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1 s than 50% of the species present (community type O).
2 2.03-3.54) compared with nonsmokers of blood type O.
3 96.4%) were White, and 104 (41.6%) had blood type O.
4 edemptions were among individuals with blood type O.
5 myocardial infarction associated with blood type O.
6 splants on average, more if the NDD is blood type O.
7 lowing exposure to either Abca4(-/-) or wild-type OS.
8 owed by a temperature shift to 37 degrees C, type O(1)C3056R-KGE colocalized with caveolin-1, while O
9 Using a genetically engineered variant of type O(1)Campos (O(1)C3056R) which can utilize both inte
13 of new multielectron catalysts for oxygenase-type O(2) activation, as well as the microscopic reverse
14 r (N-acetylglucosamine or GlcNAc), show wild-type O(2) dependence of culmination, cells lacking AgtA,
15 can American (23 777 [47.0%]), had ABO blood type O (22 879 [45.2%]), and were Rhesus factor positive
17 s. 25 kg/m2, p = .03), less frequently blood type O (36% vs. 80%, p < .001), and had higher eGFR (99
19 ian wait times were 108 days (<=25 kg, blood type O), 80 days (<=25 kg, non-O), 47 days (>25 kg, O),
22 ation assays; GST-VP8* P[11] hemagglutinates type O, A, and B red blood cells as well as pooled umbil
24 nal antibody was shown to recognize the wild-type O-acetylated CPS, but not the CPS of the mynC mutan
28 ths after KPD entry included recipient blood type O and calculated panel reactive antibodies >=98%.
30 n pathway and can produce well defined human-type O- and N-linked glycans on recombinant therapeutics
31 ation, and global deprotection of all benzyl-type O- and N-protecting groups furnished the desired la
34 ype (4.9% stillbirths, 3.0% live births) (vs type O; AOR, 1.96 [95% CI, 1.16-3.30]); history of drug
36 -list mortality; however, infants with blood type O assigned an ABO-I listing strategy were more like
37 <0.003), UNOS status I and II (P<0.007), ABO type O, B, and AB (P<0.03), and reduced-size/split liver
38 bAC) 103 (7%), alpha thalassaemia 438 (28%), type O blood group 621 (40%), and G6PD deficiency 72 (9%
39 re COVID-19 illness or death associated with type O blood group versus all others (aRR, 0.87 [CI, 0.7
43 accomplishes the conversion of regular human type-O blood into a potential blood substitute for the r
44 nts) and deaths would have shifted away from type O candidates (4.6 [95% CI: 2.7, 6.8] fewer deaths).
45 wever, transplants would have shifted toward type O candidates (57.8 [95% CI: 35.1, 80.9] additional
46 al of increasing transplant access for blood type O candidates after an error was discovered in the s
47 ed mortality incidence (95% CI) decreased in type O candidates from 3.6% (3.0%, 4.3%) premodification
48 LTx candidates with other blood types, blood type O candidates have longer waiting times and higher p
50 pe-compatible transplant is a gold standard, type O candidates might benefit from listing for A2 dono
54 ct of initial policy implementation on blood type-O candidates has not been rigorously evaluated.
58 2 and protein tyrosine phosphatase, receptor type, O cooperated with the v-raf murine sarcoma viral o
59 s hypothesis, we perfused blood from healthy type O donors (n = 33) or non-O donors (n = 54) over poo
60 Our results demonstrate that platelets from type O donors interact less with VWF at arterial shear t
61 lturing NELL1 knockout sarcoma cells on wild-type OS-enriched matricellular proteins reversed the phe
63 orm of protein tyrosine phosphatase receptor type O expressed predominantly in hematopoietic cells, i
64 se that the lower polymerase fidelity of the type O FMDV could contribute to its dominance worldwide.
