ライフサイエンスコーパス: Ki

1 Ki-67 and proliferating cell nuclear antigen were used t

2 Ki-67 and RepoMan have key roles during mitotic exit.

3 Ki-67 depletion disrupted nucleologenesis but did not in

4 Ki-67 expression was assayed by immunohistochemistry.

5 Ki-67 is also a fundamental component of the perichromos

6 Ki-67 LI and age remained significantly associated with

7 Ki-67 LI is a strong prognostic indicator and should be

8 Ki-67 mutant mice developed normally and cells lacking K

9 Ki-67 silencing also had wide-ranging effects on chromat

10 ffinity at the DAT (Ki=3 muM) than JJC8-016 (Ki=116 nM).

11 ccessfully achieved to fabricate arrays of 1 Ki cells that have sub- 15 nm nanowires distant by 28 nm

12 tive inhibition at the high-affinity Site 1 (Ki = 720 +/- 340 nm) and non-essential activation at the

13 ne fragment with a weak binding affinity (1, Ki = 160 muM).

14 -dicyclopropylmethyl 4'-CH2OH derivative 14 (Ki 11 nM).

15 t attractive ligand of the series [(+/-)16b, Ki = 24.3 nM] was resolved into its two enantiomers by c

16 Compound 2 (Ki = 19 nM) binds within the aldehyde-binding site of th

17 t analog non-competitively inhibits Nedd4-2 (Ki = 2.0 +/- 0.5 mum), consistent with the presence of t

18 Moreover, bioactive peptide 25 (Ki = 9 nM) achieved oral bioavailability of 18% in rats,

19 erved for the C26-des-methyl analogues WN-3 (Ki = 63.9 nM) and WN-7 (Ki = 63.1 nM).

20 ore biopsies (proliferation decrease >/= 30% Ki-67 or cellularity response).

21 oximately 3 log-orders to yield compound 35 (Ki = 43 nM).

22 thyl analogues WN-3 (Ki = 63.9 nM) and WN-7 (Ki = 63.1 nM).

23 In particular, fluoroderivative 7w (Ki = 0.44 nM) resulted in the most potent ligand among t

24 ptimize the inhibitor structure to achieve a Ki of 110 nM, with 15-60-fold selectivity across a serie

25 ence, the tightest cyclic peptide achieved a Ki value of 2.9 muM against DENV3 wild-type (WT) proteas

26 receptors, and binding studies established a Ki value of 4.4 nM at a known allosteric binding site.

27 d progesterone receptor expression and had a Ki-67 score of 15% (> 20% is considered high according t

28 esterone receptor expression (40%) and had a Ki-67 score of 20%.

29 progesterone receptor expression, and had a Ki-67 score of 60%.

30 ng with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein.

31 ve a very high affinity to the enzyme with a Ki equal to 7 nM.

32 and binds to all forms of the enzyme with a Ki near 200 nM, more than 300 times more tightly than ly

33 t cancer-associated isozyme, hCA XII, with a Ki of 0.79 nM.

34 e than any of our previous inhibitors with a Ki of 1.0 nM.

35 egative to inhibit TGF-beta signaling with a Ki of 20-70 nm Investigation of the mechanism showed tha

36 osaminyl)-4(5)-(2-naphthyl)-imidazole with a Ki value of 143 nM against human liver GPa.

37 (68)Ga-DOTATATE SUVmax between tumors with a Ki-67 of less than 5% and tumors with a Ki-67 of more th

38 th a Ki-67 of less than 5% and tumors with a Ki-67 of more than 5% (P = 0.004), without significance

39 es were particularly potent, with human A3AR Ki values of 6 and 42 nM, respectively.

40 Mitotic figures were abundant (Ki-67 stain 80% to 90% positive) and there were multiple

41 )H]NMS) binding to M1, left-shifting the ACh Ki approximately 19-fold at 10 muM.

42 y inhibits recombinant Drp1 GTPase activity (Ki > 1.2 mM).

