ライフサイエンスコーパス: ext

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 es with increasing external Ca(2+), [Ca(2+)](ext), for small levels of [Ca(2+)](ext).

5 [Ca(2+)](ext), for small levels of [Ca(2+)](ext).

6 ) whose activity is reduced by high [Ca(2+)](ext).

7 tical performance; that is, r(2) = 0.89, r(2-ext) = 0.72 and 0.73 for training and external validatio

8 take of (131)I- and (111)In-labeled antiPSMA(ext) mAbs (J415, J533, and J591) and their potential uti

9 ATP(ext) also induced a slower process of DNA fragmentation

10 ATP(ext) had an additive effect with TCR cross-linking in th

11 receptors in thymocytes is reflected by ATP(ext)-induced intracellular calcium increases and by thym

12 Described here, the properties of ATP(ext) and adenosine are consistent with their involvement

13 t-specific sensitivity to the effects of ATP(ext) and adenosine.

14 death, but, unexpectedly, the effects of ATP(ext) at high concentration were antagonistic to steroid-

15 Only ATP(ext), but not the ATP catabolites, adenosine, dexamethas

16 of extracellular adenosine triphosphate (ATP(ext)) and adenosine on TCR- and steroid hormone-triggere

17 ng independent measurements of b(scat) and b(ext).

18 light scattering (b(scat)) and extinction (b(ext)) coefficient by dispersed aerosols.

19 While measurement standard deviations for b(ext) and b(scat) were generally <1 Mm(-1) when the measu

20 hat reduce Ca(2+) influx, indicating that Ca(ext)(2+) is a source for the transient.

21 be induced by elevated external Ca2+ ([Ca2+](ext)), which promoted very rapid spiking of [Ca2+](cyt)

22 Our data indicate that elevated [Ca2+](ext) acts to disrupt Ca2+ homeostasis which induces defl

23 Elevated [Ca2+](ext) also results in further [Ca2+](cyt) elevations afte

24 Although basal DA(ext) did not differ, cocaine-evoked DA(ext) was greater

25 Extracellular DA concentration (DA(ext)) and extraction fraction (E(d)), an indirect measur

26 nd cocaine-evoked extracellular dopamine (DA(ext)) levels as well as basal DA uptake rate and cocaine

27 It increased cocaine-evoked DA(ext) and decreased the cocaine-induced inhibition of upt

28 The finding that cocaine-evoked DA(ext) is higher in naive and cocaine-exposed HRs suggests

29 al DA(ext) did not differ, cocaine-evoked DA(ext) was greater in HRs.

30 Basal uptake, but not DA(ext), was lower in HRs, indicating lower basal DA releas

31 r domain of the Notch ligand, Delta-1 (Delta(ext-myc)), induces apoptosis in peripheral blood monocyt

32 However, Delta(ext-myc) permitted differentiation into immature dendrit

33 Results showed that immobilized Delta(ext-myc) inhibited differentiation of monocytes into mat

34 endritic cells (51% in the presence of Delta(ext-myc) versus 10% in control cultures), whereas a decr

35 With GM-CSF and TNF-alpha, exposure to Delta(ext-myc) increased the proportion of precursors that dif

36 h increasing densities of immobilized Delta1(ext-IgG) consisting of the extracellular domain of Delta

37 of purified immobilized Notch ligand (Delta1(ext-IgG)) induced increased expression of Notch targets

38 h exogenously presented Notch ligand, Delta1(ext-IgG), consisting of the extracellular domain of Delt

39 Higher densities of Delta1(ext-IgG) also enhanced the generation of Sca-1(+)c-kit+

40 Lower densities of Delta1(ext-IgG) enhanced the generation of CD34+ cells as well

41 nd that relatively lower densities of Delta1(ext-IgG) enhanced the generation of Sca-1(+)c-kit+ cells

42 er, culture with increased amounts of Delta1(ext-IgG) induced apoptosis of CD34+ precursors resulting

43 findings demonstrate the potential of Delta1(ext-IgG)-cultured cells for accelerating early immune re

44 w that culture of LSK precursors with Delta1(ext-IgG) increases the number of progenitors that are ab

45 tion of murine marrow precursors with Delta1(ext-IgG), a Notch ligand consisting of the Delta1 extrac

46 formance (30 000 cd/m(2) luminance; 2.0% eta(ext); 4.0 V turn-on voltage).

