ライフサイエンスコーパス: Kr

1 Kr mutation affects the temporal fate of the neuroblast

2 Kr-h1 maintains the immature stage by suppressing E93 (e

3 the transcription factors Kruppel-homolog 1 (Kr-h1) and Broad-Complex (BR-C) during the last juvenile

4 Interestingly, Kruppel homolog 1 (Kr-h1) knockdown in the adult females did not reduce the

5 ncrease of mRNA levels of Kruppel homolog 1 (Kr-h1), a juvenile hormone-dependent transcription facto

6 nger transcription factor Kruppel homolog 1 (Kr-h1), one of the key players in juvenile hormone signa

7 transcription factor (TF) Kruppel homolog 1 (Kr-h1).

8 sis showed high levels of Kruppel homolog 1 [Kr-h1, a transcription factor that plays key roles in ju

9 tized by the dominant Kr(irregular facets-1)(Kr(If-1)) allele, we show that the Piwi-interacting RNA

10 At present, ATTA (81)Kr analysis requires a 40-80-kg ice sample; as sample re

11 ample requirements continue to decrease, (81)Kr dating of ice cores is a future possibility.

12 Radiokrypton isotopes ((81)Kr and (85)Kr) are ideal tracers and chronometers of var

13 The analysis by using ATTA of (81)Kr in naturally occurring gases of interest, e.g., disso

14 We present successful (81)Kr-Kr radiometric dating of ancient polar ice.

15 We estimate the error in the (81)Kr ages due to past geomagnetic variability to be below

16 The (81)Kr radiometric ages agree with independent age estimates

17 bumin and simultaneous ventilation with (81m)Kr gas.

18 s in hyperpolarized spin state of either (83)Kr or (129)Xe.

19 uclear spin polarizations were P =29% for(83)Kr and P= 63% for (129)Xe.

20 ensity for the advancement of in vivo hp (83)Kr MRI.

21 xplored approach in the generation of hp (83)Kr that can likewise be used for the production of hp (1

22 ast also complicate the production of hp (83)Kr.

23 Hyperpolarized (hp) (83)Kr is a promising MRI contrast agent for the diagnosis o

24 only NMR active, stable krypton isotope (83)Kr (spin I = (9)/(2)) is explored as a novel probe for p

25 Chemical shifts and line widths of (83)Kr are moderately dependent on small fluctuations in the

26 ver, the distinct physical properties of (83)Kr that enable unique MRI contrast also complicate the p

27 Highly spin-polarized (83)Kr can now be purified for the first time, to our knowle

28 It is demonstrated that (83)Kr NMR spectroscopy of nanoporous or microporous materia

29 The (83)Kr chemical shifts observed in the investigated material

30 omagnetic ratio and low abundance of the (83)Kr isotope.

31 The (83)Kr line width in most of the studied cases is quadrupola

32 atmospheric noble gases ((20)Ne, (36)Ar, (84)Kr, (132)Xe) with respect to air-saturated water (ASW).

33 Additionally, lack of correlation of (84)Kr/(36)Ar and (132)Xe/(36)Ar fractionation levels along

34 noble gases, with particular emphasis on (84)Kr and (132)Xe.

35 Radiokrypton isotopes ((81)Kr and (85)Kr) are ideal tracers and chronometers of various enviro

36 d sampling strategy are validated by (i) (85)Kr and (39)Ar analyses that show the samples to be free

37 radionuclides such as tritium, (14)C, or (85)Kr will become blurred in the significant background of

38 H, (14)C, (35)S), gaseous radionuclides ((85)Kr, (133)Xe, (135)Xe) or radionuclides with very long ha

39 laser-induced fluorescence detection using a Kr+ ion laser.

40 a was determined to be 33 m2 g(-1) according Kr sorption data.

41 ontaining an E-box-like motif from the Aedes Kr-h1 gene promoter specifically interacted with a prote

42 transcription factors such as S59, eve, and Kr, all of which are observed in subsets of the nautilus

43 s, osmium-isotope ratios and D/H, Ar/H2O and Kr/Xe ratios such that no primitive material similar to

44 ith a precision of better than 4% for He and Kr, and with a precision of 1% for Ar, N(2), and O(2) in

45 ) specifies the third-born U3 motoneuron and Kr misexpression induces ectopic U3 cells.

