ライフサイエンスコーパス: KI

1 KI and wild-type mice received PPIs or PBS intraperitone

2 KI enamel also exhibited hypoplasia and numerous surface

3 KI mice also showed an altered eicosanoid profile of red

4 KI mice displayed deficits in multiple behaviors, includ

5 KI mice expressing functional human BCRs promise to acce

6 KI mice were again innately resistant to doxorubicin-ind

7 KI-67 index was low (5%).

8 KI-MS2-008 suppresses cancer cell grown both in vitro an

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

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

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

12 The Cfl2A35T/A35T (KI) mice were indistinguishable from their wild-type lit

13 In addition, KI mice demonstrated a marked reduction in Cfl2 mRNA lev

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

15 In AKT-KI(+/+) mice, expressing the pathogenic human Tau mutant

16 In a transgenic knockin mouse (AKT-KI(+/+)) that lacked sulfhydrated AKT, the interaction b

17 Similarly, mice with the alpha1A KI mutation had increased mortality after transverse aor

18 ng this mouse model denoted knock-in alpha2 (KI alpha2), our electrophysiological studies showed that

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

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

21 that in the absence of phosphorylated AMELX, KI enamel lacks enamel rods, the hallmark component of m

22 4 in the RPE of the KI, KI;Fatp4 (+/-) , and KI;Fatp4 (-/-) mice.

23 The KI/KI and KI/KO mice both have significantly smaller muscle fiber

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

25 on P4 secretion was abolished in both KO and KI cells.

26 ype, compound heterozygote knockout (KO) and KI mP215L mice were generated to establish whether furth

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

28 = 0.5 +/- 0.2 muM, KI = 0.7 +/- 0.3 muM, and KI = 2.9 +/- 0.27 muM, respectively, whereas, analogues

29 luntary movement compared with wild-type and KI/KI mice in the open field starting at 7 months.

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

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

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

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

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

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

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

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

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

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

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

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

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

43 ng in amyloid precursor protein knockin (APP-KI) mice with impaired spatial memory.

44 ion of MEC grid cells emerged in younger APP-KI mice, although the spatial memory and CA1 remapping o

45 its soluble extracellular domain (APPsalpha-KI).

46 to determine trace amounts of total arsenic, KI and l(+) ascorbic acid were used to reduce As(V) to t

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

48 ology with the rapid generation of three BCR KI lines expressing native human precursors, instead of

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 highly variable mosaic structures with both KI and WT features.

52 10 DKO mice partially phenocopied mutant C10 KI mice with the development of cardiomyopathy and activ

53 UCHL1 C152A KI and WT mice underwent middle cerebral artery occlusio

54 Here we report a one-step CRISPR/Cas9 KI methodology to combine the insertion of human germlin

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

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

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

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

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

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 , the absence of prestin protein in DeltaIDR KI OHCs may be due to the unexpected splicing of the hyb

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

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

66 TT accumulation in the striatum in different KI mice.

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

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

69 S) to study FeSb(2), a correlated d-electron KI candidate that also exhibits a low-temperature resist

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

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

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

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

74 pyrin stimuli and in myeloid cells from FMF-KI mice.

75 ase in the levels of TNF are observed in FMF-KI mice, and many features of FMF overlap with the autoi

76 FMF-knockin (FMF-KI) mice that express chimeric pyrin protein with FMF mu

77 wasting, anemia, and neutrophilia in the FMF-KI mice.

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

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

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

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

82 Neurons derived from KI mice had less cell death and neurite injury after hyp

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

84 ll-like receptor stimulated macrophages from KI mice secreted high levels of IL-1beta, IL-18, and IL-

85 bstantially impaired in sensory neurons from KI mice.

86 itro, primary dermal fibroblasts (pDFs) from KI mice showed substantially increased collagen depositi

87 eurons in the adult nAc expressed functional KI GlyRs that were rather insensitive to ethanol when co

88 Furthermore, KI alpha2 mice consumed higher amounts of ethanol in the

89 Furthermore, optimal conditions to generate KI marmoset embryos were investigated using CRISPR/Cas9

90 We generated KI mice by engineering the N475K mutation, which is asso

91 GRTH-KI mice are sterile with reduced testis size, lack sperm

92 e mRNAs and half-lives were observed in GRTH-KI mice.

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

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

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

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

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

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

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

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

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

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

103 1-cis-RAL in fully dark-adapted heterozygous KI mice were similar to that in WT mice.

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

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

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

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

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

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

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

111 G2, we generated immunoglobulin knock-in (Ig KI) mice that express a prototypical celiac patient-deri

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

113 ce/absence of autoantigen by crossing the Ig KI mice to Tgm2-/- mice.

114 osaic mutations with KI and KO, or imprecise KI, of c-kit.

115 peralgesia was only marginally attenuated in KI mice.

116 matter injury was significantly decreased in KI compared with WT mice 7 d after MCAO.

117 nsformation occurred significantly faster in KI enamel.

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

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

120 ecreased tissue loss at 21 d after injury in KI mice.

121 yperalgesia induced by PMA or burn injury in KI was identical to WT.