47 observed (64 000 cd/m(2) luminance; 2.3% eta(ext); turn-on voltages as low as 3.5 V).

48 .6% forward external quantum efficiency (eta(ext)), and 5 V turn-on voltages are achieved, affording

49 reading frame [ORF]), an AT-rich extension (ext-a1) of the core ORF and an AT-rich region following

50 ulated efficiencies of mispair extension ( f ext) were, in general, not significantly decreased from

51 sion efficiencies just beyond the lesions (f(ext)) are generally smaller than f(ins) and also depend

52 equency of translesion synthesis (F(ins) x F(ext)) of dC.dG-N(2)-BPDE pairs was 2-6 orders of magnitu

53 This identifies Glu(ext) as a major component of the gating charge underlyin

54 an inward movement of the side chain of Glu(ext), followed by the binding of extracellular Cl(-) ion

55 extets in the Mossbauer spectrum at 4.2 K (H(ext) = 0) which converge to a single six-line pattern in

56 ailable from the following URL: http://igrid-ext.cryst.bbk.ac.uk/portal_guide/.

57 ) (K(int) = [E.P.UCGA]/[E.S.UCG] = 4.6 and K(ext) = [P][UCGA]/[S][UCG] = 1.9).

58 unperturbed from the solution equilibrium, K(ext) (K(int) = [E.P.UCGA]/[E.S.UCG] = 4.6 and K(ext) = [

59 ux at low external K(+) concentration ([K(+)]ext = 22.5 microm) was predominantly mediated by AtAKT1

60 m active to passive K(+) uptake at low [K(+)]ext and yielding fluxes as high as 36 micromol g (root f

61 kt1, athak5, and athak5 atakt1) at low [K(+)]ext, revealing the concerted involvement of several tran

62 (root fresh weight)(-1) h(-1) at 5 mm [K(+)]ext, among the highest transporter-mediated K(+) fluxes

63 "IB" (interburst) state, and a set of [K(+)](ext) and voltage-dependent "C" (closed) states.

64 to the Myb domain called Myb-extension (Myb-ext) that is absent in TRFL family 2 and hTRF1/hTRF2.

65 Removal of the Myb-ext domain from TRFL1, a family 1 member, abolished DNA

66 However, when the Myb-ext domain was introduced into the corresponding region

67 Thus, Myb-ext is required for binding plant telomeric DNA and defi

68 f extracellular Na(+) concentration ([Na(+)](ext)).

69 Na(X) channel and regulates the high [Na(+)](ext)-evoked Na(+) current via influencing the Na(+) infl

70 )/K(+)-ATPase play a central role in [Na(+)](ext) detection.

71 isoform is specifically involved in [Na(+)](ext) detection.

72 intracellular regulatory pathway of [Na(+)](ext) detection in MnPO neurons.

73 vations, we suspect a translation product of ext-a1 affects different regulatory mechanisms that cont

74 The localization of radiolabeled anti-PSMA(ext) antibodies in PSMA-positive LNCaP tumors was highly

75 of necrosis whereas J415 and J591 (anti-PSMA(ext)) demonstrated a distinct preferential accumulation

76 ty to the extracellular domain of PSMA (PSMA(ext)).

77 ause J591 and J415 mAbs are specific to PSMA(ext), thus targeting viable tumor, these immunoconjugate

78 (S(int)), central (S(cen)), and external (S(ext)).

79 (ex)) residue acts as a gate competing for S(ext).

80 (ex) is essential for Cl(-) transport from S(ext) to S(cen).

81 ociated with transport of a Cl(-) ion from S(ext) to S(int), depending on the Cl(-) occupancy of othe

82 Cl(-) favorably occupies an exterior site, S(ext), to form a queue of anions in the pore.

83 attering (sigma(scat)) and extinction (sigma(ext)) cross sections for size-selected ammonium sulfate

84 ooxygenation product is the less stable SREP-ext stereoisomer with the endoperoxide unit directed out

85 ent reactivity of mechanically strained SREP-ext depend on the size of the end groups of the encapsul

86 he interlocked components, the strained SREP-ext stereoisomer undergoes clean thermal cycloreversion.

87 sure ( P (0)) and at ambient temperature ( T ext).

88 verexpression of the ext-a1 sequence and the ext-a1 3' region, which includes a partial sequence of d

89 we study the effect of overexpression of the ext-a1 sequence and the ext-a1 3' region, which includes