46 e identify the relative affinities of Xe and Kr atoms for as many as seven distinct binding sites.

47 Kr, and 2.5% or better for Ne/Xe, Ar/Xe, and Kr/Xe using air as the only calibration standard.

48 oves to 0.6% or better for Ne/Xe, Ar/Xe, and Kr/Xe when the data is calibrated using discrete water s

49 Using an Ar+/Kr+ laser, the fluorophore moieties were bleached to cre

50 that between Au(-) and a noble-gas atom (Ar, Kr, or Xe).

51 ng chain molecule (n-heptane) and atoms (Ar, Kr, and Xe).

52 ll gases (H2, D2, Ne, N2, CO, CH4, C2H6, Ar, Kr, and Xe) on the metal-organic framework (MOF) NU-1000

53 artial pressures of He, Ne (in dry gas), Ar, Kr, N2, O2, CO2, and CH4 in gaseous and aqueous matrices

54 e concentrations of dissolved gases (He, Ar, Kr, N(2), and O(2)) in groundwater to be determined quas

55 ysis of 2-formyl phenylazide isolated in Ar, Kr, and Xe matrixes and characterized by IR, UV-vis, and

56 ontinuous, real-time measurements of Ne, Ar, Kr, and Xe mole ratios in natural waters.

57 ontinuous or pulsed beams of 500 keV Ne, Ar, Kr, or Xe ions.

58 s (GaSb, GaAs, GaP) and ion species (Ne, Ar, Kr, Xe) to determine new parametric trends regarding nan

59 spectrometer (GC-MS) for analysis of Ne, Ar, Kr, Xe, N2, and O2 and an electron capture detector (GC-

60 taneous measurement of dissolved He, Ne, Ar, Kr, Xe, SF6, N2, and O2 concentrations in a single water

61 We studied Ar, Kr, CO, and N(2) going into and out of a chemically open

62 y is 0.7% or better for Ne/Kr, Ne/Ar, and Ar/Kr, and 2.5% or better for Ne/Xe, Ar/Xe, and Kr/Xe using

63 These data show interactions between Kr-h1, E93 and JH in the regulation of metamorphosis in

64 The transcriptional co-regulation by Kr-h1 and dFOXO may represent a broad mechanism by which

65 find that hunchback (Calb-hb), Kruppel (Calb-Kr), knirps (Calb-knl), giant (Calb-gt) and tailless (Ca

66 </= 1) clathrates (guest = H2O, N2, Ar, CH4, Kr, Xe, C2H4, C2H6, CH3F, CO2, H2S, CH3Cl, CH3OCH3, CH3B

67 of several clathrates (guest = H2O, N2, CO2, Kr, CH3F) is shown to occur in a single-crystal-to-singl

68 A newly developed Kr purification system is based on conventional cryogeni

69 Similar work with dilute Kr and Xe in argon finds small frequency shifts in new f

70 e-outgrowth assay sensitized by the dominant Kr(irregular facets-1)(Kr(If-1)) allele, we show that th

71 ity was due to radionuclides of the elements Kr, Te, I, Xe, and Cs.

72 Dopants did enhance Kr lamp APPI sensitivity when MeOH was used as the mobil

73 ied by a combination of Sp1 and gut-enriched Kr uppel-like factor.

74 The FMOFCu shows an estimated Kr/Xe selectivity of 36 at 0.1 bar and 203 K.

75 stem described here is capable of extracting Kr of >98% purity from 5-125 L STP (standard temperature

76 tter than 1% for N2, O2, CO2, He, Ar, 2% for Kr, 8% for Xe, and 3% for CH4, N2O and Ne.

77 The dual-regulation models developed for Kr also explain some of the properties of the even-skipp

78 l practical potential for separating Xe from Kr.

79 , the expression of two JH-responsive genes, Kr-h1 and Hairy, was dependent on both the ratio of ligh

80 terized by the successive expression of Hb-->Kr-->Pdm-->Cas-->Gh in many, but not all, neuroblasts.