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

123 tion velocity recovered by 21 d post MCAO in KI mice in corpus callosum.

124 ed in penumbra of WT mouse brains but not in KI mouse brains at 24 h post MCAO.

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

126 inflamed masseter muscle was also reduced in KI mice, and was further inhibited by the TRPV1 antagoni

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

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

129 The artifactual splicing seen in KI mouse models is not present; additionally, two novel

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

131 42, production of Abeta43 is undetectable in KI/KI brains and reduced in KI/+ brains.

132 Wounds in KI mice displayed increased infiltration of dermal fibro

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

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

135 Target-gene-KO/knock-in (KI) efficiency of CRISPR/Cas9 has not been extensively i

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

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

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

139 s macaques and bnAb immunoglobulin knock-in (KI) mice expressing diverse precursors of CD4 binding si

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

141 ) mice lacking cPLA(2)alpha and in knock-in (KI) mice in which endogenous cPLA(2)alpha was replaced w

142 Nox5 knock-in (KI) mice represent the first mechanism-based animal mode

143 attern in sensory neurons of S801A knock-in (KI) mice was comparable to that in WT controls.

144 Psen1 KO mice and knock-in (KI) mice with homozygous FAD-associated L435F mutations

145 in affected tissues of mutant C10 knock-in (KI) mice, demonstrating that L-OPA1 cleavage is a novel

146 e full-length mutant HTT in HD140Q knock-in (KI) mice, we show that exon 1 HTT is stably present in t

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

148 rains of Huntington's disease (HD) knock-in (KI) mice.

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

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

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

152 ction following ischemic injury, a knock-in (KI) mouse expressing the UCHL1 C152A mutation was genera

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

154 We sought to develop a novel Nlrp3 knock-in (KI) mouse model of CAPS to study amyloidosis, a severe C

155 genic-genes using the AF-2 mutated knock-in (KI) mouse model, AF2ERKI.

156 Mutagenesis of exon 2 in Knock-in (KI) mouse models of the R47H variant introduced a crypti

157 B-cell receptor (BCR) knock-in (KI) mouse models play an important role in vaccine devel

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

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

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

161 vation, atrial fibrosis, and AF in knock-in (KI) rats.

162 Because a homozygous knock-in (KI) strain for the mP215L mutation homologous to the hum

163 Intriguingly, a knock-in (KI) Tonsl mouse model leads to embryonic lethality, impl

164 ermatogenesis, we generated a GRTH Knock-In (KI) transgenic mice with the R242H mutation.

165 uronal endolysosomal network by knocking in (KI) an engineered ascorbate peroxidase (APEX) gene to th

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

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

168 eads to discontinuation of kinase inhibitor (KI) treatment.

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

170 tivity saturation in the 4f Kondo insulator (KI) SmB(6) has spurred proposals of a correlation-driven

171 eawater (AS) than buffered potassium iodide (KI) solutions.

172 dine, with the addition of potassium iodide (KI) to assess a potential matrix effect; and 3) an aqueo

173 roponic system applying two forms of iodine, KI and KIO(3) in different concentrations was set up and

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

175 altered MHC II ubiquitination: MHCIIKR(KI) (/KI) mice that express a mutant MHC II unable to be ubiqu

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

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

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

179 ession levels of FATP4 in the RPE of the KI, KI;Fatp4 (+/-) , and KI;Fatp4 (-/-) mice.

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

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

182 Knockin (KI) strategies mimicking TBK1-DRP1 signaling produced do

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

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

185 open unc-64/syntaxin by generating knockin (KI) worms.

186 ated and characterized a hemizygous knockin (KI) mouse model with a phosphorylation-defective Ser-16

187 Using a humanized knockin (KI) mouse model and in vitro organotypic cultures, we fo

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

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

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

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

192 function of rods in the Rpe65 R91W knockin (KI) mouse model of Leber congenital amaurosis (LCA).

193 Here, using knockin (KI) mice harboring cancer-associated and functionally re

194 e, we employ a germline D620N VPS35 knockin (KI) mouse model of PD to formally establish the age-rela

195 the phenotype in DeltaIDR prestin knockins (KI) was similar to that in prestin knockouts: thresholds

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

197 at CRISPR/Cas9 may be utilized to produce KO/KI marmosets via gene editing.

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

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

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

201 13.5-fold greater than those in age-matched KI mice.

202 T(reg) were significantly reduced in MHCIIKR(KI/KI) mice, but not March8 (-/-) mice, whereas splenic

203 In MLRs, March8 (-/-), but not MHCIIKR(KI/KI), CD4(+) T cells had reduced reactivity to both se

204 ions in thymus, blood, and spleen of MHCIIKR(KI/KI) and March8 (-/-) mice were largely unaltered.

205 ls of altered MHC II ubiquitination: MHCIIKR(KI) (/KI) mice that express a mutant MHC II unable to be

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

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

208 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

209 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

210 Nlrp3 KI mice displayed a CAPS phenotype with many characteris

211 Mutant Nlrp3 KI mice displayed features that recapitulate the immunol

212 nd functional outcomes were worsened in NOX5-KI mice.

