ライフサイエンスコーパス: proliferating-cell

1 mes are essential for protein degradation in proliferating cells.

2 ts, primarily by inhibiting DNA synthesis in proliferating cells.

3 required to maintain metabolic stability in proliferating cells.

4 e normally activated during cell division in proliferating cells.

5 be higher in spontaneously quiescent versus proliferating cells.

6 duced G2 checkpoint control and apoptosis in proliferating cells.

7 alterations and genetic diversity in normal proliferating cells.

8 ses the expression of some of these genes in proliferating cells.

9 ested cells, whereas the opposite is true in proliferating cells.

10 e, highly vascularized tumors that contained proliferating cells.

11 cells, including at genes also repressed in proliferating cells.

12 eneity, and spatial distribution of necrotic/proliferating cells.

13 herapeutic agents that indiscriminately kill proliferating cells.

14 olysis, and a Warburg metabolic phenotype in proliferating cells.

15 tant functions in cytokinesis in mitotically proliferating cells.

16 nd contained a higher frequency of TNFR2(hi) proliferating cells.

17 o undergird future work on the metabolism of proliferating cells.

18 uired to fulfill the high demands of rapidly proliferating cells.

19 formation on metabolic flux distributions of proliferating cells.

20 uvate kinase (PK) in directing metabolism of proliferating cells.

21 limiting the spread of enveloped viruses in proliferating cells.

22 tablishing highly active metabolic states in proliferating cells.

23 activator MYB3R4 was in complex with E2FB in proliferating cells.

24 lization and availability of beta-catenin in proliferating cells.

25 he time window of mitotic gene expression in proliferating cells.

26 tivates the expression of IGFBP3 in actively proliferating cells.

27 n family, known to regulate cell division in proliferating cells.

28 ining cellular redox homoeostasis in rapidly proliferating cells.

29 ating cells and the latter being enhanced in proliferating cells.

30 ding cells were at least as high as those of proliferating cells.

31 s peroxide-dependent uptake and retention in proliferating cells.

32 KB1 induces a progrowth metabolic program in proliferating cells.

33 ed villus height and a compensatory shift in proliferating cells.

34 ll viability was maintained but declined for proliferating cells.

35 tissue maintenance by a single population of proliferating cells.

36 and reveals plasticity in lipid synthesis of proliferating cells.

37 reduce genome-wide DNA methylation levels in proliferating cells.

38 d DNA replication during latent infection in proliferating cells.

39 lular geometry maintenance in populations of proliferating cells.

40 surement of deuterium enrichment into DNA of proliferating cells.

41 Tumors initiate when a population of proliferating cells accumulates a certain number and typ

42 Proliferating cells acquire genome alterations during th

43 Proliferating cells actively control their size by mecha

44 Proliferating cells actively coordinate growth and cell

45 Proliferating cells adjust their cell size depending on

46 2 may neutralize and elevate p53 in actively proliferating cells and also provides a rationale for us

47 PKM2 is a known metabolic regulator in proliferating cells and cancer.

48 pression of LAT induced a reduction of brain proliferating cells and concomitant microcephaly.

49 SL baboons had lower numbers of proliferating cells and immature neurons than socially d

50 ineages showed a reduction in populations of proliferating cells and intermediate cells, and overall

51 ered every 3 days to determine the number of proliferating cells and the number of newly maturing neu

52 protein accumulation pattern correlated with proliferating cells and was sub-localized to the nucleus

53 colony physically constrains the packing of proliferating cells and, thus, controls colony shape.

54 ped in-house, allowing for quantification of proliferating cells, and BM blood volume was estimated b

55 l gap, number of macrophages, blood vessels, proliferating cells, and collagen content in the connect

56 icited a relative reduction in tumor growth, proliferating cells, and microvessel density.

