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1 acellular domain of human Jagged-1 (Jagged-1(ext)).
2 ents indicated that the chimeric IL-15Ralpha(ext)/IL-2Ralpha(int) receptor still supports trans-prese
3 racellular domain of IL-2Ralpha (IL-15Ralpha(ext)/IL-2Ralpha(int)) and examined its function in 32D c
4 etrics exceeding 0.8 (Q(2)cv = 0.864 and Q(2)ext = 0.873).
5 ds the best result (R(2)(train) = 0.93, R(2)(ext) = 0.70).
6 es with increasing external Ca(2+), [Ca(2+)](ext), for small levels of [Ca(2+)](ext).
7  [Ca(2+)](ext), for small levels of [Ca(2+)](ext).
8 ) whose activity is reduced by high [Ca(2+)](ext).
9 tical performance; that is, r(2) = 0.89, r(2-ext) = 0.72 and 0.73 for training and external validatio
10 ch fraction after thioglycolysis, a dimer A2-ext and a molecule that corresponds to a linkage between
11 take of (131)I- and (111)In-labeled antiPSMA(ext) mAbs (J415, J533, and J591) and their potential uti
12                                          ATP(ext) also induced a slower process of DNA fragmentation
13                                          ATP(ext) had an additive effect with TCR cross-linking in th
14  receptors in thymocytes is reflected by ATP(ext)-induced intracellular calcium increases and by thym
15        Described here, the properties of ATP(ext) and adenosine are consistent with their involvement
16 t-specific sensitivity to the effects of ATP(ext) and adenosine.
17 death, but, unexpectedly, the effects of ATP(ext) at high concentration were antagonistic to steroid-
18                                     Only ATP(ext), but not the ATP catabolites, adenosine, dexamethas
19 of extracellular adenosine triphosphate (ATP(ext)) and adenosine on TCR- and steroid hormone-triggere
20 ng independent measurements of b(scat) and b(ext).
21 light scattering (b(scat)) and extinction (b(ext)) coefficient by dispersed aerosols.
22  While measurement standard deviations for b(ext) and b(scat) were generally <1 Mm(-1) when the measu
23 2) affinity, external carbonic anhydrase (CA(ext) ), isotopic signatures (d(13) C) and growth among s
24 2) affinity, external carbonic anhydrase (CA(ext) ), isotopic signatures (delta(13) C) and growth amo
25 ecies, with higher CO(2) affinity, higher CA(ext) and higher d(13) C.
26 ecies, with higher CO(2) affinity, higher CA(ext) and higher delta(13) C.
27 hat reduce Ca(2+) influx, indicating that Ca(ext)(2+) is a source for the transient.
28 be induced by elevated external Ca2+ ([Ca2+](ext)), which promoted very rapid spiking of [Ca2+](cyt)
29       Our data indicate that elevated [Ca2+](ext) acts to disrupt Ca2+ homeostasis which induces defl
30                              Elevated [Ca2+](ext) also results in further [Ca2+](cyt) elevations afte
31                            Although basal DA(ext) did not differ, cocaine-evoked DA(ext) was greater
32           Extracellular DA concentration (DA(ext)) and extraction fraction (E(d)), an indirect measur
33 nd cocaine-evoked extracellular dopamine (DA(ext)) levels as well as basal DA uptake rate and cocaine
34               It increased cocaine-evoked DA(ext) and decreased the cocaine-induced inhibition of upt
35           The finding that cocaine-evoked DA(ext) is higher in naive and cocaine-exposed HRs suggests
36 al DA(ext) did not differ, cocaine-evoked DA(ext) was greater in HRs.
37                     Basal uptake, but not DA(ext), was lower in HRs, indicating lower basal DA releas
38 r domain of the Notch ligand, Delta-1 (Delta(ext-myc)), induces apoptosis in peripheral blood monocyt
39                               However, Delta(ext-myc) permitted differentiation into immature dendrit
40        Results showed that immobilized Delta(ext-myc) inhibited differentiation of monocytes into mat
41 endritic cells (51% in the presence of Delta(ext-myc) versus 10% in control cultures), whereas a decr
42 With GM-CSF and TNF-alpha, exposure to Delta(ext-myc) increased the proportion of precursors that dif
43 h increasing densities of immobilized Delta1(ext-IgG) consisting of the extracellular domain of Delta
44 of purified immobilized Notch ligand (Delta1(ext-IgG)) induced increased expression of Notch targets
45 h exogenously presented Notch ligand, Delta1(ext-IgG), consisting of the extracellular domain of Delt
46                   Higher densities of Delta1(ext-IgG) also enhanced the generation of Sca-1(+)c-kit+
47                    Lower densities of Delta1(ext-IgG) enhanced the generation of CD34+ cells as well
48 nd that relatively lower densities of Delta1(ext-IgG) enhanced the generation of Sca-1(+)c-kit+ cells
49 er, culture with increased amounts of Delta1(ext-IgG) induced apoptosis of CD34+ precursors resulting
50 findings demonstrate the potential of Delta1(ext-IgG)-cultured cells for accelerating early immune re
51 w that culture of LSK precursors with Delta1(ext-IgG) increases the number of progenitors that are ab
52 tion of murine marrow precursors with Delta1(ext-IgG), a Notch ligand consisting of the Delta1 extrac
53 formance (30 000 cd/m(2) luminance; 2.0% eta(ext); 4.0 V turn-on voltage).