43 hybrids with high CXCR7 binding affinities (Ki < 100 nM) and measurable passive permeability (Papp >

44 , endowed with a picomolar binding affinity (Ki = 38 pM), coupled with a single-digit micromolar acti

45 as the ligand with the highest CB2 affinity (Ki = 0.39 nM) and selectivity over those of CB1 (factor

46 5a, and 15c revealed favorable D3R affinity (Ki = 12-25.6 nM) and were highly selective for D3R vs D3

47 s 11b, which demonstrated high DAT affinity (Ki = 2.5 nM) and selectivity without producing concomita

48 antagonistic effect with excellent affinity (Ki < 10 nM) and outstanding selectivity profiles, provid

49 )-16b enantiomer retaining all the affinity (Ki = 15.1 nM), as predicted earlier by molecular modelin

50 t potent dual acting human (h) A1AR agonist (Ki = 0.45 nM) and A3AR antagonist (Ki = 0.31 nM) and hig

51 32, which was 10-fold selective for ALDH1A1 (Ki = 1.2 muM) versus ALDH1A2.

52 ompound 36, a selective inhibitor for ALDH2 (Ki = 2.4 muM), and compound 32, which was 10-fold select

53 r donor-matched kidney used in kidney-alone (Ki) or simultaneous pancreas kidney (SPK) transplants.

54 immunohistochemistry for cytokeratin 19 and Ki-67.

55 Compounds 4-7 have weak agonist activity and Ki's in the 1-30 muM range; compounds 8-14 are antagonis

56 mputed tomographic pulmonary angiography and Ki-67 immunohistochemistry revealed abundant lung neovas

57 y liver was delineated in the whole-body and Ki images, and tumor-to-liver ratios were calculated to

58 BrdU and Ki-67 detection at neonatal and adult ages showed that a

59 Multi-label immunofluorescence for CD163 and Ki-67 confirmed that the vast majority of Ki-67+ nuclei

60 uction as well as the expression of CD25 and Ki-67 by activated CD4+ T cells.

61 s against the pan-macrophage marker CD68 and Ki-67 showed that there was a significant increase in CD

62 Mitotic count and Ki-67 labelling index (LI) were detected as prognostic f

63 atification of patients by mitotic count and Ki-67 LI correlated significantly with overall survival

64 Risk evaluation combining mitotic count and Ki-67 LI predicts prognosis.

65 uvant therapy, recurrence occurred early and Ki-67 LI predicted prognosis.

66 epidermal growth factor receptor (EGFR) and Ki-67.

67 beta-catenin expression and Ki-67 labeling index (LI) were evaluated by immunostaini

68 uding (18)F-FLT in addition to (18)F-FDG and Ki-67 could not be found.

69 For OS, only (18)F-FDG and Ki-67 remained significant.

70 e correlation between the levels of FEN1 and Ki-67 staining was identified in these NSCLC tissues (r

71 (68)Ga DOTATATE SUVmax relates to grade and Ki-67 and can be used prognostically.

72 : Hematoxylin &Eosin, CD31 &Hematoxylin, and Ki-67 and where most of the nuclei were unevenly and imp

73 Additionally, for almost all cases, k3 and Ki had a significant strong correlation for all tissue t

74 of Arabidopsis subtilase SBT4.13 with Kd and Ki values in the picomolar range.

75 r of ETC with the kinetic constants, Ki' and Ki determined as 30.62 +/- 7.73 nM and 153.75 +/- 17.96

76 sferase-mediated dUTP nick-end labeling, and Ki-67 immunoreactivity were evaluated.

77 -associated transcription factor (MiTF), and Ki-67 for calculating the proliferation index are illust

78 e, tumor weight, somatic TP53 mutations, and Ki-67 LI were associated with prognosis.

79 d for the nucleolar localization of NADs and Ki-67 during interphase.

80 ative, CD5 negative, cyclin D1 negative, and Ki-67 index of less than 5%.

81 ence with antibodies against SIV-Gag-p28 and Ki-67, showed that the population of Ki-67+ cells were p

82 mor grade (available in 43,590 patients) and Ki-67 status (available in 7692 patients), which are str

83 e in NEN patients but when (18)F-FDG PET and Ki-67 index are also available, a multivariate model rev

84 or NENs in comparison with (18)F-FDG PET and Ki-67 index.

85 strogen receptor, progesterone receptor, and Ki-67 expression levels.

86 ariate analyses adjusting for MIPI score and Ki-67 index (hazard ratio [HR], 2.0; P = .0054 for TTF,

87 d poor OS independent of both MIPI score and Ki-67 index.

88 sessed immunohistochemically by survivin and Ki-67 staining.

