ライフサイエンスコーパス: MIT

1 MIT contains two duplicated 6- or 7-amino acid motifs wi

2 MIT differed among treatment groups (P=.009), showing an

3 MIT has only three charged amino acids within predicted

4 MIT helices alpha2 and alpha3 recognize a (D/E)xxLxxRLxx

5 MIT-MIM2 interactions appear to be common throughout the

6 xR198'L199'xxL202'R203', identical to type 1 MIT-interacting motif (MIM1) (D/E)xxLxxRLxxL(K/R) of CHM

7 ESCRT-III proteins) through canonical type 1 MIT-interacting motif (MIM1) interactions.

8 : standard care only, 192; prayer only, 182; MIT therapy only, 185; and both prayer and MIT therapy,

9 e pyrochlore Cd2Os2O7 nonetheless exhibits a MIT entwined with magnetic order phenomenologically simi

10 nding region of Vta1 unexpectedly revealed a MIT-like region.

11 nic and magnetic phases are separated across MIT which appears compelling for bulk systems has been e

12 The presence of an MIT and the accompanying atypical electronic characteris

13 ing edge of migrating cells and show that an MIT complex drives these protrusions.

14 All code is released under an MIT licence.

15 The library is available under an MIT license and can be downloaded from http://software.s

16 3 and Javascript, and is maintained under an MIT license.

17 SI (www.sbsi.ed.ac.uk) plug-in, all under an MIT open-source license.

18 he tensile strained film, which undergoes an MIT, but is absent in the compressively strained film.

19 ere differentially expressed between ATH and MIT, including 443 that were up-regulated and 373 that w

20 s or no off-site prayer (double-blinded) and MIT therapy or none (unmasked).

21 igher dosages, the effects of ethonafide and MIT on EAE were identical, whereas in lower dosages, MIT

22 ng data from 68 MOOCs offered by Harvard and MIT between 2012 and 2014, we found that course particip

23 atform at the Broad Institute of Harvard and MIT.

24 unction, which was prevented by both HIT and MIT.

25 l gradient across the parasite membrane, and MIT is a prototype for understanding the function of an

26 support a model wherein a network of MIT and MIT-like domain interactions with ESCRT-III subunits con

27 ; MIT therapy only, 185; and both prayer and MIT therapy, 189.

28 H. bilis, H. mastomyrinus, H. rodentium, and MIT 96-1001 was also encountered, as were mice infected

29 shed that Sp1 is a critical target of TA and MIT in human pancreatic cancer therapy, rationalizing cl

30 bacter canis, Helicobacter winghamensis, and MIT 99-5504).

31 on the oocyte surface at a similar level as MIT wild type, confirming that these mutations affect tr

32 prayer and 377 no prayer; 374 were assigned MIT therapy and 374 no MIT therapy.

33 ade in facilitating our research programs at MIT and later at Caltech.

34 Then, in 1964, a graduate student at MIT discovered the power of sodium dodecyl sulfate (SDS)

35 There was a significant correlation between MIT and II in those who had acute rejection in the late

36 hway partners, with CHMP1-3 proteins binding MIT domain-containing proteins, such as VPS4 and Vta1/LI

37 on revealed that structural features in both MIT and MIM contribute to determine the specific binding

38 uctural transition that accompanies the bulk MIT.

39 Active transport by MIT is driven by the proton electrochemical gradient acr

40 1 complex shows that Vfa1 adopts a canonical MIT-interacting motif 2 structure that has been observed

41 Vps4 and Vta1 both contain MIT domains, which bind to "MIT-interacting motifs" (MIM

42 recipients were divided into DA group (DA+; MIT>/=0.5 mm, n=23) or non-DA group (DA-; MIT<0.5 mm, n=

43 +; MIT>/=0.5 mm, n=23) or non-DA group (DA-; MIT<0.5 mm, n=15).