81 fating factors, including Chinmo and the Hb/Kr/Pdm/Cas transcriptional cascade, within this diverse

82 1b function are expected to reduce cardiac I Kr and enhance drug sensitivity, and represent a potenti

83 Cardiac I Kr is a critical repolarizing current in the heart and a

84 subunits, yet our current understanding of I Kr functional properties derives primarily from studies

85 by decreasing and/or increasing the rapid (I Kr) and slow (I Ks) components of delayed rectifying K(+

86 Upon reducing I Kr, the APs without EADs (no-EAD response) showed gradua

87 functional studies have demonstrated that I Kr channels are heteromers composed of both hERG 1a and

88 ristics (HERG versus guinea pig and mouse I (Kr)), tissue (oocytes versus myocytes), or specific drug

89 K-499 are potent and specific blockers of I (Kr) in cardiac myocytes.

90 I(Kr) block with d-sotalol (LQT2) and augmentation of late

91 147 amino acids (HERG(Delta147)) abolished I(Kr), whereas a larger, 159-amino acid deletion (HERG(Del

92 In contrast, an I(Kr) chemical activator of primary effects in slowing cha

93 els of LQT1 and LQT2, which lack I(Ks) and I(Kr) (slow and fast components of delayed rectifying K(+)

94 drugs of the potassium currents I(Ks) and I(Kr) and the sodium current I(Na) give rise to several ty

95 In rats, ERG1 protein (and I(Kr)) expression is higher in atria than ventricles, wher

96 These two potassium currents, I(Ks) and I(Kr), provide the principal repolarizing currents in card

97 zing potassium currents known as I(Ks) and I(Kr).

98 itro increases in outward currents such as I(Kr) or I(Kl) when extracellular potassium concentration

99 Baseline I(Kr) was negligible at CLs of 1000 to 320 ms, but increas

100 tone, d-sotalol (100 micromol/L) to block I(Kr) (LQT2 model), and ATX-II (20 nmol/L) to augment late

101 In this model, drugs that block I(Kr) but not I(Ks) prolong repolarization in a way that s

102 Although many commonly used drugs block I(Kr), in certain individuals, this action evokes a parado

103 currents investigated (I(Na)(+)/I(CaL)(+)/I(Kr)(+)/I(NCX)(+)/I(f)(+)/I(to)(+)/I(K1)(-)/I(Ks)(-)), we

104 es in the generation of functional cardiac I(Kr) channels.

105 gely indistinguishable from native cardiac I(Kr), a role for minK in this current is suggested by the

106 ating delayed rectifier potassium channel (I(Kr)) which plays an important role in cardiac repolariza

107 a subunit of the cardiac potassium channel I(Kr) that has been associated previously with inherited L

108 xpression of the cardiac potassium channel I(Kr)/human ether a-go-go-related gene (hERG).

109 HERG increased the rapid component, I(Kr), of the delayed rectifier current, thereby accelerat

110 Consequently, I(Kr) was expected to contribute more to AP repolarization

111 y activating delayed rectifier K+ current (I(Kr)) at physiological temperatures.

112 f the delayed rectifier potassium current (I(Kr)) by verapamil is frequency-dependent.

113 pinavir of repolarising potassium current (I(Kr)) channels in neonatal mouse cardiac myocytes.

114 ions, the rapid delayed rectifier current (I(Kr)) density was increased.

115 hus rapid delayed rectifying K(+) current (I(Kr)) density, served to generate APD dispersion, high-fr

116 The rapidly delayed rectifier current (I(Kr)) has been described in ventricular myocytes isolated

117 mponent of delayed rectifier K(+) current (I(Kr)) in rabbit ventricular myocytes were similar to thos

118 activating delayed rectifier K(+) current (I(Kr)).

119 he delayed rectifier repolarizing current (I(Kr)).

120 f the delayed rectifier potassium current (I(Kr)).

121 t of the cardiac delayed rectifier current I(Kr) is encoded by the human ether a-go-go related gene (

122 e rapid, outwardly rectifying K(+) current I(Kr) that is critical for repolarization of the cardiac a

123 g the rapid delayed rectifier K(+) current I(Kr), account for a significant proportion of congenital

124 to a cardiac delayed rectifier K+ current I(Kr), but had dissimilar pharmacological properties.

