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1 PMA also increased internalization and accelerated recep
2 PMA doping over a limited depth of bulk heterojunction p
3 PMA significantly reduced tenting height, tenting area,
4 PMA treatment also caused impairments in insulin-signali
5 PMA, but not DiC8, targeted PKCalpha to detergent-resist
6 PMA- and BzATP-stimulated increases in [Ca2+]i were addi
7 PMA-doped films show increased electrical conductivity a
8 PMA-induced Erk phosphorylation was reduced by ErbB2 inh
9 PMA-induced shedding of Tim-3 was abrogated by deletion
10 PMA-induced shedding was abrogated by an ADAM (A disinte
11 PMA-stimulated ERK activity was also inhibited by 1-buta
12 PMA/Ionomycin treatment of DOCK8-deficient NK cells resc
16 n electron-rich aldehyde and 5-methoxy-ABAO (PMA), which was observed at pH 4.5, places this reaction
19 lon), while phorbol 12-myristate 13-acetate (PMA) activation of PKCepsilon drives inducible TSPO expr
20 li, such as phorbol-12-myristate-13-acetate (PMA) and androgens, but show differential responses to s
23 reated with phorbol 12-myristate 13-acetate (PMA) and ionomycin, which signal via protein kinase C (P
25 e show that phorbol 12-myristate 13-acetate (PMA) immediately activates the expression of HCMV MIE RN
26 bination of phorbol 12-myristate 13-acetate (PMA) plus ionophore A23187 (Io), which induces NFAT acti
27 sponsive to phorbol 12-myristate 13-acetate (PMA) reactivation in the absence of CYLD, indicating tha
28 C activator phorbol 12-myristate 13-acetate (PMA) stimulated apoE secretion, and both PMA-induced and
29 release by phorbol-12-myristate-13-acetate (PMA) stimulation was demonstrated using T-47D human brea
30 tivation by phorbol 12-myristate 13-acetate (PMA) than cells isolated by conventional mucolytic metho
31 ivated with phorbol-12-myristate-13-acetate (PMA) were added back into whole blood, the extent and ra
32 nists (e.g. phorbol 12-myristate 13-acetate (PMA)) indicate that prolonged stimulation leads to PKCal
33 ork we used phorbol 12-myristate 13-acetate (PMA), a well recognized agonist of classical and non-con
34 opoietin or phorbol 12-myristate 13-acetate (PMA), alphaIIbbeta3 became activated as evidenced by bin
36 activator, phorbol 12-myristate 13-acetate (PMA), in primary HUVECs was found to require PKCeta- and
37 e (ATP) and phorbol 12-myristate 13-acetate (PMA), results in a cation influx via P2X(4) receptors at
38 peroxide or phorbol 12-myristate 13-acetate (PMA), U6 promoter activity was down regulated and this i
41 le of PK in phorbol 12-myristate 13-acetate (PMA)-induced megakaryocytic differentiation in human leu
42 h basal and phorbol 12-myristate 13-acetate (PMA)-induced MMP13 promoter activity; conversely, Ankrd1
43 h basal and phorbol 12-myristate 13-acetate (PMA)-induced NADPH oxidase activity were increased in Ra
44 itutive and phorbol 12-myristate 13-acetate (PMA)-induced ubiquitination of the receptor at the cell
51 oduction of phorbol 12-myristate 13-acetate (PMA)/ionomycin-stimulated human peripheral blood mononuc
54 th the ability of phorbol myristate acetate (PMA) to promote FLNB-mediated cytoplasmic accumulation o
55 fluidic device to phorbol myristate acetate (PMA), a known promoter of oxidative burst, and the produ
56 nregulated during phorbol myristate acetate (PMA)-induced monocyte-to-macrophage differentiation, whi
60 by phorbol ester (phorbol myristate acetate [PMA]) reduced insulin-induced p-Tyr-IRS2 by 46% +/- 13%
62 icacious, we conjugated polymannuronic acid (PMA), containing the blocks of mannuronic acid conserved
65 articles grafted with poly(methyl acrylate) (PMA) chains anchored by a maleimide-anthracene cycloaddu
66 l activity was mimicked by the PKC activator PMA, occurred without activation of PKA, and persisted i
67 but was inhibited by the PKC-theta activator PMA, or by CD28 crosslinking, which enhances PKC-theta a
70 ent HEK293 cells failed to shed IL-23R after PMA stimulation, demonstrating that ADAM17 but not ADAM1
72 mediated increase in IEC wound closure after PMA stimulation was mediated by increased cell spreading