44 that requires both their previously defined MIT interacting motifs and approximately 50 amino acids

45 that the IST1 terminus contains two distinct MIT interacting motifs (MIM1 and MIM2) that wrap around

46 AE were identical, whereas in lower dosages, MIT seemed more effective.

47 lating domains across the temperature-driven MIT in NdNiO3 epitaxial thin films.

48 t makes only limited contacts with the first MIT module.

49 Tested upon a total of 107049 beats from MIT-BIH arrhythmia database, our method has achieved ave

50 In particular, we show that two further MIT domain-containing proteins (AMSH/STAMBP and LOC12953

51 helical bundles, which interact with helical MIT-interacting motifs in ESCRT-III subunits.

52 were CMV-positive had a significantly higher MIT compared with those in the late group with negative

53 MIT), and the Massachusetts General Hospital/MIT Morris Udall Center of Excellence in Parkinson Disea

54 B(1)), Asp(300)(A(2)), and Glu(429)(B(2)) in MIT, are highly conserved with 96, 78, and 96% amino aci

55 hnology advances, additional developments in MIT are likely.

56 we explore the nature of a disorder induced MIT in functionalized graphene, a model 2D system.

57 ults of a project at the Whitehead Institute/MIT Center for Genome Research to construct such a physi

58 he STSs published by the Whitehead Institute/MIT Genome Center, we have identified 47 new DNA sequenc

59 the pRML vector from the Whitehead Institute/MIT-820 mouse YAC library and from BACs in pBeloBAC11.

60 ina MiSeq sequencing, for H. saguini isolate MIT 97-6194-5, consisting of approximately 2.9 Mb with a

61 ed: Vps2 can directly stimulate Vps4 via its MIT domain, whereas Vps60 stimulates via Vta1.

62 In contrast, the second LIP5 MIT module binds with unusually high affinity to a novel

63 aps almost completely around the second LIP5 MIT module but makes only limited contacts with the firs

64 trafficking (MIT) module of the tandem LIP5 MIT domain binds CHMP1B (and other ESCRT-III proteins) t

65 Mean MIT and mean II were significantly greater in the late g

66 substrates are initially recruited by an MIM-MIT interaction that activates the Vps4 central pore to

67 st1 interacts with the Did2 C-terminal MIM1 (MIT-interacting motif 1) via a novel MIM-binding structu

68 Mithramycin (MIT) and tolfenamic acid (TA) inhibit the activity of th

69 hemotherapeutic agents such as mitoxantrone (MIT) in multiple sclerosis (MS) patients justify the sea

70 ubule-interacting and trafficking molecules (MIT) at its N-terminus, and most proteins with MIT domai

71 ubule-interacting and trafficking molecules (MIT) domains comprising asymmetric three-helical bundles

72 15.0%) for a 1 degrees C increase in monthly MIT at <15, 15-64, and >/=65 years of age, respectively,

73 ties in electron-lattice dynamics and a Mott MIT where strong electron-electron correlations drive ch

74 st, at the surface, an unusual inherent Mott MIT is observed at 130 kelvin, also on cooling but witho

75 Ca(1.9)Sr(0.1)RuO4, such a first-order Mott MIT occurs in the bulk at a temperature of 154 kelvin on

76 As new MIT domain proteins are rapidly being identified, these

77 er; 374 were assigned MIT therapy and 374 no MIT therapy.

78 nths was lower with MIT therapy than with no MIT therapy (hazard ratio 0.35 (95% CI 0.15-0.82, p=0.01

79 Neither masked prayer nor MIT therapy significantly improved clinical outcome afte

80 sp19 may be important for proton coupling of MIT.

81 red to be critical for transport function of MIT, with a reduction of inositol transport to about 2%

82 (429) are critical for transport function of MIT.

83 se data support a model wherein a network of MIT and MIT-like domain interactions with ESCRT-III subu

84 of such phase coexistence in the vicinity of MIT leads to first-order transition in these manganites.

85 lifestyle or 8-10 weeks of isocaloric HIT or MIT.