89 Analysis of wild-type and Ki-67-depleted chromosomes reveals that the periphery co

90 A reduction in (18)F-FHNP tumor uptake and Ki values was observed in the presence of estradiol or g

91 correlations were found between M value and Ki in multiple tissues: the gluteus muscle (r = 0.875; P

92 Associations between M value and Ki were studied in multiple tissues by using the Pearson

93 Markers of proliferation and angiogenesis (Ki-67, vascular endothelial growth factors A/C, vascular

94 agonist (Ki = 0.45 nM) and A3AR antagonist (Ki = 0.31 nM) and highly selective versus A2A; 11 and 26

95 The cell proliferation antigen Ki-67 is widely used in cancer histopathology, but estim

96 -regulated proteins is proliferation antigen Ki-67, whose depletion also decreases the nucleolar asso

97 p to 4-fold) and an increase in the apparent Ki of the inhibitor HQNO (up to 8-fold).

98 ossessed nanomolar affinity for the hA2A AR (Ki = 2.9-10 nM) and some, very interestingly, also showe

99 id receptors subtype 1 (GluK1) was attained (Ki = 4 muM).

100 agreement between NLR- and parametric-based Ki values was found, showing that Ki images are quantita

101 agreement between NLR- and parametric-based Ki values was found, showing that Ki images are quantita

102 was no bias between NLR and parametric-based Ki values.

103 of progesterone receptor status or baseline Ki-67 expression.

104 ed in 11 new submicromolar KOR binders (best Ki = 90 nM).

105 The good correlation between Ki values observed in the sigma1 assays and calculated f

106 6 and 2.0 times higher in the parametric BFM Ki images and 2.3 and 3.0 times in the Patlak images tha

107 pyrrolidine improves the human GPR40 binding Ki and agonist efficacy.

108 pound cellular activity correlated with both Ki and koff.

109 LR assessed by Ki-67 and proliferating cell nuclear antigen was markedl

110 tokeratin-19 expression and proliferation by Ki-67 immunohistochemistry (IHC).

111 he estimates of dopamine synthesis capacity (Ki) using 6-[(18)F]fluoro-l-m-tyrosine ([(18)F]FMT; a su

112 tion in the fraction of proliferating CD4(+) Ki-67(+) TSCM in blood (but not lymph nodes).

113 hat there was a significant increase in CD68+Ki-67+ cells in macaques with SIV encephalitis (SIVE) co

114 In normal cells, Ki-67 was a late marker of cell-cycle entry; Ki-67 mRNA

115 Multivariable analysis confirmed Ki-67 response to the combination treatment of patients

116 ace, that has an MMP-14 inhibition constant (Ki ) of 0.9 pm, the strongest MMP-14 inhibitor reported

117 ement with the in vitro inhibition constant (Ki) of 6.3 nM and regional Bmax in humans.

118 [(11)C]carfentanil and influx rate constant (Ki) values for [(18)F]fluorodopa were analyzed with regi

119 The specific uptake constant, Ki, a measure of DDC activity, was estimated for striata

120 inhibitor of ETC with the kinetic constants, Ki' and Ki determined as 30.62 +/- 7.73 nM and 153.75 +/

121 selected based on its in vitro profile: D3R Ki = 6.84 nM, 1700-fold D3R versus D2R binding selectivi

122 ive, but had much lower affinity at the DAT (Ki=3 muM) than JJC8-016 (Ki=116 nM).

123 ition for CCA as knockdown of NGAL decreased Ki-67 expression in SNU308 cells and rendered SNU308 cel

124 e Cell Lymphoma Pathology Panel to determine Ki-67 index by using published guidelines, cytology, and

125 that was recently evolved by phage display (Ki = 0.84 +/- 0.03 nM).

126 e caused G1 cell-cycle arrest and eliminated Ki-67 mRNA in RB1-positive cells but had no effect in RB

127 Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, i

128 Ki-67 was a late marker of cell-cycle entry; Ki-67 mRNA oscillated with highest levels in G2 while pr

129 hyl)propoxy]methylphosphonic acid, exhibited Ki values of 6 and 70 nM for human HGPRT and Pf HGXPRT,

130 , which continued to proliferate and express Ki-67.

131 subpopulations of resident PVM that express Ki-67 and are SIV-infected, suggesting a mechanism of ma

132 in regions and in striatal [(18)F]fluorodopa Ki compared with controls.

133 ate with no differences in [(18)F]fluorodopa Ki compared with controls.

