ライフサイエンスコーパス: Ki

1 Ki(cer) showed significant positive correlations with im

2 Ki(cer) was significantly higher in responders compared

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

4 Ki-67 expression correlated with K(app) (rho = 0.53, P =

5 Ki-67 expression was assayed by immunohistochemistry.

6 Ki-67 forms repulsive molecular brushes during the early

7 Ki-67 indices for 50 GI-NETs were quantitated using SKIE

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

9 Ki-67 LI and age remained significantly associated with

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

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

12 is (OR = 6.32, 95% CI 1.33-30.01, P = 0.02), Ki-67 <10% (OR = 14.07, 95% CI 2.09-94.9, P = 0.007), an

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

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

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

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

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

22 -67 index of less than or equal to 55% and a Ki-67 index of greater than 55%.

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

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

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

26 Parameters associated with lower OS were a Ki-67 of more than 10%, performance status of at least 1

27 ower PFS in the multivariate analysis were a Ki-67 of more than 5%, previous treatment with interfero

28 -SKIE, a deep learner-based approach where a Ki-67 index heatmap is generated throughout the tumor.

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

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

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

32 9 mm small cell neuroendocrine cancer with a Ki-67 index of 80%.

33 Patients with a Ki-67 index of greater than 55% (n = 11) had a median PF

34 For G3 NENs with a Ki-67 index of less than or equal to 55% (n = 53), the m

35 ding a subgroup analysis for patients with a Ki-67 index of less than or equal to 55% and a Ki-67 ind

36 was promising, especially in patients with a Ki-67 index of less than or equal to 55% and even in pat

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 (G3) neuroendocrine neoplasms (NENs) with a Ki-67 proliferation index of greater than 20%.

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 sum tests assessed uptake differences across Ki-67 thresholds, and Spearman correlation tested associ

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

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

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

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

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

48 )-16b enantiomer retaining all the affinity (Ki = 15.1 nM), as predicted earlier by molecular modelin

49 SUV(max), and SUV ratios were tested against Ki-67.

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

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

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

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

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

59 during mitotic exit the brushes collapse and Ki-67 promotes chromosome clustering.

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

61 CRP and Ki-67 index were also prognostic and remained independen

62 in jejunal epithelium at the ulcer edge, and Ki-67 staining was unchanged in jejunal mucosa.

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

64 aining the mucosa for phosphorylated FAK and Ki-67 and measuring mucosal ulcer area, serum creatinine

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

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

67 roliferative markers, phospho-histone H3 and Ki-67, were substantially suppressed in samples treated

68 feration were quantified using histology and Ki-67 immunohistochemistry.

69 immunohistochemical (p16, SOX10, HMB45, and Ki-67) findings were recorded.

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

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

72 e activation, epidermal thickness, KRT16 and Ki-67 expression, and immune cell infiltrates CD3(+)/CD8

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

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

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

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

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

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

79 nd counting the number of Ki-67-positive and Ki-67-negative tumor cells within a subjectively picked

80 strogen receptor, progesterone receptor, and Ki-67 labeling index expression levels.

81 ertib reduced phosphorylation of RPS6KB1 and Ki-67 and increased levels of cleaved caspase 3 in tumor

82 CK7, CK14, CK19, CD3, CD20, S100, and Ki-67 antibodies were used for comparative immunohistoch

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

84 ly studied PD-L1 tumour proportion score and Ki-67 index in pleural biopsies or cytologies from 123 p

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

86 Myriocin and SKI-II decreased tumor size and Ki-67 staining of xenografted MKL-1 and WaGa tumors on t

87 sessed immunohistochemically by survivin and Ki-67 staining.

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

89 ation tested associations between uptake and Ki-67.

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

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

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

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

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

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

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

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

98 Complete cell-cycle arrest was defined as Ki-67 less than or equal to 2.7%.

99 cell cycle were evaluated by the MTS assay, Ki-67 staining, and flow cytometry, respectively.