86 d the structural basis that governs pairwise MIT-MIM interaction.

87 h two alternative starting points: a Peierls MIT driven by instabilities in electron-lattice dynamics

88 is open-source and free under the permissive MIT License (opensource.org/licenses/mit-license.php).

89 characterized ESCRT-III interacting protein, MIT-domain containing protein 1 (MITD1).

90 the Open Source Initiative (OSI) recognized MIT license.

91 tion to the uncharged amides greatly reduced MIT transport function to 23% (E187Q), 1.4% (D300N), and

92 H. saguini MIT 97-6194-5 induced significant levels of interleukin-

93 To simulate MIT in NP films, we developed a hierarchical Kinetic Mon

94 Available under the open source MIT license at http://sourceforge.net/projects/seqpig/

95 It is released under an Open source MIT license.

96 g/software, distributed under an open source MIT license.

97 annotare/ under the terms of the open-source MIT License.

98 The software is open source (MIT license) and executable with Python 2.7 or iPython n

99 Both tools are open source (MIT license) and freely available for use online through

100 on Package Index via pip; it is open source (MIT license).

101 Helicobacter hepaticus, and Helicobacter sp. MIT 94-022.

102 low-light-adapted strain Prochlorococcus sp. MIT 9313 has one iron-stress-induced pcb gene encoding a

103 based amino acid substitution in the spartin MIT domain (F24D) blocks the spartin-Ist1 interaction.

104 ance assays, we demonstrate that the spartin MIT domain binds with micromolar affinity to the endosom

105 infected with novel Helicobacter sp. strain MIT 96-1001.

106 oposed name Helicobacter aurati (type strain MIT 97-5075c) has been isolated from the inflamed stomac

107 Helicobacter cetorum, sp. nov. (type strain MIT 99-5656; GenBank accession number AF 292378), was cu

108 flexispira taxon 3, Helicobacter sp. strains MIT 94-022 and MZ 640285, and Helicobacter suis, respect

109 onovani has a myo-inositol/proton symporter (MIT) that is a member of a large sugar transporter super

110 has an active myo-inositol/proton symporter (MIT), which is driven by a proton gradient across the pa

111 isruption of the MRL protein-integrin-talin (MIT) complex markedly impairs cell protrusion.

112 Our studies thus reveal how the tandem MIT domain of LIP5 binds different types of ESCRT-III pr

113 ates and binds ESCRT-III subunits via tandem MIT domains, and thereby, delays abscission in response

114 The use of minimally invasive techniques (MIT) in patient care is well documented in ancient histo

115 t the Massachusetts Institute of Technology (MIT) Research Reactor.

116 arch, Massachusetts Institute of Technology (MIT), and the Massachusetts General Hospital/MIT Morris

117 l influenza and monthly minimum temperature (MIT), monthly vapor pressure, school calendar pattern, a

118 f VPS4, LIP5, and Spartin via its C-terminal MIT-interacting motif (MIM).

119 (MIT) domains initially bind the C-terminal MIT-interacting motifs (MIMs) of ESCRT-III subunits, but

120 ain architecture that features an N-terminal MIT (microtubule interacting and trafficking) domain fol

121 n part by binding of Vps4 via its N-terminal MIT (microtubule interacting and trafficking) domain to

122 Deleting the N-terminal MIT domain and adjacent linker from VPS4A increased both

123 stinct elements: a poorly ordered N-terminal MIT domain that binds ESCRT-III substrates, large (mixed

124 The N-terminal MIT domains of the upper ring localize on the symmetry a

125 sted a bioassay, the mouse infectivity test (MIT), in this model.

126 oscopy of oocyte cryosections confirmed that MIT mutants were expressed on the oocyte surface in simi

127 icroscopy of oocyte cryosections showed that MIT mutants were expressed on the oocyte surface at a si

128 The MIT domain forms an asymmetric three-helix bundle that r

129 The MIT domain of Vps4 binds to the C-terminal 17 residues o

130 e change of the crystal structure across the MIT at finite temperature.