134 BPND was 30-34% lower and [(18)F]fluorodopa Ki was 20% lower in BED compared with PG and controls (p

135 ed a positive correlation between [(18)F]FMT Ki and the baseline (placebo) [(11)C]raclopride measure,

136 Then, tissue was harvested for Ki-67 proliferative indexes and CD34 microvascular densi

137 f a potent FXIa clinical candidate, 55 (FXIa Ki = 0.7 nM), with excellent preclinical efficacy in thr

138 ries, exemplified by compound 16, had a FXIa Ki = 0.16 nM with potent anticoagulant activity in an in

139 ia published quantitative binding data (e.g. Ki, IC50 or Kd).

140 cited a spectral response in CYP27A1 and had Ki values for cholesterol 27-hydroxylation either in the

141 The resulting compounds have Ki values in the two-digit nanomolar range, are not cyto

142 igh expression of Kv1.3 correlated with high Ki-67 and granzyme B expression.

143 mples, and positively correlated with higher Ki-67 index.

144 Here we show how Ki-67 and RepoMan form mitotic exit phosphatases by recr

145 K1/2 dual inhibitor 20l (SLC4011540) (hSphK1 Ki = 120 nM, hSphK2 Ki = 90 nM) and SphK2 inhibitor 20dd

146 20l (SLC4011540) (hSphK1 Ki = 120 nM, hSphK2 Ki = 90 nM) and SphK2 inhibitor 20dd (SLC4101431) (Ki =

147 It has high affinity at human 5-HT6R (Ki = 2.04 nM) and selectivity over 100 target sites whic

148 was accompanied by a significant decrease in Ki-67 index (proliferation on day 7: mean reduction, 81%

149 mean kidney allograft lifespan was higher in Ki/SPK compared with SLK transplants by 0.99 years in th

150 alphaq binding affinity (10-fold increase in Ki compared with WT RGS2 in a flow cytometry competition

151 We detected an increase in Ki-67+ PD-1+ CD8 T cells following therapy in approximat

152 ting in an approximately 8-fold reduction in Ki compared with TFPI alone.

153 xpression changes were partially relieved in Ki-67-depleted hTERT-RPE1 cells by codepletion of the Rb

154 chemical cancer subtypes were made including Ki-67 intensity and Nottingham grade (NG).

155 Overexpression of miR-10b increased Ki-67 staining in human organ-cultured corneas and proli

156 y), chromogranin A, and proliferation index (Ki-67).

157 D68 at 7 days), tumor proliferative indexes (Ki-67 and CD34 at 7 days), and serum and tissue levels o

158 n (compound 16) displayed potent inhibition (Ki = 11.45 nM) and was 84-fold more selective toward the

159 -1) produced a potent cathepsin G inhibitor (Ki = 0.89 nM).

160 ide moiety, proved to be a potent inhibitor (Ki = 8.2 nM) of the Thermotoga maritima TmGH1 beta-gluco

161 inhibitor of human cathepsins B, K, and L ( Ki = 6.87, 0.49, and 0.34 nM, respectively).

162 tux enabled selective uptake of FITC-labeled Ki-67 antibody TuBB-9 in EGFR-positive cells pre-loaded

163 nt mice developed normally and cells lacking Ki-67 proliferated efficiently.

164 splayed noncompetitive inhibition of the LC (Ki approximately 1 muM), while mercury (II) cations were

165 ation in G1 After cell-cycle exit, low-level Ki-67 expression persisted but was undetectable in fully

166 These low Ki values were achieved by inserting an extra carbon ato

167 n the expression of the proliferation marker Ki-67 and the aromatase enzyme.

168 actor-kappaB p65(+)), proliferation markers (Ki-67(+)), and class-switched B cells (IgG(+)); and (5)

169 ocessed for DCX, cell proliferation markers (Ki-67, BrdU), pallial/subpallial developmental origin (T

170 ) increased levels of proliferation markers (Ki-67, p-Erk, p-Akt and PCNA); (3) decreased apoptosis m

171 d two additional adult neurogenesis markers, Ki-67 and doublecortin, in the hippocampus was evaluated

172 ere was significantly greater geometric mean Ki-67 suppression of 83.8% (one-sided 95% CI, >/= 79.0%)

173 on of CDK4/CDK6 revealed proteasome-mediated Ki-67 degradation in G1 After cell-cycle exit, low-level

174 ptosis were determined by methyltetrazolium, Ki-67, proliferating cell nuclear antigen, bromodeoxyuri