57 two distinct subsets, one that is induced in proliferating cells, and repressed otherwise, and anothe

58 In proliferating cells, APOBEC3A modestly elicited ATR but

59 Patterns of epigenetic heritability in proliferating cells are important for understanding long

60 Highly proliferating cells are particularly dependent on glucos

61 , protein, and fatty acid synthesis found in proliferating cells as well as for neutralizing high lev

62 these tissues contain a small proportion of proliferating cells (assessed by both Ki67 and PCNA) but

63 The proliferating cells attained a steady state, their slow

64 In proliferating cells, B-Myb interacts with the MuvB core

65 During ontogeny, proliferating cells become restricted in their fate thro

66 ata indicate that La is required not only in proliferating cells but also in nondividing postmitotic

67 to be completely reprogrammed to support the proliferating cells, but 3 additional clusters of EBV-re

68 P-1) is overexpressed in various cancers and proliferating cells, but the functional significance rem

69 Nucleotide synthesis is essential to proliferating cells, but the preferred precursors for de

70 omal fragments are generally eliminated from proliferating cells, but we know little about how mammal

71 us RNA-Seq (sNuc-Seq) with pulse labeling of proliferating cells by 5-ethynyl-2'-deoxyuridine (EdU) t

72 that methylation of newly synthesized DNA in proliferating cells can be altered by oxidants that targ

73 In proliferating cells, cell size is regulated by coordinat

74 tional compensation is most prominent in non-proliferating cells, clearly delineating two temporally

75 In proliferating cells, cohesin also mediates sister chroma

76 ited reduced cell density and fewer actively proliferating cells compared to the control and bexarote

77 sive crypt degeneration and lower numbers of proliferating cells compared with wild-type control mice

78 When proliferating cells complete mitosis, a fraction of newl

79 It is not clear how stem and proliferating cells cope with accumulating endogenous DN

80 lockade of WNT/beta-catenin signaling in the proliferating cells decreases proliferation activity, bu

81 However, proliferating cells depend on growth-factor-induced incr

82 e concurrent with myocardial infiltration of proliferating cells displaying a poorly differentiated m

83 We find that proliferating cells divide at a similar rate, and place

84 al precursor cells that can be maintained as proliferating cells due to the expression of a tetracycl

85 It is unclear how proliferating cells elicit suppression on cell prolifera

86 (ADC) distinguishes meningioma regions with proliferating cells enriched for developmental gene expr

87 tors involved in renal repair, the number of proliferating cells, especially at the injured edge, the

88 tive DNA damage response are well studied in proliferating cells, especially with regards to the deve

89 iferating human CD4(+) T cells, we show that proliferating cells express multiple IC molecules at hig

90 Normal proliferating cells express sense (SncmtRNA) and antisen

91 Latent infection was enriched in proliferating cells expressing PD-1.

92 elonging to the TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTOR (TCP) protein family are known

93 TCP (for Teosinte branched1, Cycloidia, and Proliferating cell factor) genes from petunia, and have

94 we report that teosinte branched1/cycloidea/proliferating cell factor1-20 (TCP20) and NIN-like prote

95 egulated TCP (TEOSINTE BRANCHED 1, CYCLODEA, PROLIFERATING CELL FACTORS) transcription factors, notab

96 In proliferating cells, formin inhibition abolishes nuclear

97 found a significantly greater percentage of proliferating cells from mice fed the high-fat/high-chol

98 hin the niche, but by prematurely displacing proliferating cells from their normal epithelial milieu.

99 Rapidly proliferating cells growing by glucose fermentation must

100 cells; however, in senescent cells, but not proliferating cells, H4K20me3 enrichment at gene bodies

101 ough the importance of folate metabolism for proliferating cells has been long recognized and attribu

102 zyme and appears on the surface of cancerous proliferating cells, has been used as a diagnostic bioma

103 Proliferating cells have been found along the entire ven

104 a potential onco-target in specifically high-proliferating cells in Burkitt's lymphoma (BL).

105 ulture apparatus (Nutrostat) for maintaining proliferating cells in low-nutrient media for long perio

106 The rapidly proliferating cells in plant meristems must be protected

107 During early gonadogenesis, proliferating cells in the coelomic epithelium (CE) give

108 Proliferating cells in the ventricular zone stem cell co

109 ;CD11b+ macrophages accounted for ~20-40% of proliferating cells in untreated tumors.

110 5-bromo-2'-deoxyuridine (BrdU; a marker for proliferating cells) in vivo, consequently interfering w

111 severe damage to tissues containing actively proliferating cells, including bone marrow and the gastr

112 istration and non-specific damages to highly proliferating cells, including immune cells.

113 Rapidly proliferating cells increase glycolysis at the expense o

114 ivity and prevents the outgrowth of cilia in proliferating cells, independent of Aurora A and HDAC6.

115 nals control keratinocyte differentiation in proliferating cells independently of actual DNA damage.