131 reedom with the crystal structure across the MIT in rare-earth nickelates.

132 O3 films with x = 0.33 and 0.375, across the MIT temperature.

133 ation length of these LPCMO films across the MIT.

134 In addition, the MIT motif-containing N-terminal domain, projected by a l

135 SCRT-III subunits with both the pore and the MIT domain simultaneously, which might be essential for

136 "working draft" of the human genome and the MIT shotgun assembly of the mouse genome, we performed a

137 rained NdNiO3 films both above and below the MIT temperature.

138 ngth for two films which increases below the MIT.

139 the 40-amino acid linker region between the MIT and the ATPase domain of Vps4 is not required for pr

140 bunits in yeast, only Vps2 and Did2 bind the MIT (microtubule interacting and transport) domain of Vp

141 IM1 mode, the additional ability to bind the MIT domain of Spartin in the MIM3 mode.

142 MP2A, a protein that normally only binds the MIT domain in the MIM1 mode, the additional ability to b

143 etion of the linker is expected to bring the MIT domains into close proximity to the central pore of

144 c and magnetic energy scales controlling the MIT.

145 bes the thermodynamic forces controlling the MIT.

146 Here we report that the entropy driving the MIT in VO2 is dominated by strongly anharmonic phonons r

147 f metallic and insulating regions during the MIT and the coupling of lattice strain to the local tran

148 ture ramp from heating to cooling during the MIT.

149 appeared, or in immunocompromised hosts, the MIT compared favorably to culture and PCR for infected N

150 Distinct pockets in the MIT domain bind three conserved leucine residues of the

151 into two groups: those with >/=0.5 mm in the MIT in any matched site (group 1) and those with MIT <0.

152 n with published maps revealed a hole in the MIT/Whitehead and CEPH YAC maps that includes the immedi

153 Our data provide new insights into the MIT of heteroepitaxial nickelates and point to a rich, n

154 We propose that this localization of the MIT domain in linker-deleted Vps4 mimics a repositioning

155 r-deleted Vps4 mimics a repositioning of the MIT domain normally caused by binding of Vps4 to ESCRT-I

156 e between the first and third helices of the MIT domain.

157 p around and bind in different groves of the MIT helical bundle.

158 bond length disproportionation model of the MIT in the rare-earth nickelates.

159 ehensively the ESCRT-III interactions of the MIT-domain family member MITD1 and identify strong inter

160 theory provides a better description of the MIT.

161 data in terms of two candidate models of the MIT: (a) as a Quantum Critical Transition, signaled by a

162 bustness of the effect shed new light on the MIT in complex oxides.

163 ection of spirochetes in the CSF by PCR, the MIT, and culture was inversely related to the concomitan

164 We show that the MIT domain binds to a subset of ESCRT-III subunits and t

165 st cancer tumorigenesis and suggest that the MIT gene product functions in the control of the tumorig

166 tion shows that it is closely related to the MIT domain of Vps4.

167 ar complexes revealed that IST1 binds to the MIT domains of VPS4, LIP5, and Spartin using two differe

168 ed an anomalously low gap region next to the MIT.

169 e open-source software distributed under the MIT licence.

170 The software is distributed under the MIT License and is accompanied by example files and data

171 DRAW+SneakPeek is released under the MIT license and is available for academic and nonprofit

172 Cordova is open source under the MIT license and is freely available for download at http

173 Available under the MIT license at http://github.com/princelab/metriculator.

174 he source code is freely available under the MIT license at https://mgymrek.github.io/pybamview.

175 nline web application is available under the MIT license at: http://github.com/brentp/gobe.

176 the full source code are available under the MIT license at: https://github.com/brentp/methylcode.

177 The package is freely available under the MIT license from CRAN.

178 age is open source and distributed under the MIT license via GitHub along with examples, documentatio

179 and SneakPeek are freely available under the MIT license, and are available as Amazon machine images

180 ps://rubygems.org/gems/bio-svgenes under the MIT license, and open source code is available at https:

181 able at github.com/mnori/foldatlas under the MIT license.