125 underlies the cardiac repolarizing current I(Kr), is the unintended target for many pharmaceutical ag

126 ect block of the cardiac potassium current I(Kr)/hERG, which is crucial for terminal repolarization i

127 ect block of the cardiac potassium current I(Kr)/hERG.

128 -related gene (hERG)-encoded K(+) current, I(Kr) is essential for cardiac repolarization but is also

129 otein underlying the cardiac K(+) current, I(Kr), cause chromosome 7-linked long QT syndrome (LQT2).

130 rapid delayed rectifier potassium current, I(Kr), which flows through the human ether-a-go-go-related

131 t or slow delayed rectifier K(+) currents (I(Kr)/I(Ks)).

132 ition of delayed K(+) rectifying currents, I(Kr) (E4031; 0.5 micromol/L, n=3), shifted FFT spectra fr

133 I(Kr) suppressed alternans and decreasing I(Kr) increased alternans.

134 his current is suggested by the diminished I(Kr) in an atrial tumour line subjected to minK antisense

135 ized that a small molecule that diminishes I(Kr) block by a known hERG antagonist would constitute a

136 molecular pathway whereby KCR1 diminishes I(Kr) drug response.

137 Although the protein level of ERG (I(Kr) pore-forming, alpha, subunit) was not altered, the K

138 To test this idea experimentally, I(Kr) was measured as the E-4031-sensitive current in isol

139 .7 nM), a value close to that reported for I(Kr) in native cardiac myocytes.

140 g a unique specific chemical activator for I(Kr) that has a primary effect of causing a right shift o

141 ort the conclusion that HERG subunits form I(Kr) channels in cardiac myocytes.

142 play roles in the generation of functional I(Kr) channels.

143 We show that complete loss of functional I(Kr) in embryonic hearts leads to ventricular cell membra

144 identified in an LQT2 kindred did generate I(Kr), albeit with reduced amplitude compared with the wil

145 olayers infected with GFP (control), hERG (I(Kr)), or dominant negative mutant hERG G628S.

146 HERG/I(Kr) channels are blocked selectively by class III antiar

147 s: a well characterized inhibition of hERG/I(Kr) trafficking and a poorly understood increase of card

148 mulations, a fivefold regional increase in I(Kr) abbreviated the APD and hyperpolarized the resting p

149 er of rotation was significantly faster in I(Kr)-infected monolayers than controls.

150 sudden cardiac death due to a reduction in I(Kr)-mediated repolarization.

151 ed on these data indicated that increasing I(Kr) suppressed alternans and decreasing I(Kr) increased

152 Ranolazine inhibited I(Kr) (IC50=11.5 micromol/L), late I(Na), late I(Ca), peak

153 (3) Alterations of I(Ks), I(Kr), and I(Na) (fast sodium current) in long-QT syndrome

154 The EC50 for the methanesulfonanilide I(Kr) blocker dofetilide was 12 +/- 2 nM.

155 Modifying I(Kr) may be a promising approach to suppressing alternans

156 Native I(Kr) channels are composed of two alpha subunits, hERG 1a

157 s using siRNA led to an increase in native I(Kr).

158 e that HERG encodes a major constituent of I(Kr) and suggest that at physiological temperatures HERG

159 A computer model of I(Kr) based on these data indicated that increasing I(Kr)

160 upport of the latter result, inhibition of I(Kr) by E-4031 increased the maximal amplitude of alterna

161 tive evaluation suggests that elevation of I(Kr) by reducing voltage sensitivity of inactivation, not

162 ions or unintended pharmaceutical block of I(Kr) can lead to life-threatening arrhythmias.

163 is unknown whether the time dependency of I(Kr) enables it to control APD, conduction velocity (CV),

164 s studies that showed significant block of I(Kr) in isolated myocytes by similar drugs, even in the a

165 nuates the RRD and proarrhythmic effect of I(Kr) inhibition.

166 enous late I(Na) contributes to the RRD of I(Kr) inhibitor-induced increases in APD and BVR and to br

167 The magnitude of I(Kr) is paradoxically increased by an increase in extrace

168 al mapping, we investigated the effects of I(Kr) upregulation on reentry frequency, APD, CV, and WL i

169 (HERG) encodes the pore-forming subunit of I(Kr), a cardiac K(+) channel.