116 phosphate (SAICAR), a metabolite abundant in proliferating cells, induces PKM2's protein kinase activ

117 s additional evidence that the metabolism of proliferating cells is adapted to facilitate producing n

118 ll orders of life, cell cycle progression in proliferating cells is dependent on cell growth, and the

119 s suggest that increased (18)F-FLT uptake by proliferating cells is due to a greater fraction of (18)

120 is modification controls SAMHD1 functions in proliferating cells is not known.

121 we show that a major role of respiration in proliferating cells is to provide electron acceptors for

122 ata argue a major function of respiration in proliferating cells is to support aspartate synthesis.

123 ent state of replicative arrest in otherwise proliferating cells, is a hallmark of aging and has been

124 l nervous system (CNS)-derived conditionally proliferating cell line that can be differentiated into

125 n also promote adaptability and diversity in proliferating cell lineages, although whether WGD is ben

126 capture the transcriptional dynamics within proliferating cells, methods to differentiate nascent tr

127 pproach that leverages error-prone PCR and a proliferating cell model to identify such gain-of-functi

128 We observed that, in the limited subset of proliferating cells, most displayed fermentation of gluc

129 To maintain the integrity of the genome, proliferating cells must be able to block progression th

130 Proliferating cells must coordinate central metabolism w

131 Proliferating cells must cross a point of no return befo

132 bacteria can promote sustained expression of proliferating cell nuclear Ag and that human PMN undergo

133 polarization, PMN-SA had sustained levels of proliferating cell nuclear Ag expression, absence of cas

134 interacting partners of EndoQ and identified Proliferating Cell Nuclear Angigen (PCNA).

135 wn as the PIP degron, which binds DNA-loaded proliferating cell nuclear antigen (PCNA(DNA)) and recru

136 Subsequently, proliferating cell nuclear antigen (PCNA) activates MutL

137 During DNA replication, proliferating cell nuclear antigen (PCNA) adopts a ring-

138 Proliferating cell nuclear antigen (PCNA) and alpha-smoo

139 Overexpression of cyclins and proliferating cell nuclear antigen (PCNA) and evidence f

140 ociated with decreased platinum drug-induced proliferating cell nuclear antigen (PCNA) and FANCD2 mon

141 Pol delta binds to proliferating cell nuclear antigen (PCNA) and functions

142 Mtp53 increased the level of proliferating cell nuclear antigen (PCNA) and minichromo

143 th muscle mass, paired box protein 7 (Pax7), proliferating cell nuclear antigen (PCNA) and nicotinami

144 omethylates non-histone substrates including proliferating cell nuclear antigen (PCNA) and promotes c

145 through its interactions with two proteins, Proliferating Cell Nuclear Antigen (PCNA) and Replicatio

146 the essential replication accessory protein proliferating cell nuclear antigen (PCNA) and the scaffo

147 e show that the ternary complexes containing proliferating cell nuclear antigen (PCNA) and two non-cl

148 Replication factor C (RFC) and the proliferating cell nuclear antigen (PCNA) are additional

149 replication factor C (RFC) and sliding clamp proliferating cell nuclear antigen (PCNA) are both essen

150 In this study, we identified the proliferating cell nuclear antigen (PCNA) as a nIGF-1R-b

151 shown previously that the sliding DNA clamp proliferating cell nuclear antigen (PCNA) associates wit

152 In human cells, the DNA replication factor proliferating cell nuclear antigen (PCNA) can be conjuga

153 n multiple transient events in the reaction: proliferating cell nuclear antigen (PCNA) clamp binding/

154 nd the homotrimeric Saccharomyces cerevisiae proliferating cell nuclear antigen (PCNA) clamps using s

155 of alpha-smooth muscle actin (alpha-SMA) and proliferating cell nuclear antigen (PCNA) compared with

156 inding protein 1 (Ebp1), a key in regulating proliferating cell nuclear antigen (PCNA) expression and

157 s a mismatch, MutSalpha/beta, and DNA-loaded proliferating cell nuclear antigen (PCNA) for activation

158 plication forks through its interaction with proliferating cell nuclear antigen (PCNA) for nucleosome

159 Proliferating cell nuclear antigen (PCNA) forms a trimer

160 Proliferating cell nuclear antigen (PCNA) forms a trimer

161 xyuridine (EdU) labeling as well as Ki67 and proliferating cell nuclear antigen (PCNA) immunofluoresc