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

214 significantly attenuated in the hindpaws of KI mice.

215 ay screen, they report the identification of KI-MS2-008, a compound that results in the stabilization

216 Although further improvement of KI strategies is required, these results indicated that

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

218 ed with drug substructures are predictive of KI-induced cardiotoxicity risk, and that they can be inf

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

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

221 matrix effect; and 3) an aqueous solution of KI as a comparator; with all 3 containing equal amounts

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

223 o integrin adhesion complexes in synapses of KI mice.

224 Treatment of KI mice with PPIs had a clear clinical effect, showing a

225 es in the inferior retinas of 4- or 6-mo-old KI;Fatp4 (-/-) mice was 7.6- or 13.5-fold greater than t

226 u foils in aqueous solutions of KCl, KBr, or KI creates surfaces of CuCl, CuBr, or CuI, respectively.

227 d closure rate was not affected in the KO or KI mice, but wound maturation was enhanced in the KI mic

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

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

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

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

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

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

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

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

236 proved sensorimotor recovery in postischemic KI mice.

237 n striatal tissue homogenates from Hdh(Q140) KI mice and in human HD postmortem cortex.

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

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

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

241 g and expression was measured in Trem2(R47H) KI rat brains and microglia by qualitative and quantitat

242 unction, a new rat KI model, the Trem2(R47H) KI rat was created.

243 Thus, Trem2(R47H) KI rats may prove valuable to define pathogenic mechanis

244 reases dementia risk, we created Trem2(R47H) KI rats.

245 nd Trem2 levels are unchanged in Trem2(R47H) KI rats.

246 s and behavioral testing, we generated a rat KI model of the Psen1(LF) mutation.

247 oes not model Trem2-R47H function, a new rat KI model, the Trem2(R47H) KI rat was created.

248 In terms of ethanol response, KI alpha2 male mice recovered faster from the administra

249 ve terminals at an earlier stage than SJ1(RQ)KI mice.

250 tors observed at synapses of cultured SJ1(RQ)KI neurons was more severe in double-mutant neurons.

251 ce carrying the SJ1 patient mutation (SJ1(RQ)KI) exhibit PD features, while Sac2 knockout mice (Sac2K

252 ha KO, phosphorylation-blocked ERalpha S216A KI mice, it is now demonstrated that, after being activa

253 Secretory KI ameloblasts also lacked Tomes' processes, consistent

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

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

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

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

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

259 x quantitation in GI-NETs: (1) Synaptophysin-KI-Estimator (SKIE), a pipeline automating Ki-67 index q

260 Unexpectedly, the open syntaxin KI partially suppresses exocytosis defects of various mu

261 The KI animals exhibit enhanced spontaneous and evoked exocy

262 The KI mice provide a useful model for further understanding

263 The KI rats may provide an inflammation-based, genetic anima

264 The KI/KI and KI/KO mice both have significantly smaller mus

265 The KI/KO mice have a significant decrease in voluntary move

266 The KI/KO mP215L strain is the first murine model of BAG3 my

267 ce, but wound maturation was enhanced in the KI mice compared to that in wild-type controls.

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

269 the lysosomes, was remarkably reduced in the KI mouse retinas lacking FATP4.

270 gulated kinase) was markedly impaired in the KI mutant myocytes, and A61603 did not protect mutant my

271 in trafficking and M-opsin solubility in the KI retinas.

272 S- and M-cones is markedly preserved in the KI;Fatp4 (-/-) mice, displaying an inverse correlation w

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

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

275 expression levels of FATP4 in the RPE of the KI, KI;Fatp4 (+/-) , and KI;Fatp4 (-/-) mice.

276 However, only the KI/KO mice have clear skeletal muscle histologic changes

277 In behavioral tests, the KI alpha2 mice did not show any difference in basal moto

278 The longer survival of these KI rats affords the opportunity to examine the effect of

279 ducted a comparative evaluation between this KI-LAMP1-APEX method and our two overexpression LAMP1-AP

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

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

282 perchlorate) showed the highest response to KI.

283 tion in Alternaria alternata-challenged TrkA-KI mice markedly inhibited eosinophilia and attenuated v

284 with 1-NM-PP1 in TrkA(F592A)-knock-in (TrkA-KI) eosinophils.

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

286 ith the nervous system, including GTML/Trp53(KI/KI) medulloblastoma (G (d) = 3.5 +/- 0.2 kPa, G (l) =

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

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

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

290 uclein-positive neuropathology in aged VPS35 KI mice, a hallmark of Lewy body pathology in PD.

291 Finally, by crossing VPS35 KI and null mice, our data demonstrate that a single D62

292 unts of PdI(2) (1 mol %) in conjunction with KI (20 mol %) and 2 equiv of diisopropylethylamine at 80

293 e Satin') were grown in soil fertilized with KI (4 kg I ha(-1)) and Na(2)SeO(4) (0.25 kg Se ha(-1)).

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

295 All embryos exhibited mosaic mutations with KI and KO, or imprecise KI, of c-kit.

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

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