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

101 n-KI-Estimator (SKIE), a pipeline automating Ki-67 index quantitation via whole-slide image (WSI) ana

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

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

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

105 6 and 2.0 times higher in the parametric BFM Ki images and 2.3 and 3.0 times in the Patlak images tha

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

107 ls to proliferate (via the protein biomarker Ki-67) and to squeeze through microfluidic channels, mim

108 pound cellular activity correlated with both Ki and koff.

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

110 reased proliferative rates, as determined by Ki-67 labeling, and reduced levels in the central tumor

111 due to a low proliferation level measured by Ki-67 staining.

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

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

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

115 re, its inhibitor-TTR dissociation constant (Ki) was used to estimate inhibition levels of T4-TTR bin

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

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

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

119 for activation (HLA-DR(+) CD38(+)), cycling (Ki-67(+)), degranulation (CD107a(+)), and the immune che

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

121 imals whose tumours also exhibited decreased Ki-67 expression.

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

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

124 he number of positive nodes, tumor diameter, Ki-67, and vascular/perineural invasion.

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

126 ron Emission Tomography scan to measure DSC (Ki(cer)) prior to antipsychotic treatment.

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

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

129 ive CatS inhibitors with picomolar enzymatic Ki values and nanomolar functional activity in human Raj

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

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

132 in the viral reservoir; these cells express Ki-67 at levels similar to or higher than the same cells

133 dx1(+)/Ptf1a(+) lineage beta-cells had fewer Ki-67(+) proliferating beta-cells, and expressed higher

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

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

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

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

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

139 mpared with ex vivo immunohistochemistry for Ki-67.

140 cells in these eyes were immunopositive for Ki 67 and incorporated BrdU.

141 g tumor tissue single-immunostained (SS) for Ki-67 and counting the number of Ki-67-positive and Ki-6

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

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

144 ceptor 2 protein, p53 tumor suppressor gene, Ki-67 proliferation marker, and tumor-infiltrating lymph

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

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

147 higher-grade (grade 3 [G3]) NENs have a high Ki-67 (>20%) and shorter overall survival (<1 y).

148 ith poor prognostic features, such as a high Ki-67 index (p = 0.048), a high TNM stage (p = 0.012), a

149 ositive staining for GFAP, Olig2, and a high Ki-67 proliferative index.

150 In the entire cohort, high Ki-67 (OR 1.369; 95% CI 1.121-1.673; P = 0.002), N-stage

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

152 Tumors stratified into the high-Ki-67 (>=20%) group had SUV(max) greater than the low-Ki

153 Conclusion: Higher Ki-67 values, as well as higher CgA levels and previous

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

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

156 20l (SLC4011540) (hSphK1 Ki = 120 nM, hSphK2 Ki = 90 nM) and SphK2 inhibitor 20dd (SLC4101431) (Ki =

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

158 rozole groups (A v B + C + D) were change in Ki-67 (protein encoded by the MKI67 gene; immunohistoche

159 Median log-fold change in Ki-67 was greater with palbociclib plus letrozole compar

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

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

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

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

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

165 from non-tumor cells can lead to inaccurate Ki-67 indices and possibly incorrect tumor grades.

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

167 ranching of the mammary glands and increased Ki-67 staining.

168 sEVs elicited by oxidative stress increased Ki-67 expression of mesenchymal stem cells (MSCs); cytos

169 grade 2 NENs have a low proliferation index (Ki-67 < 20%) and longer overall survival (>10 y), wherea

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

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

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

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

174 Interestingly, Ki-67 index and CRP influenced the prognostic power of P

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

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

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

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

179 ciated with PFS were primary tumor location, Ki-67 percentage, neutrophil-to-lymphocyte ratio, alkali

180 They also displayed low Ki-67, CD49d, cell-surface immunoglobulin M (IgM) expres

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

182 20%) group had SUV(max) greater than the low-Ki-67 (<20%) group (P = 0.02).