54 observed (64 000 cd/m(2) luminance; 2.3% eta(ext); turn-on voltages as low as 3.5 V).
55 .6% forward external quantum efficiency (eta(ext)), and 5 V turn-on voltages are achieved, affording
56  reading frame [ORF]), an AT-rich extension (ext-a1) of the core ORF and an AT-rich region following
57 ulated efficiencies of mispair extension ( f ext) were, in general, not significantly decreased from
58 sion efficiencies just beyond the lesions (f(ext)) are generally smaller than f(ins) and also depend
59 equency of translesion synthesis (F(ins) x F(ext)) of dC.dG-N(2)-BPDE pairs was 2-6 orders of magnitu
60                          This identifies Glu(ext) as a major component of the gating charge underlyin
61  an inward movement of the side chain of Glu(ext), followed by the binding of extracellular Cl(-) ion
62 extets in the Mossbauer spectrum at 4.2 K (H(ext) = 0) which converge to a single six-line pattern in
63 ) (K(int) = [E.P.UCGA]/[E.S.UCG] = 4.6 and K(ext) = [P][UCGA]/[S][UCG] = 1.9).
64 unperturbed from the solution equilibrium, K(ext) (K(int) = [E.P.UCGA]/[E.S.UCG] = 4.6 and K(ext) = [
65 ux at low external K(+) concentration ([K(+)]ext = 22.5 microm) was predominantly mediated by AtAKT1
66 m active to passive K(+) uptake at low [K(+)]ext and yielding fluxes as high as 36 micromol g (root f
67 kt1, athak5, and athak5 atakt1) at low [K(+)]ext, revealing the concerted involvement of several tran
68  (root fresh weight)(-1) h(-1) at 5 mm [K(+)]ext, among the highest transporter-mediated K(+) fluxes
69 "IB" (interburst) state, and a set of [K(+)](ext) and voltage-dependent "C" (closed) states.
70  to the Myb domain called Myb-extension (Myb-ext) that is absent in TRFL family 2 and hTRF1/hTRF2.
71                           Removal of the Myb-ext domain from TRFL1, a family 1 member, abolished DNA
72                        However, when the Myb-ext domain was introduced into the corresponding region
73                                    Thus, Myb-ext is required for binding plant telomeric DNA and defi
74 f extracellular Na(+) concentration ([Na(+)](ext)).
75 Na(X) channel and regulates the high [Na(+)](ext)-evoked Na(+) current via influencing the Na(+) infl
76  isoform is specifically involved in [Na(+)](ext) detection.
77 )/K(+)-ATPase play a central role in [Na(+)](ext) detection.
78  intracellular regulatory pathway of [Na(+)](ext) detection in MnPO neurons.
79 vations, we suspect a translation product of ext-a1 affects different regulatory mechanisms that cont
80 this limitation by using an extended pegRNA (ext-pegRNA) with modified 3' extension, and an additiona
81   The localization of radiolabeled anti-PSMA(ext) antibodies in PSMA-positive LNCaP tumors was highly
82 of necrosis whereas J415 and J591 (anti-PSMA(ext)) demonstrated a distinct preferential accumulation
83 ty to the extracellular domain of PSMA (PSMA(ext)).
84 ause J591 and J415 mAbs are specific to PSMA(ext), thus targeting viable tumor, these immunoconjugate
85 capacity for the test set with R(ext)(2) = Q(ext)(2) values in the range of 0.639-0.823 and 0.767-0.8
86  predictive capacity for the test set with R(ext)(2) = Q(ext)(2) values in the range of 0.639-0.823 a
87  (S(int)), central (S(cen)), and external (S(ext)).
88 (ex)) residue acts as a gate competing for S(ext).
89 (ex) is essential for Cl(-) transport from S(ext) to S(cen).
90 ociated with transport of a Cl(-) ion from S(ext) to S(int), depending on the Cl(-) occupancy of othe
91 Cl(-) favorably occupies an exterior site, S(ext), to form a queue of anions in the pore.
92 y two components: dCas9 and extended sgRNAs (ext-sgRNAs).
93 attering (sigma(scat)) and extinction (sigma(ext)) cross sections for size-selected ammonium sulfate
94 ooxygenation product is the less stable SREP-ext stereoisomer with the endoperoxide unit directed out
95 ent reactivity of mechanically strained SREP-ext depend on the size of the end groups of the encapsul
96 he interlocked components, the strained SREP-ext stereoisomer undergoes clean thermal cycloreversion.
97 sure ( P (0)) and at ambient temperature ( T ext).
98 verexpression of the ext-a1 sequence and the ext-a1 3' region, which includes a partial sequence of d
99 we study the effect of overexpression of the ext-a1 sequence and the ext-a1 3' region, which includes
100 ciently perform editing on both sides of the ext-pegRNA nick, a task that is unattainable by canonica
101 base pairs within the upstream region of the ext-pegRNA nick.
102 -sgRNA) targeting the upstream region of the ext-pegRNA.
103 k, we develop a tumor phylogeny method, TUSV-ext, which incorporates SNVs, CNAs and SVs into a single

 
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