170 Inadvertent block of I(Kr), known as the acquired long QT syndrome (aLQTS), is

171 HERG is the molecular basis of I(Kr), which plays a critical role in repolarization.

172 increasing [K+]o decreases the potency of I(Kr)-blocking drugs in vitro.

173 everse rate dependence (RRD) of actions of I(Kr)-blocking drugs to increase the action potential dura

174 indicating a heterogeneous distribution of I(Kr).

175 at rapid rates and a predominant effect on I(Kr) at slow rates.

176 and Endo but had no significant effect on I(Kr) in either Epi or Endo.

177 estigated the effects of reducing I(Ks) or I(Kr) or enhancing late I(Na) (to simulate the 3 forms of

178 Peak I(Kr) increased initially as CL was shortened from 1000 to

179 During APD alternans, peak I(Kr) was larger for the short than for the long action po

180 During an action potential, I(Kr) increased gradually to a maximum at -55 to -60 mV.

181 Slowly (I(Ks)) and rapidly (I(Kr)) activating delayed rectifier K(+) currents were rec

182 nd KvLQT1+minK that encode native rapidly (I(Kr)) and slowly (I(Ks)) activating delayed rectifier K(+

183 rapid component of delayed rectification, I(Kr), in cardiac myocytes.

184 rapid component of the delayed rectifier (I(Kr)) may contribute importantly to action potential dyna

185 subunit for the cardiac delayed rectifier I(Kr), these results suggest that this peptide may have th

186 eir effect on the rapid-delayed rectifier, I(Kr).

187 uce loss-of-function phenotypes and reduce I(Kr) currents either by the heteromeric assembly of non-

188 l or acquired LQTS is secondary to reduced I(Kr) or I(Ks) but less so when it is due to augmented lat

189 observed after chronic amiodarone (reduced I(Kr), I(Ks), late I(Na), and I(Ca)).

190 atory protein KCR1, which markedly reduces I(Kr) drug sensitivity, protects HERG through glucosyltran

191 that this heteromultimerization regulates I(Kr) activity.

192 tated to LGL (HERG(Delta147-LGL)) restored I(Kr).

193 e increase in TDR induced by the selective I(Kr) blocker d-sotalol.

194 In all dogs, the selective I(Kr) blocker dofetilide was used to examine susceptibilit

195 s of repolarization delay as the selective I(Kr) blocker dofetilide, the combined ion-channel blocker

196 A selective I(Kr) blocker, E-4031 (1 microm), completely blocked mI(Kr

197 ssess the presence and behaviour of single I(Kr) channels in adult mouse cardiomyocytes (mI(Kr)).

198 This was confirmed by specific I(Kr) block with dofetilide, which prolonged AP significan

199 Conversely, HERG-G628S suppressed I(Kr) without significantly delaying repolarization.

200 An important observation is that I(Kr) block or late I(Na) acts to increase APD differences

201 These results indicate that I(Kr) contributes importantly to rate-related alterations

202 The I(Kr) blocker dofetilide prolonged APD in female and ORCH

203 The I(Kr) blocker E4031 (0.5 microM) together with 50 % reduct

204 riants showed decreased sensitivity to the I(Kr) inhibitor dofetilide, these changes could not be cor

205 2-G628S, a dominant negative mutant of the I(Kr) potassium channel alpha-subunit (G628S animals).

206 Reentry frequency was higher in the I(Kr)-infected monolayers (21.12 +/- 0.8 Hz; n=43 versus 9

207 APD(80) in the I(Kr)-infected monolayers was shorter (>50%) than control

208 The I(Kr)-specific blockers, E-4031 and dofetilide, do not inh

209 sed sensitivity to QT prolongation by this I(Kr)-specific blocker.

210 1+/-0.1 versus 0.43+/-0.07 pA/pF), whereas I(Kr) density was similar between Epi and Endo (0.31+/-0.0

211 However, whether I(Kr) is present in the adult mouse heart remains controve

212 tassium channels encoded by HERG underlie I:(Kr), a sensitive target for most class III antiarrhythmi

213 idly activating cardiac delayed rectifier (I[Kr]).