175 itumor effects of CFI-402257, a potent (Mps1 Ki = 0.09 +/- 0.02 nM; cellular Mps1 EC50 = 6.5 +/- 0.5

176 e was potent and selective at A3AR (MRS7220, Ki 60 nM) and also completely reversed mouse sciatic ner

177 -1)) and substrate inhibition above 0.5 mum (Ki = 2.5 +/- 1.3 mum) that tends to zero velocity, requi

178 ocker Ki16425 (cells, 10 muM; lungs, 25 muM; Ki, 0.34 muM) or cellular knockdown of LPAR type 1 decre

179 d to high-affinity analogs (medium nanomolar Ki) for the GHB high-affinity binding sites as the most

180 binds to WDR5 with an IC50 value of 0.90 nM (Ki value <1 nM) and inhibits the MLL H3K4 methyltransfer

181 factor (LF) protease (IC50 = 390 +/- 20 nM, Ki = 365 +/- 20 nM) and a weak inhibitor of other mammal

182 inhibiting LF protease (IC50 = 43 +/- 3 nM, Ki = 18 +/- 1 nM).

183 preserves excellent potency with human nNOS (Ki = 30 nM) and very high selectivity over other NOS iso

184 Immunohistological staining of occludin, Ki-67, NF-kappaB-p65, and terminal deoxynucleotidyl tran

185 whether the equally weighted combination of Ki-67 index (dichotomized at the validated 30% cutoff) a

186 Here we demonstrate that depletion of Ki-67 in human hTERT-RPE1, WI-38, IMR90, and hTERT-BJ ce

187 Notably, induction of p21 upon depletion of Ki-67 was a consistent hallmark of cell types in which t

188 in cancer histopathology, but estimations of Ki-67 expression levels are inconsistent and understandi

189 A reduced expression of Ki-67 and survivin in tumor tissues accompanied the obse

190 that p150N is required for normal levels of Ki-67 accumulation on the PCL.

191 in the tissue model coincided with a loss of Ki-67, a protein strictly associated with cell prolifera

192 nd Ki-67 confirmed that the vast majority of Ki-67+ nuclei were localized to CD163+ macrophages in pe

193 Comparison of the expression pattern of Ki-67, a protein that acts as a cellular marker for prol

194 ing slowly, as measured by the percentage of Ki-67(+) cells.

195 p28 and Ki-67, showed that the population of Ki-67+ cells were productively infected and expanded pro

196 bination:anastrozole geometric mean ratio of Ki-67 suppression was 0.37 (95% CI, </= 0.67; P = .008),

197 Conversely, upregulation of Ki-67 expression in differentiated tissues did not preve

198 tumor size, Scarf-Bloom-Richardson grade, or Ki-67 expression.

199 Parametric Ki images were computed using a basis function method (B

200 d agreement between VOI-based and parametric Ki values were assessed using regression and Bland-Altma

201 metric methods for computation of parametric Ki images by comparison to volume of interest (VOI)-base

202 iver contrast was superior in the parametric Ki images compared with whole-body images for both (68)G

203 kout of RCN2 inhibited EGFR phosphorylation, Ki-67 expression and tumor growth in nude mice.

204 selectivity with a good stability in plasma (Ki = 1.63 +/- 0.18 nM, >27000-fold selectivity, t1/2(pla

205 ighly-positive (SOX-2), moderately-positive (Ki-67) and weakly-positive (betaIII-tubulin) protein tar

206 ion in number of bromodeoxyuridine-positive, Ki-67(+), and doublecortin(+) cells in the subgranular z

207 pyrrolidine ring was identified as a potent (Ki = 0.63 nM) and highly selective kappa agonist (EC50 =

208 anidyl-l-phenylalanine) to produce a potent (Ki = 1.6 nM) and the most selective (>/=360-fold) engine

209 n expansion of the fraction of proliferating Ki-67(+) cells, and (iii) high levels of SIV DNA.

210 expression of markers of cell proliferation (Ki-67), decreased neovascularization (laminin and alphaS

211 ar-complete inhibition of CLL proliferation (Ki-67) by cycle 2.

212 ncluded distant tumor growth, proliferation (Ki-67 percentage), and microvascular density.