182 om/danmaclean/bioruby-svgenes also under the MIT License.

183 The source code is released under the MIT license.

184 .github.com/hemberg-lab/MPRAnator/ under the MIT license.

185 http://github.com/whitehead/plaac under the MIT license.

186 .github.com/ElofssonLab/pcons-fold under the MIT license.

187 mplemented in C++ and is available under the MIT License.

188 The source code is distributed under the MIT Open Source license agreement and is available for d

189 BioBIKE is distributed under the MIT Open Source license.

190 munities, all software is released under the MIT open source license.

191 hase that is observed in films for which the MIT is absent.

192 tal structure of LIP5NTD in complex with the MIT (microtubule-interacting and transport)-interacting

193 n PROS that mediate the interaction with the MIT domain of SKD1.

194 re of meiotic clade AAA ATPases may be their MIT domain, which is a module that is found in a wide va

195 that bind and recruit VPS4 ATPases via their MIT domains.

196 defined by ICUS as a mean intimal thickness (MIT) > or =0.3 mm in any coronary artery segment.

197 formed, including maximal intimal thickness (MIT) and intimal index (II).

198 On the basis of maximum intimal thickness (MIT) at BL, recipients were divided into DA group (DA+;

199 The change in maximal intimal thickness (MIT) from baseline to one year was recorded for several

200 croscopically for maximal intimal thickness (MIT), percentage of luminal circumference involved (PLCI

201 ular interactions between IST1 and the three MIT domain-containing proteins to understand the structu

202 ues (ATH) and macroscopically intact tissue (MIT) sampled from 32 patients were compared and an integ

203 romosome 17, approximately 3.77 cR distal to MIT framework marker UTR-9641.

204 on the oocyte surface in similar quantity to MIT wild type.

205 With reference to MIT, we examined the effect of ethonafide on experimenta

206 ast, showed an inhibition profile similar to MIT wild type.

207 hracene-based antineoplastic drug similar to MIT.

208 ta1 both contain MIT domains, which bind to "MIT-interacting motifs" (MIMs) of ESCRT-III proteins.

209 essory prayer and music, imagery, and touch (MIT) therapy.

210 h a microtubule-interacting and trafficking (MIT) domain at the N terminus and a unique, unanticipate

211 the microtubule-interacting and trafficking (MIT) domain of Vps4.

212 its microtubule interaction and trafficking (MIT) domain, NRBF2 binds Atg14L directly and enhances At

213 ps4 microtubule-interacting and trafficking (MIT) domains initially bind the C-terminal MIT-interacti

214 the microtubule interacting and trafficking (MIT) domains of VPS4, LIP5, and Spartin via its C-termin

215 rst microtubule-interacting and trafficking (MIT) module of the tandem LIP5 MIT domain binds CHMP1B (

216 is superior to moderate-intensity training (MIT) in counteracting obesity-induced impairment of left

217 O3 exhibits a metal-to-insulator transition (MIT) as the temperature is lowered that is also seen in

218 ty change at the metal-insulator transition (MIT) has been extensively considered for the near-future

219 e existence of a metal-insulator transition (MIT) in highly disordered RuO2 nanoskins with carrier co

220 (LMR) and the metal-to-insulator transition (MIT) induced by magnetic field in heavily-doped Nb:STO (

221 ts a first-order metal-insulator transition (MIT) near room temperature, where conductivity is suppre

222 ng a first-order metal-insulator transition (MIT) offers unique opportunities to uncover their drivin

223 The metal-insulator transition (MIT) remains among the most thoroughly studied phenomena

224 gnetoresistance, metal-insulator transition (MIT) that may result from coexistence of ferromagnetic,

225 lic state is the metal-insulator transition (MIT).

226 films across the metal-insulator transition (MIT).

