ライフサイエンスコーパス: KI

1 KI hearts exhibited atrial enlargement, papillary muscle

2 KI mice displayed deficits in multiple behaviors, includ

3 KI mice had significantly fewer lineage-Sca1(+)c-Kit(+)

4 KI mice were again innately resistant to doxorubicin-ind

5 experiment: (1) control without N and I, (2) KI application without N, (3) KIO3 application without N

6 duction of nonneutralizing serum IgGs in 2F5 KI mice is T dependent and originates from a subset of s

7 thout N, (3) KIO3 application without N, (4) KI+Ca(NO3)2, (5) KIO3+Ca(NO3)2, (6) KI+(NH4)2SO4 and (7)

8 ortantly, serum IgGs from naive 2F5 and 4E10 KI strains selectively eliminate gp41 and lipid binding,

9 t N, (4) KI+Ca(NO3)2, (5) KIO3+Ca(NO3)2, (6) KI+(NH4)2SO4 and (7) KIO3+(NH4)2SO4.

10 protein expression is decreased by over 80%, KI/KI mice retinae retain comparable 11-cis-retinal leve

11 afforded SAM resulted in the production of a KI-sensitive sensor.

12 Remarkably, a KI mutation of LCK Ser59, previously suggested to be key

13 ively inhibited GLUT5 fructose uptake with a KI of 3.2 +/- 0.4 muM.

14 ptamer selectively inhibited GluA1/2R with a KI of approximately 5 mum, along with GluA1 and GluA2 AM

15 agement, but data on practice patterns after KI discontinuation and optimal sequencing are limited.

16 Au(3+) in the presence of the masking agent KI to minimize Hg(2+) interference; however, RQ-2 select

17 ntolerant patients treated with an alternate KI was not reached vs 7 months for patients with CLL pro

18 due to toxicity can respond to an alternate KI, and that these responses may be durable.

19 were recorded in intact KI-TnC-A8V(+/-) and KI-TnC-A8V(+/+) cardiomyocytes.

20 The global kinetic parameters kinact and KI have been used to characterize MBIs, but they provide

21 mixed type inhibition with KI = 1.4 muM and KI = 5.5 muM, respectively.

22 = 0.5 +/- 0.2 muM, KI = 0.7 +/- 0.3 muM, and KI = 2.9 +/- 0.27 muM, respectively, whereas, analogues

23 n using ethylene bromide, triethylamine, and KI at 80 degrees C.

24 nce of functional HSCs between wild-type and KI mice.

25 doxorubicin-induced cardiomyopathy in WT and KI mice was investigated.

26 d neurons (SCNs) were similar between WT and KI mice.

27 graphy (micro-CT) analysis in homozygous Ank KI/KI mice, a model for CMD, showed that molars can be m

28 Histological analysis of molars in Ank KI/KI mice revealed decreased numbers of TRAP+ osteoclas

29 tosis of mandibles, which distinguishes Ank (KI/KI) mice from the other Ank mouse models.

30 AP-positive cells in the apical ends of Ank (KI/KI) incisors revealed decreased osteoclast numbers an

31 ections in Ank (+/+) mice replicate the Ank (KI/KI) incisor phenotype.

32 ased in APOE4 KI animals compared with APOE3 KI animals.

33 Aged apoE4-KI mice had fewer SWRs than apoE3-KI mice and significantly reduced slow gamma activity du

34 als and was significantly increased in APOE4 KI animals compared with APOE3 KI animals.

35 Genetic reduction of synj1 in ApoE4 KI mouse models restores PIP2 levels and, more important

36 Aged apoE4-KI mice had fewer SWRs than apoE3-KI mice and significan

37 ancing GABA signaling by treating aged apoE4-KI mice with a GABAA receptor potentiator pentobarbital

38 ancing GABA signaling by treating aged apoE4-KI mice with the GABAA receptor potentiator pentobarbita

39 efore MWM abolished the rescue in aged apoE4-KI mice, suggesting the importance of continuously enhan

40 low gamma deficit emerged only in aged apoE4-KI mice.