183 chemistry demonstrates a significantly lower Ki-67 proliferation index in size matched larynx SCC com

184 d reduced levels of the proliferation marker Ki-67 as well as decreased expression of leptin-regulate

185 VEGFA) and CD31 and the proliferation marker Ki-67.

186 s the expression of the proliferation marker Ki-67.

187 s and expression of the proliferative marker Ki-67 and the reactive oxygen species scavenger receptor

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

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

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

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

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

193 tissue-based assay of proliferation, namely Ki-67 expression.

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

195 epidermal growth factor receptor type 2/neu, Ki-67) were extracted and compared with preoperative MRI

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

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

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

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

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

201 ained (DS) slides to improve the accuracy of Ki-67 index quantitation in GI-NETs: (1) Synaptophysin-K

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

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

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

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

206 y-like CD4(+) T cells had high expression of Ki-67, indicative of cell division, and CD5, a surrogate

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

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

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

210 ed (SS) for Ki-67 and counting the number of Ki-67-positive and Ki-67-negative tumor cells within a s

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

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

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

214 sion of p57 with concomitant upregulation of Ki-67 while maintaining glucose-sensing functionality.

215 es from the nucleus after mitosis depends on Ki-67-regulated chromosome clustering.

216 There was a significant effect of group on Ki(cer) in associative striatum (F((2, 37)) = 7.9, p = 0

217 ing, HPV E6/E7 messenger RNA (mRNA), and p16/Ki-67 dual stain in a population of HIV+ MSM.

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

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

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

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

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

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

224 effect in generating frequent polyfunctional Ki-67(+), IFN-gamma(+), CD107(+), and CD8(+) T cells.

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

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

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

228 t eligibility criteria included GEP primary, Ki-67 of 20% or less, and first-line SSA monotherapy for

229 Proliferating (Ki-67+) CD8 T cells expressed high levels of granzyme B

230 suppression of malignant cell proliferation (Ki-67) in primary ER-positive BC, but did not increase t

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

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

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

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

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

236 We quantified both proliferative (Ki-67 immunohistochemistry) and immature (doublecortin i

237 sm that involves the surfactant-like protein Ki-67.

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

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

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

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

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

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

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

245 etastasis, which was associated with reduced Ki-67 level and augmented CD8+ T cell infiltration in xe

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

247 </= 0.67; P = .008), whereas no significant Ki-67 response was observed for pictilisib in luminal A

248 0 nM) and SphK2 inhibitor 20dd (SLC4101431) (Ki = 90 nM, 100-fold SphK2 selectivity).

249 ranting a lead compound with a submicromolar Ki.

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

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

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

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

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

255 The Ki values correlated well with ERbeta expression but not

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

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

258 The Ki-67 index is an established prognostic factor in gastr

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

260 Chromogranin A expression was lost, and the Ki-67 index increased to 90%.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 troduce two computational tools that utilize Ki-67 and synaptophysin double-immunostained (DS) slides

276 K-RAS (V-Ki-ras2 Kirsten rat sarcoma viral oncogene) gene was pre

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

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

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

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

281 2.8 min) and D-alpha-(1'-fluoro)vinyllysine (Ki = 470 +/- 30 muM; t1/2 = 3.6 min).

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

283 nical manifestation of IRI, these cells were Ki-67+IL-18R1+ and could be expanded ex vivo in response

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

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

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

287 ribution volume ratio did not correlate with Ki-67 (P > 0.05).

288 Dnmt1 expression was correlated with Ki-67 expression (Spearman correlation, 0.483; P < 0.001

289 cted SUV(max) was positively correlated with Ki-67 for invasive ductal carcinoma (rho = 0.51, P = 0.0

290 V(max) exhibited a positive correlation with Ki-67 across all breast cancer subtypes (rho = 0.46, P =

291 They rapidly entered the cell cycle with Ki-67-positive staining, which started at 1 h and peaked

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

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

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

295 bound to chromatin through interaction with Ki-67 in response to IR treatment and facilitates the re

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

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

298 .5% compared with 96.2% for 29 patients with Ki-67 LI < 15% (log-rank P = .002), and the rate of rela

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

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