B cell phenotype, and type III latency with an activated B cell (ABC) phenotyp
149 e whether EBV enters the highly transforming type III latency, versus the more restricted type I late
154 lvability, while non-neutral correlations of type iii) may instead facilitate evolutionary exploratio
155 hase-variable methylation by both Type I and Type III methyltransferases is associated with altered g
162 that soluble ectodomains of both type I and type III NRG1 significantly increased expression of Abet
163 test this possibility, full-length type I or type III NRG1 was overexpressed via lentiviral vectors i
166 B cells support a highly transforming form (type III) of viral latency; however, long-term EBV infec
167 Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian
168 opsis showed that exposure to LS upregulated type III peroxidase genes, of which some are involved in
169 led by NADPH oxidases as well as by secreted type III peroxidases has a great impact on cell wall pro
171 istical association between strains from the type III phylogenetic lineage and PMH lesions (P = 0.001
173 oding proteins of several families including type-III polyketide synthases, hydrolases, and cytochrom
174 ecies (type II), Staphylococcus epidermidis (type III), Porphyromonas and Peptoniphilus species (type
175 ganization of the collagen network, collagen type III predominance, and lack of collagen fiber insert
181 The Chromodomain-Helicase-DNA binding (CHD) Type III proteins are a subfamily of SWI2/SNF2 proteins
183 ly secreted from cardiomyocytes, as were the type III repeat (T3R) and TSP-C domains, while the LamG
184 tural comparisons revealed that the targeted type III repeat epitopes cluster on the inner strands of
186 icryptic heparin-binding region of the first type III repeat of fibrillar FN (FNIII1H) mediates vasod
190 a combination of random fragmentation and a type III restriction enzyme to derive a densely covering
191 tion system as a molecular syringe to inject type III secreted effector (T3SE) proteins in plants.
193 e roles of toxins, type II secreted enzymes, type III secreted effectors and motility as well as thei
199 , a direct physiologic role for the Shigella type III secretion apparatus (T3SA) in mediating phagoso
200 recisely with the activation of the Shigella type III secretion apparatus, thus evidencing injectisom
201 free cytosolic complexes, which include the type III secretion ATPase, constitute a highly dynamic a
202 g a microcompartment shell protein (PduA), a type III secretion effector protein (SteA), and a metabo
206 ation and characterization of the Salmonella type III secretion machine in live bacteria by 2D and 3D
207 situ structure of the Salmonella Typhimurium type III secretion machine obtained by high-throughput c
208 reviously unknown effectors, suggesting that type III secretion may have evolved prior to the archaea
209 epends in part on its pathogenicity island 2 type III secretion system (SPI-2 T3SS), which is require
210 inflammasome upon sensing components of the type III secretion system (T3SS) and flagellar apparatus
211 ne and expression dose of the antiphagocytic type III secretion system (T3SS) and induces functions c
212 opathogenic Escherichia coli (EPEC) uses the type III secretion system (T3SS) effector EspL to degrad
213 . Typhimurium pathogenicity island-1 (SPI-1) type III secretion system (T3SS) effectors and transloca
216 e receptors sense host-cell targeting by the type III secretion system (T3SS) of pathogenic Yersinia.
217 ny pathogenic Gram-negative bacteria use the type III secretion system (T3SS) to deliver effector pro
218 tive pathogens infect eukaryotes and use the type III secretion system (T3SS) to deliver effector pro
221 gative pathogens, Shigella rely on a complex type III secretion system (T3SS) to inject effector prot
224 rV is an essential part of the P. aeruginosa type III secretion system (T3SS), and its oligomeric nat
225 and regulatory components of the P. syringae type III secretion system (T3SS), essential for coloniza
226 m-negative bacteria secrete proteins using a type III secretion system (T3SS), which functions as a n
227 e characterize a regulatory node involving a type III secretion system (T3SS)-exported protein, BtrA,
229 d P. aeruginosa virulence determinant is the type III secretion system (T3SS); the production of T3SS
230 is organism requires a horizontally acquired type III secretion system (T3SS2) to infect the small in
231 B, are required for activating the virulence type III secretion system 2 in response to bile salts.
232 he epithem and is actively suppressed by the type III secretion system and its effector proteins.
233 syringae and Xanthomonas campestris, use the type III secretion system as a molecular syringe to inje
234 's immune response, Y. enterocolitica uses a type III secretion system consisting of an injectisome a
236 fication of two homologous Shigella flexneri type III secretion system effector E3 ligases IpaH1.4 an
238 tium strains bearing deletions in individual type III secretion system effector genes to determine wh
241 mbrella term given to E. coli that possess a type III secretion system encoded in the locus of entero
242 leum, a virulence process carried out by the type III secretion system encoded within Salmonella path
243 depends on effector proteins secreted by its type III secretion system for the pathogenesis of plants
245 er Gram-negative bacterial pathogens, uses a type III secretion system to deliver multiple proteins,
248 hogens use a syringe-like apparatus called a type III secretion system to inject virulence factors in
251 at the introduction of a functional Shigella type III secretion system, but none of its effectors, in
252 -silenced plants are more susceptible to the type III secretion system-deficient bacterial strain Pse
264 he injectisome (iT3SS) and flagellar (fT3SS) type III secretion systems are 2 virulence factors assoc
266 sponse, attaching and effacing pathogens use type III secretion systems to introduce effectors target
267 e homology to ring-forming proteins found in type III secretion systems, assembles into an oligomeric
270 of proteins involved in central metabolism, type III secretion, and protein synthesis were associate
279 the natural history of mucopolysaccharidosis type III syndromes, neurocognitive progression was impro
280 lfataricus has two divergent subtypes of the type III system (Sso-IIID and a Cmr7-containing variant
284 mild post-systolic shortening (n = 35); and type III: systolic stretching with large post-systolic s
285 e information involves communication between Type III taste cells and 5-HT3 -expressing afferent nerv
286 um imaging, we identified AI salt-responsive type III taste cells and demonstrated that they compose
287 o separate populations of AI salt-responsive type III taste cells distinguished by their sensitivity
288 bsence of TPs, many (66%) AI salt-responsive type III taste cells still exhibited the anion effect, d
289 chanisms could underlie AI salt responses in type III taste cells, one of which may contribute to the
292 ular PAR levels were up to 2-fold greater in type III than type I latently infected EBV B cells.
293 study, we show that a representative of fold type III, the Escherichia coli alanine racemase (ALR), i
299 of structural staged mutation carriers were type III, whereas a large proportion of both electrical
300 ine (Type II) or manifest as a chronic form (Type III) with a wide spectrum of neurological signs.
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