41 as reduced similarly in young and aged apoE4-KI mice; however, the full SWR-associated slow gamma def

42 We previously reported that female apoE4-KI mice had an age-dependent decline in hilar GABAergic

43 Here we report two functional apoE4-KI phenotypes involving sharp-wave ripples (SWRs), hippo

44 However, treating apoE4-KI mice during middle adulthood (9-11 months of age) wit

45 However, treating apoE4-KI mice during middle adulthood with PB for a short peri

46 its soluble extracellular domain (APPsalpha-KI).

47 fied as the most common clinically available KI effective in overcoming venetoclax resistance.

48 lash stimuli also show no difference between KI/KI and WT mice.

49 Here, we review insights gained from bnAb KI studies regarding the regulation and induction of bnA

50 In this regard, bnAb KI models expressing deduced precursor V(D)J rearrangeme

51 ng of the fluorescence of the organic NPs by KI was investigated.

52 Findings from Chn1KI/KI Epha4KO/KO mice demonstrated that mutant alpha2-chima

53 ort a knockin alpha2-chimaerin mouse (Chn1KI/KI) that models DRS.

54 Whole embryo imaging of Chn1KI/KI mice revealed stalled abducens nerve growth and selec

55 ens nerve wandering distinct from the Chn1KI/KI phenotype.

56 The first cohort (KI) was collected from the Memory Clinic at Karolinska U

57 Consequently, KI mice with dominant negative mutations had much less w

58 In contrast, KI mice were markedly resistant to the dysfunction induc

59 has emerged as an alternative way to create KI mice.

60 Our results establish the Car1(CreER) KI as a valuable mouse model to study colon-specific tum

61 or suppressor gene Apc using the Car1(CreER) KI caused tumor formation in the cecum but did not yield

62 Homozygous MLL4 enzyme-dead KI (Mll4(KI/KI)) mice are embryonic lethal and die aroun

63 ed knock-in of inducible degron tags (Degron-KI) that provides a versatile approach for the functiona

64 The Degron-KI system allows for highly specific, inducible, and all

65 demonstrate the broad utility of the Degron-KI system for the functional characterization of cancer

66 The Degron-KI system was able to faithfully recapitulate the effect

67 sensor sensitivity and its ability to detect KI in artificial saliva, we could conclude that this sen

68 This sensor selectively determined KI compare to different alkali metal iodides: NaI, RbI,

69 scontinuation, that patients who discontinue KI due to toxicity can respond to an alternate KI, and t

70 nib = 143; idelalisib = 35) who discontinued KI therapy.

71 nned fibers increased with mutant gene dose: KI-TnC-A8V(+/+)>KI-TnC-A8V(+/-)>wild-type, whereas KI-Tn

72 nase 2 (ErbB2)-positive breast cancer (ErbB2(KI)), which exhibits aberrant beta-catenin nuclear signa

73 Furthermore, treatment of ErbB2(KI) or human ERBB2-overexpressing tumor cells with a sel

74 In contrast to the ErbB2(KI) basal tumor model, modulation of beta-catenin levels

75 on of both beta-catenin alleles in the ErbB2(KI) model had only a minor impact on tumor onset that fu

76 Overall response rate (ORR) to first KI was 62% (complete response 14%).

77 eceived subsequent salvage therapy following KI discontinuation with an ORR to subsequent KI at 50% a

78 that toxicity was the most common reason for KI discontinuation, that patients who discontinue KI due

79 The most common reasons for KI discontinuation were toxicity (51%), CLL progression

80 erived the following optimum thresholds: for KI 1.05/1.15/1.31/1.49 and for KMI 0.77/0.32/-0.08/-0.3.

81 We found three InDels in four KI mice but not in a control mouse.

82 namics of ventricular myocytes isolated from KI hearts are altered in a manner consistent with impair

83 progression-free survival (PFS) and OS from KI initiation were 10.5 and 29 months, respectively.

84 analysis of synaptic currents recorded from KI mice showed that the glycinergic synaptic transmissio

85 ore, the glycine-evoked current in SCNs from KI was resistant to ethanol and G-protein activation by

86 In this study, we generate KI models expressing H chains from two other HIV-1 Abs,

87 nse that are characteristic of other glycine KI mouse lines with markedly impaired glycine receptor f

88 Mice expressing PI3K-insensitive GSK3 (gsk3(KI)) and wild-type mice (gsk3(WT)) were fed a high-fat d

89 t/PKB/SGK-resistant GSK3alpha/GSK3beta (gsk3(KI)) exhibit enhanced sympathetic nervous activity and p

90 calcium were measured by photometry in gsk3(KI) and gsk3(WT) mice, before and after 1 wk of oral tre

91 phosphate concentrations were lower in gsk3(KI) mice than in gsk3(WT) mice.