80 TI) scans, early in life (postmenstrual age [PMA] = 32.3 weeks) and at term-equivalent age (PMA = 40.
81 (imaged from 30-36 weeks postmenstrual age [PMA]); 78% of term-aged preterm infants (imaged from 37-
82 Circulating platelet-monocyte aggregates (PMAs), p-selectin expression (P-SEL), and integrin alpha
84 erellins (GA) in pre-maturity alpha-amylase (PMA) formation in developing wheat grain, two glasshouse
86 actor required for Th17 differentiation, and PMA markedly stimulated the expression of Stat3 in WT bu
91 mulated by uridine-5'-triphosphate (UTP) and PMA, agonists inducing LB fusion with the PM, but not ac
95 undersizing restrictive mitral annuloplasty (PMA) associated with complete surgical myocardial revasc
99 therapy devices, via the premarket approval (PMA) process, during which manufacturers submit clinical
108 metformin and AICAR significantly attenuated PMA-induced monocyte-to-macrophage differentiation and p
109 t-mediated uptake requires macrophages to be PMA-primed, untreated cells phagocytose nonopsonized sil
110 lls with the protein kinase C activator beta-PMA and concomitantly decreases PMA-elicited SERT phosph
113 te (PMA) stimulated apoE secretion, and both PMA-induced and apoAI-induced apoE secretion were inhibi
114 tobacillus rhamnosus strain GG inhibits both PMA- and Staphylococcus aureus-induced formation of NETs
116 induced NF-kappaB, or NF-kappaB activated by PMA or MyD88 overexpression, whereas a mutant protein la
118 on, and viable cell quantities determined by PMA real-time PCR were approximately 10(4) greater than
119 and this inhibition was further enhanced by PMA and p38 kinase inhibitors reversed this inhibition.
123 o cAMP signaling, including ERK induction by PMA, and ERK activation and neuritogenesis induced by NG
124 of dopamine neurons after internalization by PMA, compared with vehicle or amphetamine treatment.
126 TE had a significant increase in circulating PMAs and CRP post-operatively, compared to those without
127 study to identify that increased circulating PMAs and CRP levels are early markers associated with po
128 uantifying the anthracene-containing cleaved PMA polymers, which are generated via retro-[4 + 2] cycl
131 cal IDR-1002 treatment successfully dampened PMA-induced ear edema, proinflammatory cytokine producti
135 play bryostatin-like behavior, WN-1 displays PMA-like behavior in U937 cell attachment and proliferat
136 racene/phorbol 12-myristate 13-acetate (DMBA/PMA) treatment developed in sites of preexisting hyperem
137 guided PK-dependent metabolic changes during PMA induction, which are important in megakaryocytic dif
139 C-theta, or WT PKC-theta activated by either PMA or TCR cross-linking, stimulated expression of a luc
140 protein kinase C (PKC) by the phorbol ester PMA has been shown to down-regulate cell surface DAT.
141 tor region is inducible by the phorbol ester PMA, a potent activator of the protein kinase C (PKC) pa
142 n contrast, the PKC-activating phorbol ester PMA, often used as a strong inducer of ADAM17, causes no
145 f the Nox4 TM and Nox2 DH domains, exhibited PMA-dependent activation that required coexpression of r
147 isk therapeutic devices approved via the FDA PMA pathway, total product life cycle evidence generatio
150 lement, is both necessary and sufficient for PMA-induced transactivator activity in PAI-2-expressing
152 BV-transformed B cell lines (resting and 6 h PMA stimulated) and purified CD4(+) and CD8(+) T cells.
155 iated by the reduction of ADAM17 activity in PMA stimulated cells although the expression ADAM17 is n
161 n rate determined by the culture-independent PMA-qPCR method (1.5-log removal at 664 mg.min/L) was lo
163 cule C-reactive protein (CRP), which induces PMA formation in vitro, along with plasma d-dimer and fi
164 extracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN me
165 f c-Jun N-terminal kinase activity inhibited PMA-induced inflammation but not differentiation, sugges
166 ore expressed by Escherichia coli, inhibited PMA-induced generation of reactive oxygen species (ROS)
167 ly, silencing of PK (PKM2 and PKR) inhibited PMA-induced megakaryocytic differentiation, as revealed
169 s which modifications occurred after initial PMA) and median number of supplements approved per devic
171 developed and applied a propidium monoazide (PMA) real-time PCR assay to quantify viable (with PMA) a
172 technique combined with propidium monoazide (PMA) to simultaneously detect viable Legionella pneumoph
173 live cells was based on propidium monoazide (PMA) treatment to selectively remove DNA from membrane-c
174 at the combination of a propidium monoazide (PMA) treatment with haRPA, the so-called viability haRPA
175 lled organisms, we used propidium monoazide (PMA), a DNA-binding dye that penetrates damaged bacteria
176 home, at 1 year, and at age 18 to 24 months' PMA and neurodevelopmental assessments at 18 to 24 month