162 Proliferating cell nuclear antigen (PCNA) is a highly co

163 Proliferating cell nuclear antigen (PCNA) is a protein w

164 Proliferating cell nuclear antigen (PCNA) is a sliding c

165 The sliding clamp proliferating cell nuclear antigen (PCNA) is an indispen

166 Proliferating cell nuclear antigen (PCNA) lies at the ce

167 Proliferating cell nuclear antigen (PCNA) loading by rep

168 early and mid-S phase and during DNA repair, proliferating cell nuclear antigen (PCNA) loading onto D

169 c expression of USP7 promoted the UV-induced proliferating cell nuclear antigen (PCNA) monoubiquitina

170 ily TLS polymerases to damaged DNA relies on proliferating cell nuclear antigen (PCNA) monoubiquityla

171 loading of cyclin-dependent kinase (CDK) and proliferating cell nuclear antigen (PCNA) onto chromatin

172 The sliding clamp proliferating cell nuclear antigen (PCNA) plays a vital

173 ns wherein the interaction between RECQ5 and proliferating cell nuclear antigen (PCNA) promotes RAD18

174 Proliferating cell nuclear antigen (PCNA) recruits Pol d

175 NA polymerase delta (Pol delta) bound to the proliferating cell nuclear antigen (PCNA) replicates the

176 e lagging strand template and anchors to the proliferating cell nuclear antigen (PCNA) sliding clamp

177 TLS requires selective monoubiquitination of proliferating cell nuclear antigen (PCNA) sliding clamps

178 eration in calcified arteries as assessed by proliferating cell nuclear antigen (PCNA) staining was a

179 in the recruitment of the DNA clamp protein proliferating cell nuclear antigen (PCNA) to DNA lesions

180 ective bioPROTAC against an oncology target, proliferating cell nuclear antigen (PCNA) to elicit rapi

181 ly, we found that AKT-mediated modulation of Proliferating Cell Nuclear Antigen (PCNA) ubiquitylation

182 show that Bub1 constitutively interacts with proliferating cell nuclear antigen (PCNA) via a highly c

183 cleotide by DNA polymerase alpha holoenzyme, proliferating cell nuclear antigen (PCNA), a homotrimeri

184 Here, we show that monoubiquitinated Proliferating Cell Nuclear Antigen (PCNA), a marker of s

185 We previously described that proliferating cell nuclear antigen (PCNA), a nuclear sca

186 entry is similar to that described for human proliferating cell nuclear antigen (PCNA), a small ubiqu

187 from Thermoplasma acidophilum interact with proliferating cell nuclear antigen (PCNA), an essential

188 n of Kdm4d impairs the recruitment of Cdc45, proliferating cell nuclear antigen (PCNA), and polymeras

189 ion, as evidenced by stabilization of Mcl-1, proliferating cell nuclear antigen (PCNA), and pro-caspa

190 reaction requiring Msh2-Msh6 (or Msh2-Msh3), proliferating cell nuclear antigen (PCNA), and replicati

191 Proliferating cell nuclear antigen (PCNA), bone sialopro

192 ssive replication with the replication clamp proliferating cell nuclear antigen (PCNA), respectively.

193 Y-family polymerases, Poliota interacts with proliferating cell nuclear antigen (PCNA), Rev1, ubiquit

194 ammatory cytokines, the proliferation marker proliferating cell nuclear antigen (PCNA), the anti-infl

195 A We show that Rad51 inhibits recruitment of proliferating cell nuclear antigen (PCNA), the platform

196 Proliferating cell nuclear antigen (PCNA), the processiv

197 The expression levels of proliferating cell nuclear antigen (PCNA), vascular endo

198 Lack of SIM, but not proliferating cell nuclear antigen (PCNA)-interacting mo

199 the density of mitotic figures, and BrdU and proliferating cell nuclear antigen (PCNA)-reactive cells

200 action between the Enok complex and the Elg1 proliferating cell nuclear antigen (PCNA)-unloader compl

201 increased expression of Nox4, TNF-alpha, and proliferating cell nuclear antigen (PCNA).

202 d together they enhance the transcription of proliferating cell nuclear antigen (PCNA).

203 strongly stimulated by its interaction with proliferating cell nuclear antigen (PCNA).