92 pose tissue was significantly higher in gsk3(KI) mice than in gsk3(WT) mice.

93 reased serum phosphate concentration in gsk3(KI) mice.

94 Compared with gsk3(WT) mice, gsk3(KI) mice were protected against the development of metab

95 the serum adiponectin concentration of gsk3(KI) mice and abrogated the difference in C/EBPalpha acti

96 eased with mutant gene dose: KI-TnC-A8V(+/+)>KI-TnC-A8V(+/-)>wild-type, whereas KI-TnC-A8V(+/+) relax

97 n, we have generated a hCD1d knock-in (hCD1d-KI) mouse.

98 loped the first humanized mouse model (hCD1d-KI) with human CD1d knocked in.

99 secreted exosomes in both female and male HD KI mouse striatum in which abundant nuclear mHtt aggrega

100 rocytic exosomes into the striatum of HD140Q KI mice reduces the density of mHtt aggregates.

101 as mHtt aggregates in the striatum of HD140Q KI mice.

102 re virulent than the parental virus in hDPP4 KI mice.

103 The hDPP4 KI mouse and the MERSMA provide tools to investigate dis

104 ce containing the A8V mutation (heterozygote=KI-TnC-A8V(+/-); homozygote=KI-TnC-A8V(+/+)) were charac

105 1-cis-RAL in fully dark-adapted heterozygous KI mice were similar to that in WT mice.

106 urons showed that Dyt1 DeltaGAG heterozygous KI mice exhibited normal miniature excitatory post-synap

107 cantly reduced in Dyt1 DeltaGAG heterozygous KI mice.

108 Furthermore, heterozygous KI mice exhibited lower A-wave recovery compared with WT

109 re were significantly slower in heterozygous KI mice compared with WT and RPE65 heterozygous knockout

110 rotein levels were decreased in heterozygous KI mice, their scotopic, maximal, and photopic electrore

111 to a lower affinity for this enzyme (higher KI) and a lower rate of enzyme inactivation (k(inact)).

112 on (heterozygote=KI-TnC-A8V(+/-); homozygote=KI-TnC-A8V(+/+)) were characterized by echocardiography

113 t700Lys patient mutation, used homozygously (KI/KI) or combined with a knockout allele (KO/KI), to st

114 However, KI-PRS preselection DP thymocytes show impaired tyrosine

115 nome editing to generate clonal HEK293 (Hrd1.KI) cells harboring a homozygous insertion of a small ta

116 Analysis of detergent-solubilized Hrd1.KI cells indicates that the composition and stoichiometr

117 Our results show that macrophages from huTNF KI mice responded to BCG and lipopolysaccharide similarl

118 control of mycobacterial infection in huTNF KI mice, leading to an increased bacterial burden and hy

119 succumbed to mycobacterial infection, huTNF KI mice survived, controlling the bacterial burden and a

120 ompounds were assayed with nNOS, their IC50, KI, and kinact values were obtained, and their crystal s

121 river in the T-cell lineage, we crossed Idh1-KI mice with conditional Trp53 null mice, a well-charact

122 n and induction of bnAbs, and discuss new Ig KI methodologies to manipulate the production and/or exp

123 nock-in (KI) mice and TCR-transgenic (OT-II) KI mice, in which the integrin/kindlin connection is dis

124 Most important, KI-PRS mice are partly protected against the development

125 Importantly, KI/KI mice show significantly increased resistance to hi

126 These pro-apoptotic events were absent in KI mice and were attenuated in WTs co-administered tadal

127 STIM2-nSOC-CaMKII pathway is compromised in KI neurons, in aging neurons, and in sporadic AD brains

128 moderate visual pigment bleach is delayed in KI/KI mice.

129 ts suggest that frequency of InDels found in KI mice generated by the CRISPR/Cas technology is not hi

130 eta42/Abeta40 ratio is slightly increased in KI/+ brains.