214 m oxyfuel plants may be strongly enriched in Kr and Xe which are potentially valuable subsurface trac

215 Methoprene induced Kr-h1 and suppressed E93 and induced formation of the su

216 aviolet second-harmonic focused tightly into Kr gas.

217 defects after irradiation using heavy ions (Kr(+), 400 keV) is inversely proportional to the grain s

218 sitized isogenic D. melanogaster strain, iso-Kr(If-1), we confirm this finding and present evidence s

219 in the presence of ADP would follow kobsd=Kf+Kr+9.2 x 10(2) s-1.

220 l), the zebrafish ortholog of mafB/Kreisler (Kr), encodes a bZip transcription factor that is require

221 Kruppel (Kr) and snail (sna), two zinc finger repressors, are ess

222 In neuroblast 7-1 (NB7-1), Kruppel (Kr) specifies the third-born U3 motoneuron and Kr misexp

223 ing development but does not effect Kruppel (Kr) activation.

224 r spatial localization of gap genes Kruppel (Kr) and giant (gt) and the pair-rule gene even-skipped (

225 f three target genes, the gap genes Kruppel (Kr) and hunchback (hb), and the pair-rule gene even-skip

226 rget genes, including the gap genes Kruppel (Kr), knirps (kni), and giant (gt), and the homeotic gene

227 anscription factors Hunchback (Hb), Kruppel (Kr), Pdm1/Pdm2 (Pdm) and Castor (Cas).

228 icient for establishing the initial Kruppel (Kr) expression pattern in central regions of the precell

229 Using Kruppel (Kr) and pannier (pnr) homologues of Megaselia as markers

230 Krypton (Kr) and xenon (Xe) adsorption on two partially fluorinat

231 separation of parts-per-million (ppm) level Kr from chemically airlike bulk gas.

232 of parts-per-million by volume (ppmv) level Kr from up to a few liters of bulk gas can be achieved b

233 ted with the clay content (relation to log10(Kr, linear), r2=0.40, n=19).

234 ity of the investigated soils (group 1, mean Kr, linear=3.7 L kg(-1), n=19), and was correlated with

235 a high retention of AgNM-300k (group 2, mean Kr, linear=1048 L kg(-1), n=6) either had a low (<5.1) o

236 TEM) and consecutive ion-irradiations: 1 MeV Kr(2+) (simulating alpha-recoil damage), followed by 400

237 Upon repolarization, ensemble-averaged mI(Kr) showed slow deactivation with a biexponential time c

238 er, E-4031 (1 microm), completely blocked mI(Kr) channel activity.

239 ) channels in adult mouse cardiomyocytes (mI(Kr)).

240 Of 314 patches, 158 (50.1%) demonstrated mI(Kr) currents as compared with 131 (42.3%) for the I(K1)

241 nnels with properties similar to those of mI(Kr), except for the more-negative activation of the HERG

242 Despite the abundant expression of mI(Kr), single-channel events were rarely observed during a

243 s of divalent cations prevent significant mI(Kr) opening under physiological conditions.

244 Single mI(Kr) channel activity was rarely observed at potentials p

245 ion potential parameters, confirming that mI(Kr) plays at best a minor role in repolarization of adul

246 ss of the colliding gas species (He, Ar, Ne, Kr, Xe, CH4, and N2).

247 rium), the accuracy is 0.7% or better for Ne/Kr, Ne/Ar, and Ar/Kr, and 2.5% or better for Ne/Xe, Ar/X

248 for four distinct CUO(Ar)(4-n)(Ng)(n) (Ng = Kr, Xe, n = 1, 2, 3, 4) complexes for each Ng.

249 Notably, Kr-h1 physically and genetically interacts with dFOXO in

250 PRC loss of function extends the ability of Kr to induce U3 fates and PRC gain of function causes pr

251 on increases during the N5 in the absence of Kr-h1 and promotes the development of adult structures.