213 or volume (p < 0.01), reduced proliferation (Ki-67 staining; p < 0.03) and apoptosis induction (cleav

214 Tumor proliferation (Ki-67 percentage) was increased for 5-W MWA (82% +/- 5)

215 A marker of cell proliferation, Ki-67, was stained, showing a significant reduction in t

216 sing catalytically inactive prostasin (Prss8(Ki/Ki)) to show that the physiological and pathological

217 Across time points, quantitative Ki-67 had weak positive correlation with SUVmax (R1 = 0.

218 te (k3) and delivery rate (K1), influx rate (Ki ) constants, and tissue-to-blood activity concentrati

219 sulin-mediated (18)F-FDG tissue influx rate (Ki) in the whole-body region by using the Patlak method.

220 However, changes in net influx rate (Ki) may better reflect treatment effects than those of t

221 lak graphical analysis gave metabolic rates (Ki, the irreversible uptake rate constant) comparable to

222 s (estrogen receptor, progesterone receptor, Ki-67, human epidermal growth factor receptor 2, and Els

223 red hHFs treated with PGD2 displayed reduced Ki-67 expression and EdU incorporation in bulge resident

224 rafts, which had reduced tumor size, reduced Ki-67, and increased terminal deoxynucleotidyl transfera

225 ylation of AKT and S6, together with reduced Ki-67 and CD31 expression.

226 a need to compute parametric images showing Ki at the voxel level.

227 </= 0.67; P = .008), whereas no significant Ki-67 response was observed for pictilisib in luminal A

228 0 nM) and SphK2 inhibitor 20dd (SLC4101431) (Ki = 90 nM, 100-fold SphK2 selectivity).

229 ranting a lead compound with a submicromolar Ki.

230 l-bowel sections were analyzed for survivin, Ki-67, and TP53 by immunohistochemistry.

231 s such as TNFalpha converting enzyme (TACE) (Ki = 4.45 +/- 0.48 muM).

232 ession but not with ERalpha, confirming that Ki is a suitable parameter to quantify ERbeta expression

233 Altogether, our results indicate that Ki-67 integrates normal S-phase progression and Xi heter

234 Unexpectedly, our data also reveal that Ki-67 and RepoMan bind PP1 using an identical, yet novel

235 Here, we show that Ki-67 controls heterochromatin organisation.

236 Previously, we showed that Ki-67 organizes the mitotic chromosome periphery and rec

237 tric-based Ki values was found, showing that Ki images are quantitatively accurate.

238 tric-based Ki values was found, showing that Ki images are quantitatively accurate.

239 Altogether, our results suggest that Ki-67 expression in proliferating cells spatially organi

240 The Ki and k3 parametric analysis provided information on tu

241 The Ki values correlated well with ERbeta expression but not

242 The Ki values for these compounds ranged from 1.2 to 21 muM,

243 The Ki-, G-, H- and F values were calculated for the estimat

244 The Ki-67 index is a strong independent prognostic factor; h

245 The Ki-67 index was assessed in 508 of 832 patients (median

246 The Ki-67 proliferation index is presently used as the key m

247 The Ki-67 protein is widely used as a tumor proliferation ma

248 for inhibition of CYP2C9 and determined the Ki values for inhibitors.

249 Nodal status, central and local grade, the Ki-67 protein encoded by the MKI67 gene, estrogen recept

250 rameter to quantify ERbeta expression is the Ki However, a simplified static imaging protocol for det

251 The modified combination of the Ki-67 index and MIPI separated four groups with 5-year O

252 The modified combination of the Ki-67 index and MIPI showed a refined risk stratificatio

253 ndently of MIPI but not independently of the Ki-67 index.

254 mmune liposomes and the high efficacy of the Ki-67 light-inactivation.

255 We examined the expression of the Ki-67 proliferation marker in the brains of uninfected a

256 led TuBB-9, which caused inactivation of the Ki-67 protein and subsequent cell death via apoptosis.

257 cer therapeutics that selectively target the Ki-67:PP1 and RepoMan:PP1 holoenzymes.

258 ositively but moderately correlated with the Ki-67 protein encoded by the MKI67 gene and grade and ne

259 state plasma concentrations exceeding their Ki values by >60-fold, plasma D-serine levels remained t

260 Thus, Ki-67 expression varies due to cell-cycle regulation, bu

261 ath was higher in SLK recipients relative to Ki/SPK recipients: 10-year cumulative incidences 0.36 (9

262 nd cell cycle distribution were sensitive to Ki-67; these responses were absent in cells that did not

263 ctivity against the serine protease trypsin (Ki = 1.5 nm).