131 , which is required to elicit fatty liver in KI mice, led to a much larger and more persistent increa

132 CaMKII activity, and mushroom spine loss in KI neurons.

133 Median PFS in KI-intolerant patients treated with an alternate KI was

134 undetectable in KI/KI brains and reduced in KI/+ brains, though the Abeta42/Abeta40 ratio is slightl

135 undetectable in KI/KI brains and reduced in KI/+ brains.

136 ndicating impaired rhodopsin regeneration in KI/KI.

137 s of Abeta40 and Abeta42 are undetectable in KI/KI brains and reduced in KI/+ brains, though the Abet

138 42, production of Abeta43 is undetectable in KI/KI brains and reduced in KI/+ brains.

139 MBL2(+/+)Mbl1(-/-)Mbl2(-/-) [MBL2 knock in (KI)] mice.

140 f MMAuria using a constitutive Mut knock-in (KI) allele based on the p.Met700Lys patient mutation, us

141 was significantly reduced in APOE2 knock-in (KI) animals and was significantly increased in APOE4 KI

142 we have generated MLL4 enzyme-dead knock-in (KI) embryonic stem (ES) cells and mice, which carry Y547

143 In this study, we used knock-in (KI) mice (Pnpla3(148M/M) ) to examine the mechanism resp

144 dy, we used TTT/AAA beta2-integrin knock-in (KI) mice and TCR-transgenic (OT-II) KI mice, in which th

145 Genetically engineered knock-in (KI) mice containing the A8V mutation (heterozygote=KI-Tn

146 Here, we used knock-in (KI) mice expressing an Itgb3 variant that phenocopies th

147 viously reported that female apoE4 knock-in (KI) mice had an age-dependent decline in hilar GABAergic

148 We used transgenic knock-in (KI) mice harboring the human pathogenic FHM1 mutation S2

149 4 carriers, in the brains of ApoE4 knock-in (KI) mice, and in primary neurons expressing ApoE4 allele

150 that hearts of Cys42Ser PKGIalpha knock-in (KI) mice, which are resistant to PKGIalpha oxidation, ha

151 ecretion from astrocytes in HD140Q knock-in (KI) mice.

152 isulfide-resistant C42S PKG Ialpha knock-in (KI) mice.

153 Using a knock-in (KI) model of 2F5, a human HIV-1 gp41 membrane proximal e

154 g treatments of the human disease, knock-in (KI) models offer advantages of genetic precision of the

155 We generated a D477G knock-in (KI) mouse and characterized its phenotypes.

156 generating a genetically modified knock-in (KI) mouse having a glycine receptor (GlyR) with phenotyp

157 tered low-dose oral rapamycin to a knock-in (KI) mouse model of authentic mtDNA disease, specifically

158 -cell compartment in a conditional knock-in (KI) mouse model of mutant Idh1.

159 o in vivo functions, we analyzed a knock-in (KI) mouse model that lacks isoforms Runx1b/cEx6(-) and R

160 In a new heterozygous Q175 knock-in (KI) mouse model, we performed an extensive evaluation of

161 lon-specific inducible Car1(CreER) knock-in (KI) mouse with broad Cre activity in epithelial cells of

162 er TBI in an AD model, the APP/PS1 knock-in (KI) mouse.

163 nt in a mouse model carrying a CMD knock-in (KI) mutation (Phe377del) in the Ank gene.

164 sgenic mice on either a human ApoE knock-in (KI) or ApoE knockout (KO) background, here we show that

165 hTau knock-in (KI) proteins were expressed at normal, endogenous levels

166 syntaxin, we generated mice with a knock-in (KI) syntaxin-1A (R151G) mutation.

167 rvival, we generated an Rpe65/P25L knock-in (KI/KI) mouse model.

168 human ortholog (human TNF [huTNF] knock-in [KI] mice) to determine resistance to Mycobacterium bovis

169 criteria, using Pentacam (Keratoconus Index [KI], Topographic Keratoconus Classification [TKC]), Topo

170 hresholds for the metric keratoconus indices KI and KMI, which allow classification of keratoconus st

171 Low nanomolar inhibition KI values were detected for all of them, with a very int

172 B-cell receptor kinase inhibitor (KI) therapy represents a paradigm shift in chronic lymph

173 Notably, initial KI choice did not impact PFS or OS; however, RT portende

174 ak neuroinflammatory response in the injured KI mice occurring at 7 d after injury.