252 Our models predict activation of Kr by Cad and clarify several other regulatory interacti

253 YC heterodimer mediates JH III activation of Kr-h1 and Hairy genes in the context of light-dependent

254 The anterior border of Kr, which lies 4-5 nucleus diameters posterior to nuclei

255 presses metamorphosis, and that depletion of Kr-h1 expression in Dicer-1 knockdown individuals rescue

256 miRNA depletion is due to a deregulation of Kr-h1 expression and that this deregulation is derived f

257 er, JH III was not effective in induction of Kr-h1 and Hairy gene expression in vitro in fat bodies o

258 Knockdown of Kr-h1 in N4 resulted in a precocious development of adul

259 However, low levels of Kr-h1 mRNA were detected in the fifth and last nymphal s

260 Down-regulation of Kr-h1 expression has been previously associated with ins

261 PR differentiation, transient repression of Kr-h1 represents a key step regulating neuronal maturati

262 ial mechanism, is required for repression of Kr.

263 We have also found that the 3'UTR of Kr-h1 mRNA contains a functional binding site for miR-2

264 ressurized at varying conditions under Xe or Kr gas, and X-ray data for six crystals, we identify the

265 A special case is the control of miR-2 over Kr-h1 transcripts, which determines adult morphogenesis

266 ed SBMOF-2) that is selective toward Xe over Kr under ambient conditions, with a Xe/Kr selectivity of

267 The high-precision Kr and Xe isotope data together suggest that Earth's int

268 Here, we report the discovery of primordial Kr in samples derived from Earth's mantle and show it to

269 s (<10(-12)) provided that 50 microL of pure Kr is available.

270 the data indicate that miR-2 miRNAs scavenge Kr-h1 transcripts when the transition from nymph to adul

271 Specifically, SAPO-34 membranes can separate Kr/Xe mixtures with Kr permeances as high as 1.2 x 10 (-

272 lite SAPO-34 membranes effectively separated Kr/Xe gas mixtures at industrially relevant compositions

273 In addition, SAPO-34 membranes separated Kr/Xe mixtures with Kr permeances as high as 1.2 x 10 (-

274 Here we show, by using in situ Kr ion irradiation in a transmission electron microscope

275 discovered during room temperature, in situ Kr ion irradiation of epitaxial nanotwinned Ag with an a

276 Here by using in situ Kr ion irradiation technique in a transmission electron

277 We found that Kr-h1 mutants show delayed larval development and altere

278 These studies indicate that Kr and sna function as short-range repressors, which can

279 Cas play no detectable role, indicating that Kr either acts outside of the cascade identified in the

280 These experiments showed that Kr broke through the column first, followed by Xe, which

281 ulk gas can be achieved by concentrating the Kr under the chromatographic tails of major components.

282 The subsequent refinement of the Kr pattern depends on the combination of Hb and the Gian

283 However, JH does not work through Kr-h1 but may work through transcription factors not yet

284 an inversion in sorption selectivity toward Kr at temperatures below 0 degrees C while FMOFZn does n

285 is present, and similarly for complexes with Kr and Ar, with single occupancy relatively more prevale

286 o a transcriptional repressor by fusion with Kr uppel-associated box (KRAB), ERD, or SID repressor do

287 os in the eggs laid by females injected with Kr-h1 double-stranded RNA.

288 of adult structures through interaction with Kr-h1 and E93 was also studied by the topical applicatio

289 4 membranes can separate Kr/Xe mixtures with Kr permeances as high as 1.2 x 10 (-7) mol/m(2) s Pa and

290 O-34 membranes separated Kr/Xe mixtures with Kr permeances as high as 1.2 x 10 (-7) mol/m(2) s Pa and

291 gle occupancy relatively more prevalent with Kr and Ar.

292 acidity of Hg(OTeF5)2 toward NgF2 (Ng = Xe, Kr) was investigated in SO2ClF solvent and shown to form

293 o calculate the binding free energies of Xe, Kr and Ar relative to a standard state at a pressure of

294 over Kr under ambient conditions, with a Xe/Kr selectivity of about 10 and a Xe capacity of 27.07 wt

295 pore spaces are predicted to be efficient Xe/Kr solid-state adsorbents, but no experimental insights

296 The demand for Xe/Kr separation continues to grow due to the industrial si

297 chmark selectivity for Xe separation from Xe/Kr mixtures.

298 ation of similarly sized molecules (e.g., Xe/Kr mixtures).

299 enon adsorption capacity and a remarkable Xe/Kr selectivity under conditions pertinent to nuclear fue

300 The Xe/Kr separation in SBMOF-2 was investigated with experimen