204 is dependent on the interaction of TDG with proliferating cell nuclear antigen (PCNA).

205 nse (p.Ser228Ile) sequence alteration of the proliferating cell nuclear antigen (PCNA).

206 in conjunction with the processivity factor proliferating cell nuclear antigen (PCNA).

207 s (RLCs) mediate chromatin engagement of the proliferating cell nuclear antigen (PCNA).

208 Small molecule inhibitors of proliferating cell nuclear antigen (PCNA)/PCNA interacti

209 be stimulated by processivity clamps such as proliferating cell nuclear antigen (PCNA); however, the

210 we explore the interactions of S. cerevisiae Proliferating Cell Nuclear Antigen (yPCNA) with modified

211 In the absence of NKT cells hepatic proliferating cell nuclear antigen and cyclin B1 decreas

212 Whereas association with proliferating cell nuclear antigen and participation in

213 We further show that proliferating cell nuclear antigen and the nucleosome co

214 show that NEIL1 binarily interacts with the proliferating cell nuclear antigen clamp loader replicat

215 l neurogenesis, measured by doublecortin and proliferating cell nuclear antigen expression, was also

216 instability 1 are responsible for unloading proliferating cell nuclear antigen from newly synthesize

217 incorporation and proportionate increases in proliferating cell nuclear antigen gene expression.

218 ither translesion DNA synthesis initiated by proliferating cell nuclear antigen monoubiquitination or

219 Proliferating cell nuclear antigen monoubiquitination po

220 The eukaryotic DNA polymerase sliding clamp, proliferating cell nuclear antigen or PCNA, is a ring-sh

221 LR assessed by Ki-67 and proliferating cell nuclear antigen was markedly decrease

222 to promote senescence, whereas cyclin D1 and proliferating cell nuclear antigen were decreased to red

223 Expression of hepatic cyclin B1 and proliferating cell nuclear antigen were evaluated by Wes

224 Ki-67 and proliferating cell nuclear antigen were used to measure

225 ersely, nascent DNA replication foci and the proliferating cell nuclear antigen(PCNA) protein have a

226 tethers it to the leading strand, and PCNA (proliferating cell nuclear antigen) binds tightly to Pol

227 Proliferating cell nuclear antigen, a DNA sliding clamp,

228 In reconstituted human systems, MutSalpha, proliferating cell nuclear antigen, and replication fact

229 were determined by methyltetrazolium, Ki-67, proliferating cell nuclear antigen, bromodeoxyuridine, a

230 olution dynamics of the human clamp protein, proliferating cell nuclear antigen, by monitoring the ch

231 o examine the mRNA and protein expression of proliferating cell nuclear antigen, cyclin D1, E-cadheri

232 and expression of the proliferation marker, proliferating cell nuclear antigen, indicative of intest

233 d DNA ligase I, which compete for binding to proliferating cell nuclear antigen, is critical to preve

234 esis phase of the cell cycle (e.g. P. patens proliferating cell nuclear antigen, ribonucleotide reduc

235 resulted in accumulation of chromatin-bound proliferating cell nuclear antigen, slowed cell division

236 synthesis as essential for cccDNA formation: proliferating cell nuclear antigen, the replication fact

237 gy with Cavalieri estimation; apoptosis with proliferating cell nuclear antigen, TUNEL, and caspase a

238 ll microscopy of cells harboring fluorescent proliferating cell nuclear antigen, we confirmed that 8a

239 (MMP) 9-, and MMP13-positive cells and more proliferating cell nuclear antigen- and pSMAD5-positive

240 or how nucleosome binding protects Set8 from proliferating cell nuclear antigen-dependent degradation

241 cluding the catalytic polymerase domain, the proliferating cell nuclear antigen-interacting region, t

242 h cyclin-dependent kinase 2 (CDK2), CDK4 and proliferating cell nuclear antigen.

243 polymerase-alpha and the replication clamp, proliferating cell nuclear antigen.