175 kine, and chemokine responses in the injured KI mice were delayed compared with the injured wild-type

176 esponses were more persistent in the injured KI mice, leading to a chronic neuroinflammation.

177 At late time points after injury, KI mice exhibited a significant impairment in radial arm

178 ntractile transients were recorded in intact KI-TnC-A8V(+/-) and KI-TnC-A8V(+/+) cardiomyocytes.

179 levels are normal in TTT/AAA beta2-integrin KI mice, but B cell numbers in lymph nodes and IgG and I

180 the seroprevalence of 10 human PyVs (BK, JC, KI, WU, MCV, HPyV6, HPyV7, TSV, HPyV9, and HPyV10) among

181 Higher basal P-selectin in Selp(KI) (/) (KI) mice compensated for this defect.

182 Selp(KI) (/) (KI) mice constitutively expressed more P-selectin on pla

183 n trauma-stimulated venules of Selp(KI) (/) (KI) mice.

184 degree of selectivity and efficiency (kinact/KI > 10(5) M(-1) min(-1)).

185 metric of irreversible inhibitors is kinact/KI not IC50.

186 A simple approach to measuring kinact/KI was developed that makes use of an irreversible probe

187 In this system, the kinact/KI value of the test compound is equal to (kinact/KI)pro

188 lue of the test compound is equal to (kinact/KI)probe x[probe]/IC50.

189 Knockin (KI) mouse carrying a point mutation has been an invaluab

190 exclusively in muscle fibres and a knockin (KI) model expressing a humanized mutant AR gene.

191 st approach consisted of studying a knockin (KI) mouse line (KI-PRS) bearing a conservative mutation

192 enerated a Cys521Ser sEH redox-dead knockin (KI) mouse model that was resistant to this mode of inhib

193 oculation with MERS-CoV, human DPP4 knockin (KI) mice supported virus replication in the lungs, but d

194 Since 2010, immunoglobulin knockin (KI) technology, involving inserting functional rearrange

195 In knockin (KI) mice, human apoE4 causes age-dependent learning and

196 neurons from the presenilin-1 M146V knockin (KI) mouse model of familial AD (FAD).

197 ired for this recruitment, p27T187A knockin (KI) mice were generated to determine the effects of syst

198 Here, we generated Psen1 knockin (KI) mice carrying the FAD mutation L435F or C410Y.

199 hat homozygous Presenilin-1 (Psen1) knockin (KI) mice carrying the familial Alzheimer's disease (FAD)

200 fferent severities, Gabrg2(+/Q390X) knockin (KI) and Gabrg2(+/-) knockout (KO) mice.

201 Previously, we used knockin (KI) mice expressing a prototypical gp41-specific BnAb, 2

202 I/KI) or combined with a knockout allele (KO/KI), to study biochemical and clinical MMAuria disease a

203 Unchanged at the transcriptional level, KI mice with severe epilepsy had neuronal accumulation o

204 we have generated a new knockin mouse line (KI-PRS) bearing a conservative mutation in the PRS resul

205 isted of studying a knockin (KI) mouse line (KI-PRS) bearing a conservative mutation in the PRS that

206 was chemically reduced to As(III) with 0.2 M KI, and total determination of arsenic could be carried

207 es more chaotropic conditions, such as 0.5 M KI.

208 hippocampal neurons obtained from PS1-M146V-KI AD mouse model.

209 MBL2 KI mice represent a novel animal model that can be used

210 Myocardial ischemia/reperfusion in MBL2 KI mice revealed that 3F8 preserved cardiac function and

211 Serum MBL2 level in MBL2 KI mice significantly increased after 7 (8 mug/mL) or 14

212 3 deposition on mannan-coated plates in MBL2 KI, but not wild-type, mice.

213 Like Mll4 knockout ES cells, Mll4(KI/KI) ES cells show reduced levels of H3K4me1/2.

214 Homozygous MLL4 enzyme-dead KI (Mll4(KI/KI)) mice are embryonic lethal and die around E10.5,

215 rved in Tph2-KI mice (wildtype = 24.25 msec, KI = 25.22 msec; p = .011).