65 es evidence that higher genetic diversity of type O FMDV could increase both virulence and transmissi
67 5% CI 1.27-51.44], p=0.025; OR for community type O for BRCA1 mutation carriers aged <35 years in the
68 BRCA1 mutation status (eg, OR for community type O for cases aged <40 years in the ovarian cancer se
70 is the Tn antigen (CD175), which is a mucin-type O-GalNAc-Ser/Thr/Tyr glycan in membrane and secrete
72 n, the protein-tyrosine phosphatase receptor type O gene, PTPRO, was frequently methylated in right-s
74 Pathway enrichment analyses show that mucin-type O-glycan biosynthesis and cardiomyocyte adrenergic
78 TCR avidities, perforin levels, and surface type O-glycan levels indicative of mature CD8(+) T cell
79 e2 O-glycan is presumably an essential mucin-type O-glycan structure found in both molecules in vivo.
80 hether such differential expression of mucin-type O-glycan structures has physiological significance
81 c-R is the precursor for many extended mucin-type O-glycan structures in animal cell surface and secr
82 e first to clearly identify functional mucin-type O-glycan structures modulating cell surface express
85 9, and T168 are modified by sialylated mucin-type O-glycan with core 1- and core 2-based structures.
86 -type N-glycans, a novel HexNAc-GalNAc-mucin-type O-glycan, and Tn-antigen; identified the glycosyltr
87 now identify a sulfated extended core1 mucin-type O-glycan, Gal beta 1-->4(sulfo-->6)GlcNAc beta 1-->
92 rate ligands that reveal how host cell mucin-type O-glycans are recognized and allow a structure-guid
93 talytic preference for core 2-branched mucin-type O-glycans as found in natural L-selectin counterrec
94 ct binding preferences for sialylated GalNAc-type O-glycans but exhibit selectivity for patterns of O
99 This study identified the most common mucin-type O-glycans in human tears and their expected biosynt
102 one Cosmc regulate the biosynthesis of mucin type O-glycans on glycoproteins, and evidence suggests t
103 ults indicate that polysialic acid and mucin type O-glycans on NCAM differentially regulate myoblast
106 tructural evidence for a novel type of mucin-type O-glycans that is strictly specific for LacdiNAc te
107 a pivotal role in the biosynthesis of mucin-type O-glycans that serve as ligands in cell adhesion.
108 cular surface epithelium to synthesize mucin-type O-glycans to maintain a wet-surface phenotype.
109 icits in aged mice by restoring core 1 mucin-type O-glycans to the brain endothelium using adeno-asso
110 However, the presence of clustered mucin-type O-glycans together with N-glycans makes the determi
113 se (C1GALT1) controls the formation of mucin-type O-glycans, far overlooked and underestimated in can
115 gates (O-fucose, O-mannose, N-glycans, mucin-type O-glycans, proteoglycans, glycosphingolipids), focu
123 nuclear O-Fuc-type and cell surface Glc-Fuc-type O-glycans; and showed that they are important for i
125 d to enrich GlcNAc-capped N-glycans or mucin type O-glycopeptides from complex samples in glycomics a
126 core 2 GlcNAc transferase acting on a mucin-type O-glycoprotein displayed increased galectin-3 bindi
127 ere, we report a comprehensive map of GalNAc-type O-glycoproteins (>800) and O-glycosites (>4000) fro
131 inyl transferases (GalNAc-Ts) initiate mucin type O-glycosylation by catalyzing the transfer of N-ace
132 mary, this study demonstrates that mammalian type O-glycosylation can be established in plants and th
134 Here we show that the N-acetylgalactosamine-type O-glycosylation enzyme GALNT11 is crucial to such d
135 reviously unrecognized requirement for mucin-type O-glycosylation in epithelial tube integrity and ha
136 have demonstrated essential roles for mucin-type O-glycosylation in protein secretion, stability, pr
147 esults and can be applied to a complex mucin-type O-glycosylation site analysis of other glycoprotein
150 In summary, stably engineered mammalian type O-glycosylation was established in transgenic plant
153 inyl-transferases (GalNAc-Ts) initiate mucin-type O-glycosylation, an abundant and complex posttransl
154 ted individuals showed abnormal N- and mucin-type O-glycosylation, and mass spectrometry indicated re