181 d sensitivity, this newly invented multiplex PMA-qPCR assay took a much shorter time than did convent
184 onstitutive endocytosis in dopamine neurons, PMA induces ubiquitination of DAT and leads to accumulat
185 FcepsilonRI-mediated degranulation, but not PMA/ionomycin-induced degranulation, as shown by beta-he
188 n (representing chromatin decondensation) of PMA-treated serpinb1-deficient neutrophils compared with
190 FAT-mediated T-cell activation in a model of PMA-elicited peritonitis, whereas topical application of
192 mulated CD4+ T cells and immune responses of PMA/ionomycin stimulated CD4+ T cells by FACS analysis p
193 ession or its inactivation on the surface of PMA-treated monocytes reduced the extent and rate of clo
195 proval of panel-track supplements (a type of PMA supplement pathway that is used for significant chan
203 using the calcium ionophore ionomycin and/or PMA on Jurkat T cells, we show that the gene expression
206 ears (IQR, 8-20), and 79% of the 77 original PMAs approved during our study period were the subject o
208 lated the number of supplements approved per PMA and analyzed trends relating to different supplement
211 thway, we treated MKs with polymethacrylate (PMA), which markedly increased MARCKS phosphorylation wh
215 WC1 cytoplasmic domain significantly reduced PMA-induced endocytosis in both cell types and enhanced
218 mic devices initially approved via the FDA's PMA pathway between January 1, 1979 and December 31, 201
219 st ophthalmic devices approved via the FDA's PMA pathway have undergone extensive revisions, includin
221 es accounted for birth gestational age, sex, PMA, dose of analgesics/sedatives (fentanyl, morphine, m
222 m hPSCs within 23 days of culture using soft PMAs were improved more than fourfold and tenfold, respe
226 he NETosis pathways induced by five stimuli; PMA, the calcium ionophore A23187, nigericin, Candida al
228 FDA approved 77 original and 5829 supplement PMA applications for CIEDs, with a median of 50 suppleme
229 oes not rely on its relocalisation, but that PMA-induced PKC activity drastically dysregulates the lo
234 Further mechanistic analysis revealed that PMA fails to promote phosphorylation of Bad in Ser(112)
237 ite-specific mutational analysis showed that PMA increased serine phosphorylation at three sites on I
238 matin immunoprecipitation assays showed that PMA treatment induced p65 binding to the TRPC6 promoter.
246 Ejection fraction was 44.1 +/- 6% in the PMA group versus 39.9 +/- 3.9% in the RA group (mean cha
248 this paper, we investigate the origin of the PMA in MgO/CoFe/metallic capping layer structures by usi
256 ruginosa, but nonetheless rabbit antibody to PMA-FLA showed evidence of protective efficacy against b
258 nors with inhibitors of molecules crucial to PMA-induced NETs including protein kinase C, calcium, re
259 4-3-3-binding site S312, whereas exposure to PMA led to phosphorylation of PDE3A2 at an alternative 1
260 t not unmodified PKCdelta, was refractory to PMA-stimulated T(505) phosphorylation, similar to PKCdel
264 H547A displays a differential sensitivity to PMA- or BIM-induced activation or inhibition of DAT func
267 Pepsilon) in MCF-7 cells and MDA-MB-231 upon PMA, FGF, and serum stimulation, which depended on EGFR
268 of CD63 and CD203c in mononuclear cells upon PMA stimulation, suggesting a role in sensitization to a
269 ted during monochloramine disinfection using PMA-pyrosequencing, while the community structure appear
270 ity on the U937 cells to confirm that it was PMA-like for growth and attachment, as predicted by the
273 ged preterm infants (imaged from 37-42 weeks PMA); 49% of term infants; and 39% of adult subjects.
275 ot improve survival without BPD at 36 weeks' PMA or respiratory and neurodevelopmental outcomes at 18
276 me at less than 90% Sao2 at 35 and 36 weeks' PMA was 106.3 (89.0) and 100.1 (114.6) s/h, respectively
280 ory impairment, the AOR and AUC at 40 weeks' PMA (AOR, 1.5, 95% CI, 1.0-2.1; AUC, 0.740) were only ma
284 (n) < 20 kDa, (ii) for high molecular weight PMAs (M(n) > 60 kDa) featuring terminal cycloaddition ad
285 phages, we treated U937 monocytic cells with PMA, which stimulates both macrophage differentiation an
287 in culture medium, whereas incubations with PMA, TNF-alpha, IL-13, or IL-4 enhanced levels of C3 1.7
288 Stimulation of Raw 264.7 macrophages with PMA augmented the amount of mu1A associated with anti-L-
289 5 years, mean LVEDD was 56.5 +/- 5.7 mm with PMA versus 60.6 +/- 4.6 mm with RA (mean change from bas
290 uman polymorphonuclear cells stimulated with PMA did not bind to zymosan or E. coli, but when incubat
292 expressed on NK cells, and stimulation with PMA or N-ethyl-maleimide resulted in the shedding of Fcg
299 real-time PCR assay to quantify viable (with PMA) and total (without PMA) E. coli O157:H7 cells on gr
300 uantify viable (with PMA) and total (without PMA) E. coli O157:H7 cells on growth chamber and field-g
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