216 CSR rates were lower in mTOR KI and KO mice, and pharmacologic inhibition of mTOR in

217 osphate synthase with KI = 1.0 +/- 0.12 muM, KI = 0.5 +/- 0.2 muM, KI = 0.7 +/- 0.3 muM, and KI = 2.9

218 KI = 1.0 +/- 0.12 muM, KI = 0.5 +/- 0.2 muM, KI = 0.7 +/- 0.3 muM, and KI = 2.9 +/- 0.27 muM, respect

219 of active TGF-beta, such as P-Smad2, C-Myc, KI-67, and markers of cell-cycle traverse.

220 tios were elevated in plasma from WT but not KI mice following NO2-OA treatment, consistent with the

221 hypertension model in wild-type (WT) but not KI mice.

222 g of multiple lines of F1 heterozygous Ntrk1 KI mice generated using the CRISPR/Cas system in compari

223 After addition of KI, the fluorescence lifetime decreased to 3.1 ns.

224 tial for application in the determination of KI in different media, such as the human body and in bio

225 fter 30 serial passages through the lungs of KI mice, a mouse-adapted virus emerged (MERSMA) that gre

226 sfully employed to determine the presence of KI in artificial saliva with a limit of detection of 3

227 s(III) and total arsenic (in the presence of KI) are 2.2 mug L(-1) and 2.4 mug L(-1), respectively, a

228 e (FAK) rescued SERT function in synapses of KI mice, demonstrating that constitutive active FAK sign

229 o integrin adhesion complexes in synapses of KI mice.

230 Thymocytes of KI-PRS mice are partly arrested at each step at which pr

231 Three-month-old KI-TnC-A8V(+/+) mice displayed decreased ventricular dim

232 regular mouse housing, homozygous Rpe65/P25L KI/KI mice are morphologically and functionally very sim

233 p27T187A KI activated an E2F1-p73-apoptosis axis in DKO prostate

234 p27T187A KI or Skp2 knockdown (KD) induced similar degrees of p27

235 n DKO prostate cells that contained p27T187A KI (AADKO prostate cells).

236 ested by p27 Thr187-to-Ala knockin (p27T187A KI), it was found dispensable for Kras(G12D)-induced lun

237 Here, we show that p27T187A KI prevented pituitary tumorigenesis in Rb1(+/-) mice an

238 rotein accumulated in prostate when p27T187A KI mice underwent DKO prostate tumorigenesis.

239 trast, gliomas arising in GFAP-HRas(V12);p53(KI/KI) mice develop in the absence of functional p53.

240 gliomas that develop in GFAP-HRas(V12);p53(+/KI) mice abrogate the p53 pathway by mutating p19(ARF)/M

241 Evaluation of OCLs from MVNP, p62-KI, and WT mice revealed increased IGF1 expression in MV

242 t, mice harboring a knockin of p62P394L (p62-KI mice), which is the most frequent PD-associated mutat

243 CO-CO2 at 70 atm in the presence of the PdI2/KI catalytic system.

244 of 9 polyomaviruses (MCPyV, BK polyomavirus, KI polyomavirus, JC polyomavirus, WU polyomavirus, Human

245 We examined responses, toxicity, post-KI therapies, and overall survival (OS).

246 TYR) coupled with markers of proliferation (KI-67) and migration (MCAM) in precursors and mature mel

247 Notably, Pten KI mice are more tumor prone and display features remini

248 At 12-16 months of age, Q175 KI mice displayed motor and cognitive deficits, which we

249 is study indicate that the heterozygous Q175 KI mouse represents a realistic model for HD and also pr

250 its were apparent at 6 months of age in Q175 KI mice and at that time, postmortem striatal gamma-amin

251 ependently found to be downregulated in Q175 KI mice compared to WT (5.2e-7 < P < 0.04).

252 al expression profile in Q175 knock-in (Q175 KI) vs Q25 WT mouse models.

253 x, prefrontal cortex and hippocampus of Q175 KI mice, compared with WT levels.

254 Heterozygous Gabrg2(+/Q390X) KI mice are associated with a severe epileptic encephalo

255 Remarkably, KI mice homozygous for either mutation recapitulate the

256 cordings of presynaptic terminals from S218L KI mice showed a strong shift of the calcium current I-V

257 Selp(KI) (/) (KI) mice constitutively expressed more P-select

258 Higher basal P-selectin in Selp(KI) (/) (KI) mice compensated for this defect.

259 ed P-selectin-dependent inflammation in Selp(KI) (/-) mice.