264 based and parametric image-based (BFM) tumor Ki values was 0.98 (slope, 0.81) and 0.97 (slope, 0.88)

265 based and parametric image-based (BFM) tumor Ki values was 0.98 (slope, 0.81) and 0.97 (slope, 0.88)

266 image-derived input function, and mean tumor Ki values were determined for 50% isocontour VOIs and co

267 LR-based and parametric-based (Patlak) tumor Ki was 0.95 (slope, 0.71) and 0.92 (slope, 0.74) for (68

268 Conversely, greater tumoral Ki-67 staining was observed in female mice (71% +/- 3% f

269 Furthermore, upon Ki-67 depletion, a subset of inactive X (Xi) chromosomes

270 gen VI hHFs by immunohistomorphometry, using Ki-67 and 5-ethynyl-2'-deoxyuridine (EdU).

271 stands out 12b for its high affinity value (Ki = 0.27 nM) and for its anxiolytic-like and ability to

272 hat cell-cycle regulation underlies variable Ki-67 expression in all situations analyzed, including n

273 ession increased lung cancer cell viability, Ki-67 intensity and clonogenicity and promoted lung canc

274 inhibition for the brain-expressed hCA VII (Ki = 0.20 nM) and selectivity over wider distributed hCA

275 2.8 min) and D-alpha-(1'-fluoro)vinyllysine (Ki = 470 +/- 30 muM; t1/2 = 3.6 min).

276 o antipodes, L-alpha-(1'-fluoro)vinyllysine (Ki = 630 +/- 20 muM; t1/2 = 2.8 min) and D-alpha-(1'-flu

277 o significantly correlated with the in vitro Ki values for NTS1.

278 However, whether Ki-67 affects cell cycle progression has been controvers

279 ibiting PARP1 and PARP2 enzyme activity with Ki = 1.2 and 0.87 nM, respectively.

280 d azide inhibited the catalase activity with Ki values of 3.8 mum and 37.7 mum, respectively.

281 re found to inhibit the enzyme activity with Ki values ranging from 3 to 24 mum PJ34, a well known in

282 vatives showed high receptor affinities with Ki values in the low nanomolar range, even when bulky fl

283 the compounds showed high CBR affinity with Ki values within the submicromolar and subnanomolar rang

284 exhibited binding affinity to PKC alpha with Ki values of 7000 +/- 990 and 4940 +/- 470 nM, respectiv

285 M range; compounds 8-14 are antagonists with Ki's in the 0.1-10 muM range for OX2 and 1-50 muM for th

286 ally inhibited FRET (i.e. CaM binding), with Ki > 10 mum, for both RyR1 and RyR2.

287 nes concentration changes were compared with Ki and H-values and safe temperatures and times for stor

288 ed for 50% isocontour VOIs and compared with Ki values based on nonlinear regression (NLR) of the who

289 a non-competitive inhibitor of CYP1A2, with Ki values no more than 2.16 muM.

290 hibition for CYP2B1, CYP2C11 and CYP2E1 with Ki values less than 9.93 muM were observed.

291 N mutant being competitively inhibited, with Ki = 31 +/- 1.5 mum and 1.5 +/- 0.1 mm, respectively, an

292 ne is a potent, reversible CE inhibitor with Ki values in the nanomolar range.

293 of low molecular weight STEP inhibitors with Ki values as low as 7.8 muM.

294 etitive inhibitors of UGM against NADPH with Ki values of 6 microM and 74 microM, respectively.

295 Three-year PFS for 27 patients with Ki-67 LI >/= 15% was 48.5% compared with 96.2% for 29 pa

296 .5% compared with 96.2% for 29 patients with Ki-67 LI < 15% (log-rank P = .002), and the rate of rela

297 molecule SW033291 (1) inhibits 15-PGDH with Ki = 0.1 nM in vitro, doubles PGE2 levels in vivo, and s

298 two compounds that inhibited PKCepsilon with Ki <20 nM, showed selectivity for PKCepsilon over other

299 noncompetitive inhibitor of 3MG uptake with Ki(app) = 0.3 mum but is a competitive inhibitor of suga

300 throcyte 3-O-methylglucose (3MG) uptake with Ki(app) = 6 mum but is a noncompetitive inhibitor of sug

301 Finally, overexpression of human or Xenopus Ki-67 induced ectopic heterochromatin formation.