244 D1, and the cell cycle genes CYCLIN A2;1 and PROLIFERATING CELL NUCLEAR ANTIGEN1 in buds was suppress

245 the first structural characterization of the proliferating-cell-nuclear-antigen-associated factor p15

246 These non-proliferating cells occupy key cellular niches and elabo

247 e characterization of gene expression in the proliferating cells of M. lignano, represented by somati

248 YAP and WPB2 are upregulated in actively proliferating cells of mouse and human epidermis and cSC

249 Proliferating cells often have increased glucose consump

250 M proteins limit Hippo regulation of YAP, in proliferating cells only, by sequestering a cytosolic Hi

251 Non-proliferating cells oxidize respiratory substrates in mi

252 nd PCL3 are E2F-regulated genes expressed in proliferating cells, PCL1 is a p53 target gene predomina

253 In proliferating cells, PhIP treatment increased the freque

254 diminished, correlating with the loss of the proliferating cell population of germinal zones.

255 etween these mechanisms can push an actively proliferating cell population to transition into a weakl

256 s chromatin patterns are being duplicated in proliferating cells, predisposing them to tumorigenesis.

257 t DC cells are recent progeny of selectively proliferating cells present prior to morphogenesis and t

258 We hypothesized that proliferating cells produce virions without HIV replicat

259 In senescent cells, but not proliferating cells, promoters of active genes are excep

260 Together, our findings suggest that proliferating cells rely on both MDH1 and LDH to repleni

261 Lipids are important nutrients that proliferating cells require to maintain energy homeostas

262 tion of normal cells into malignant, rapidly proliferating cells requires major alterations in cell p

263 In contrast to the role of nuclear RNF8 in proliferating cells, RNF8 operates in the cytoplasm in n

264 In proliferating cells, SAFA and PANDA recruit PRC complexe

265 likely to arrest than to die, whereas slowly proliferating cells showed a higher probability of death

266 Proliferating cells showed undifferentiated morphology a

267 our results suggest that Ki-67 expression in proliferating cells spatially organises heterochromatin,

268 biosynthetic and energetic demand of rapidly proliferating cells such as cancer cells is met by metab

269 ation, similar to that seen in other rapidly proliferating cells such as cancer cells.

270 Rapidly proliferating cells switch from oxidative phosphorylatio

271 ling centres are specialized clusters of non-proliferating cells that direct the development of many

272 In those proliferating cells that do make a cilium, it is a trans

273 together with perforin and (2) induction of proliferating cells that had greater capacity to produce

274 vulnerability of proteostasis maintenance in proliferating cells that may be compromised by diverse g

275 n program, which culminates in immortalized, proliferating cells that partially resemble plasmablasts

276 The proportion of proliferating cells that were Olig2(+) was similar throu

277 In proliferating cells, the largest contributor to cytosoli

278 Unknown mechanisms commit rapidly proliferating cells to post-mitotic terminal differentia

279 ence, but the contribution of these clonally proliferating cells to the rebounding virus is unknown.

280 s, and with KLF4 in differentiating, but not proliferating, cells to promote expression of specialize

281 As proliferating cells transit from interphase into M-phase

282 Although its role in proliferating cell types and tissues has been extensivel

283 Proliferating cells, typically considered "nonexcitable,

284 RNA was extracted from proliferating cells versus differentiated neural cells a

285 insight about proteins apportioned for newly proliferating cells versus for somatic maintenance.

286 es, and the resolution of SEs in mitotically proliferating cells via SCML2, a germline-specific Polyc

287 y all animals and only limited cell death of proliferating cells was found within the generative zone

288 In proliferating cells, we found that hnRNPA1 binds and des

289 These proliferating cells were able to produce HAP stem cell c

290 However, proliferating cells were found only in the CMZ of turtle

291 9-23 peptide in proliferation assays and the proliferating cells were highly enriched in certain T-ce

292 ion of mTORC1 and likely most predominant in proliferating cells where mTORC1 is highly active.

293 to the nucleus and endogenously expressed in proliferating cells whereas p22(CBX7) was localized to t

294 assical signaling via RelA was essential for proliferating cells, whereas the alternative signaling p

295 ccumulation of SMN in Cajal bodies of intact proliferating cells, which actively assemble snRNPs, as

296 resses stem cell-promoting genes in actively proliferating cells, which is essential for the progress

297 small number of stem cells or is composed of proliferating cells with approximate phenotypic equivale

298 unohistochemistry and identify central canal proliferating cells with Ki67 and newly generated cells

299 Hdac7 was highly expressed in proliferating cells within the growth plate.

300 sponses to cisplatin and suggest that slowly proliferating cells within tumors may be acutely vulnera