260 electin in trauma-stimulated venules of Selp(KI) (/) (KI) mice.

261 r with the corresponding SELP sequence (Selp(KI)).

262 rm water maze performance compared with sham KI mice or injured wild-type mice.

263 In behavioral studies, KI mice did not display the foot-clasping behavior upon

264 KI discontinuation with an ORR to subsequent KI at 50% and a median PFS of 11.9 months.

265 The KI mice provide a useful model for further understanding

266 Heterozygosity for the KI mutation decreased production of Abeta40 and Abeta42,

267 In the KI cohort, depression was assessed using the Cornell Sca

268 persistent increase in PNPLA3 protein in the KI mice than in wild-type (WT) mice.

269 lar clamp involved in exocytosis, and in the KI mice, recruitment of complexin to the SNARE complex w

270 iac troponin C ( approximately 21%) into the KI-TnC-A8V(+/-) cardiac myofilament.

271 The most notable characteristic of the KI mice was their significant lower sensitivity to ethan

272 tation, it would confound phenotyping of the KI mice.

273 lly occurred during the establishment of the KI mouse line and potentially have larger impact than a

274 n a new model of HD with an expansion of the KI repeats (Q175).

275 ral rapamycin was sufficient to extend Tk2KI/KI mouse lifespan significantly, and did so in the absen

276 ed that rapamycin may have enabled the Tk2KI/KI mice to utilize alternative energy reserves, and poss

277 perchlorate) showed the highest response to KI.

278 Using INK128 as a prototype TOR-KI, we demonstrate potent inhibition of both R5 and X4 H

279 Transient treatment of mice with the TOR-KI compound AZD8055 increased titers of class-switched h

280 etinal content were found in DAT-KO and Tph2-KI mice, respectively.

281 ic b-wave implicit time was observed in Tph2-KI mice (wildtype = 24.25 msec, KI = 25.22 msec; p = .01

282 R439H tryptophan hydroxylase 2 knockin (Tph2-KI) mice that have an approximately 80% decrease in brai

283 between Th-MYCN mice heterozygous for Trp53(KI) (n = 188) and Th-MYCN mice with wild-type p53 (n = 1

284 ressed from a knock-in allele (Th-MYCN/Trp53(KI)).

285 Conversely, the survival of Th-MYCN/Trp53(KI/KI) mice lacking functional p53 (n = 60) was greatly

286 We found that Th-MYCN/Trp53(KI/KI) tumors were resistant to ionizing radiation (IR),

287 nsitivity to IR in only 50% of Th-MYCN/Trp53(KI/KI) tumors, indicating the acquisition of additional

288 ctional imaging to provide a signature for V-KI-RAS2 Kirsten rat sarcoma viral oncogene homolog (KRAS

289 l B cell deletion in 4E10, but not in 48d VH KI mice.

290 ion, and enhanced systolic function, whereas KI-TnC-A8V(+/-) mice displayed cardiac restriction at 14

291 -A8V(+/+)>KI-TnC-A8V(+/-)>wild-type, whereas KI-TnC-A8V(+/+) relaxed more slowly on flash photolysis

292 allylic halide, reacts 30 times faster with KI/acetone than does benzyl chloride at room temperature

293 SPP/SPP displayed mixed type inhibition with KI = 1.4 muM and KI = 5.5 muM, respectively.

294 d sample with NaBH4 after pre-reduction with KI-ascorbic acid for total As and Sb, and boiling with H

295 of avian farnesyl diphosphate synthase with KI = 1.0 +/- 0.12 muM, KI = 0.5 +/- 0.2 muM, KI = 0.7 +/

296 ge ability was found for carrot treated with KI without N.

297 ng the RA overexpressed hCA IX and XII, with KI values in the low nanomolar-subnanomolar ranges.

298 a DNA-binding domain mutation knocked in (WT/KI) to produce WT, ERalpha KO, or ERalpha KIKO females l

299 that cannot signal through its hemITAM (Y7A KI).

300 However, treatment of Y7A KI mice with Fab' fragments of the function-blocking ant