227 undergo a metal-insulator phase transition (MIT), the origin of which is still under debate.

228 ions, which are metal-insulator transitions (MITs) driven by electron-electron interactions, are usua

229 and manifested metal-insulator transitions (MITs).

230 VPS4A microtubule interacting and transport (MIT) domain and demonstrate that the VPS4A MIT domain bi

231 t the microtubule interacting and transport (MIT) domains of human VPS4A and VPS4B bind conserved seq

232 their microtubule interacting and transport (MIT) N-terminal domains and Vta1p co-factors.

233 otubule interacting and organelle transport (MIT) domain.

234 source code and binaries are available under MIT license at http://noble.gs.washington.edu/proj/qvali

235 l are open-source and freely available under MIT License from http://prody.csb.pitt.edu/.

236 The software is currently distributed under MIT artistic license and freely available at http://bioi

237 It is implemented in C ++, distributed under MIT license and supported on Linux, OS X and Windows (wi

238 he source and executables are released under MIT style license at http://obi-warp.sourceforge.net/.

239 role in 5d(5) iridates (Ir(4+)), undergoing MITs both concurrent (pyrochlores) and separated (perovs

240 The performance evaluation using MIT-BIH arrhythmia database shows that our approach comp

241 ng and linkage analysis of hybrid mice using MIT microsatellite marker sequences localized the seizur

242 that recruitment to the protein lattice via MIT domains also relieves autoinhibition and primes the

243 Mutations that block VPS4 MIT-MIM2 interactions inhibit VPS4 recruitment, lysosoma

244 We now report that VPS4 MIT domains also bind a second, "MIM2" motif found in a

245 ratricopeptide-like repeat (TPR) of the VPS4 MIT domain, but in the opposite orientation to that of a

246 e Vps2 C terminus in a complex with the Vps4 MIT domain, explaining the basis for selective ESCRT-III

247 The solution structure of the VPS4 MIT-CHMP6 MIM2 complex revealed that MIM2 elements bind

248 Structures of VPS4A MIT-CHMP1A and VPS4B MIT-CHMP2B complexes reveal that th

249 (MIT) domain and demonstrate that the VPS4A MIT domain binds the C-terminal half of the ESCRT-III pr

250 Structures of VPS4A MIT-CHMP1A and VPS4B MIT-CHMP2B complexes reveal that the C-terminal CHMP mot

251 ate engagement is autoinhibited by the Vps4p MIT domain and that this inhibition is relieved by bindi

252 or Type 2 MIM elements, which bind the Vps4p MIT domain through different interfaces.

253 The structures suggest models in which Vps4p MIT and Vta1p domains engage ESCRT-III substrates above

254 .20 mm; SE = 0.03 mm) (both P<.025), whereas MIT in infected/treated versus control rabbits did not d

255 method to the leukemia data of the Whitehead/MIT group that attempts to differentially diagnose two k

256 tromeric and telomeric ends of the Whitehead/MIT recombinational maps.

257 YAC targeting technology (YTT) uses the WIBR/MIT-820 C57BL/6-mapped YAC library derived from the C57B

258 fide has less cardiac toxicity compared with MIT.

259 egalovirus (CMV) status were correlated with MIT and II.

260 Mortality at 6 months was lower with MIT therapy than with no MIT therapy (hazard ratio 0.35

261 he HbA(1c) level was higher in patients with MIT > or =0.3 mm than in those with MIT <0.3 mm (6.4% vs

262 T) at its N-terminus, and most proteins with MIT domains interact with specific ESCRT-III proteins.

263 nts with MIT > or =0.3 mm than in those with MIT <0.3 mm (6.4% vs. 5.7%, p < 0.05).

264 in any matched site (group 1) and those with MIT <0.5 mm (group 2).

265 reatment of pancreatic tumor xenografts with MIT and TA produced dose-dependent antitumor activity, a

266 oteins' extreme C-termini that overlap with "MIT interacting motifs" (MIMs) known to bind to VPS4.