155 l-D-galactosamine (GalNAc) (core-1) in mucin type O-glycosylation, and thus terminates chain extensio
156 (EC 2.4.1.41) of enzymes that initiate mucin-type O-glycosylation, are structurally composed of a cat
157 ransferases (GalNAc-Ts), that initiate mucin-type O-glycosylation, consist of a catalytic and a lecti
162 ate the involvement of GalNAc-type (or mucin-type) O-glycosylation in EMT process, induced with trans
163 Mucin-type (N-acetylgalactosamine [GalNAc]-type) O-glycosylation is found in eumetazoan cells but a
165 ycosylation of the protein CST1 by the mucin-type O-glycosyltransferase T. gondii (Txg) GalNAc-T3 inf
167 (302) or Q(375) in VA387 affected binding to type O HBGA only, while switch mutants with three amino
171 bling species Paramecium septaurelia, mating type O is determined by coding-sequence deletions in a d
172 e transmembrane protein mtA, and the default type O is determined during development by scnRNA-depend
176 n addition, GalNAz efficiently labeled mucin-type O-linked glycoproteins expressed at endogenous leve
177 erein we present a method for labeling mucin-type O-linked glycoproteins with a unique chemical tag,
179 in (also known as proteoglycan 4) is a mucin-type O-linked glycosylated biological lubricant implicat
180 the ppGalNAcTs makes the prediction of mucin-type O-linked glycosylation difficult based on primary s
183 ere, we provide the first example that mucin-type O-linked glycosylation is involved in a development
185 ium, but not Plasmodium, possesses an animal-type O-linked glycosylation pathway, along with >30 pred
187 hanistically similar to that of animal mucin type O-linked glycosylation, except that it occurs in th
192 (ppGaNTases) initiate the formation of mucin-type, O-linked glycans by catalyzing the transfer of alp
195 tcomes of listing for A2 donors among 67 756 type O LT candidates listed between 2010 and 2023 using
196 r older had a higher prevalence of community type O microbiota (81 [61%] of 133 ovarian cancer cases
197 e stronger the association between community type O microbiota and ovarian cancer or BRCA1 mutation s
198 ears were also more likely to have community type O microbiota than age-matched controls (OR 2.79 [95
199 significantly higher prevalence of community type O microbiota than did age-matched controls under a
202 n = 90) was greater than the number of blood type O-non-directed donors (n = 32) initiating chains.
203 d with the MBL genotype (A/A indicating wild type, O/O indicating homozygous for MBL structural-gene
205 od type, but no correlation was observed for type O patients, suggesting that von Willebrand factor (
209 he rat protein tyrosine phosphatase receptor type O (PTPRO) and one amplified gene as rat C-MYC.
210 ne for protein tyrosine phosphatase receptor-type O (PTPRO) in primary and established rat hepatomas.
211 elated)] and the type III RPTP, PTP receptor type O (PTPRO), have been implicated in the regulation o
213 orm of protein-tyrosine phosphatase receptor-type O (PTPROt) is specifically expressed in hematopoiet
219 plants performed prior to CD, 48% were blood type-O recipients compared to 40% post-CD, representing
222 Incubation of RBC from universal donors (type O, Rh negative) with trauma sera (n = 10) promoted
223 s indicate that in vitro cultivation of FMDV type O selects viruses that bind to heparin and that vir
224 n those with blood type O; The <25 kg, blood type O subgroup experiences longer wait times and higher
225 lood, Dunne et al report that platelets from type O subjects bound poorly to von Willebrand factor (V
227 in candidates <25 kg and in those with blood type O; The <25 kg, blood type O subgroup experiences lo
228 k from MST1/2 via BUB3 and forkhead homeobox type O to the abnormal proliferation and survival of pul
231 a nonischemic cause of heart failure, blood type O, United Network for Organ Sharing status 2 at lis
234 problematic because it harms standard blood type O wait-list candidates who already have the longest
235 ncreased among AB and B types, compared with type O, while risk of death was increased for type AB an
236 Transplantation of bone marrow from wild-type o XBP1ecko mice could also slightly improve the foo