ライフサイエンスコーパス: hyperproliferation

1 oplasmic reticulum stress, inflammation, and hyperproliferation.

2 om binding to the kinetochore does not cause hyperproliferation.

3 estored microabscess formation and epidermal hyperproliferation.

4 oxide synthase expression, and keratinocyte hyperproliferation.

5 uses cutaneous inflammation and keratinocyte hyperproliferation.

6 ced paradoxical ERK activation, resulting in hyperproliferation.

7 catenin, which maintain Hras(G12V)-dependent hyperproliferation.

8 at signaling in the regulation of intestinal hyperproliferation.

9 stion revolves around the nature of cellular hyperproliferation.

10 preting studies of both normal and malignant hyperproliferation.

11 of activated BRAFV600E resulted in astrocyte hyperproliferation.

12 and retinal degeneration associated with RPE hyperproliferation.

13 geing intestines required Wg and Myc for ISC hyperproliferation.

14 crease in basal cell number and luminal cell hyperproliferation.

15 , over time, could not prevent CD4(+) T cell hyperproliferation.

16 Egfr signaling suppresses Apc1-dependent ISC hyperproliferation.

17 ssociated with diminished p21 expression and hyperproliferation.

18 liminated cilia, and many (not Kif3a) caused hyperproliferation.

19 activation and cell-cycle arrest to prevent hyperproliferation.

20 2+)](i) in cholangiocytes is associated with hyperproliferation.

21 ar senescence, whereas in others it produces hyperproliferation.

22 eases, cyst formation involves cholangiocyte hyperproliferation.

23 in the surface pit epithelium, resulting in hyperproliferation.

24 ns junction component alphaE-catenin lead to hyperproliferation.

25 cts may be avoided through control of B-cell hyperproliferation.

26 CDK4-induced, but not myc-induced epidermal hyperproliferation.

27 dent of their ability to prevent unwarranted hyperproliferation.

28 bined Mek1/2 loss also abolished Raf-induced hyperproliferation.

29 rmalizes KITD814V-induced ligand-independent hyperproliferation.

30 s significantly inhibited UV-induced rebound hyperproliferation.

31 scale, and exhibits features consistent with hyperproliferation.

32 on and polarity, while c-Jun is required for hyperproliferation.

33 signaling, resulting in SMC misalignment and hyperproliferation.

34 in tumors or in Rasopathies correlates with hyperproliferation.

35 nd by p53-dependent parietal epithelial cell hyperproliferation.

36 metabolism, higher rates of glycolysis, and hyperproliferation.

37 l role of the gut microbiota in heme-induced hyperproliferation.

38 -secreting capacity, suggesting compensatory hyperproliferation.

39 tion of VEGF-R2 tyrosine, thus preventing EC hyperproliferation.

40 contribute to enhanced inflammation and cell hyperproliferation.

41 search for novel agents against keratinocyte hyperproliferation.

42 xposure but are dispensable for premalignant hyperproliferation.

43 ositive cells, but there was no evidence for hyperproliferation.

44 in expression and resulted in ex vivo B-cell hyperproliferation, a phenotype similar to that of the P

45 Prior studies showed that Hmga1 drives hyperproliferation, aberrant crypt formation and polypos

46 ence is thought to be invariably preceded by hyperproliferation, aberrant replication, and activation

47 We did not identify signs of hyperproliferation, abnormal growth, or immune mediated

48 henotype characterized by basal keratinocyte hyperproliferation, acanthosis, hyperkeratosis, intraepi

49 tic ablation of N-cadherin (N-cad KO) caused hyperproliferation, accelerated mPanIN progression, and

50 of CDK2 is sufficient to induce keratinocyte hyperproliferation, activation of CDK2 alone does not in

51 Kidneys from these mice demonstrated marked hyperproliferation and a concomitant increase in label-r

52 scular injury, they display a marked intimal hyperproliferation and abnormal activation of mitogen-ac

53 K14cre;Dlx3(Kin/f) mice exhibited epidermal hyperproliferation and abnormal differentiation of kerat

54 , inflammatory skin disease characterized by hyperproliferation and abnormal differentiation of kerat

55 Knockdown of RUNX1 causes hyperproliferation and abnormal morphogenesis, both of w

56 I receptor (IGF-IR) hyperstimulation induced hyperproliferation and antiapoptotic activities that wer

57 The T cell hyperproliferation and autoimmune phenotypes that manife

58 ay is constitutively active, reversed T-cell hyperproliferation and autoimmunity.

59 e of which results in p38 activation, T cell hyperproliferation and autoimmunity.

60 mediated mTORC1 induction, resulting in cell hyperproliferation and cancer growth.

61 A in maximizing MYC expression, resulting in hyperproliferation and cellular transformation into canc

62 decanoylphorbol-13-acetate-induced epidermal hyperproliferation and closure rates of full-thickness s

63 gen-induced airway smooth muscle cell (ASMC) hyperproliferation and cyclin D1 (an important cell prol

64 homozygous PRKCD mutation results in B-cell hyperproliferation and defective apoptosis with conseque

65 , embryo arrest is associated with endosperm hyperproliferation and delayed development similar to pa

66 strong hyperactivation of ERK1/2, promoting hyperproliferation and depletion of HSCs and expansion o

67 N signaling by Irgm1 is necessary to prevent hyperproliferation and depletion of the stem cell compar

68 nse (DDR), which may follow oncogene-induced hyperproliferation and ensuing DNA replication stress.

69 is responsible for costimulation independent hyperproliferation and excess cytokine production in TRA

70 on or localization could contribute to tumor hyperproliferation and explain how polarity disruption c

71 and expands the Axin2(+) cell pool to cause hyperproliferation and gland hyperplasia.

72 iota is required for heme-induced epithelial hyperproliferation and hyperplasia because of the capaci

73 arget for epidermal diseases associated with hyperproliferation and impaired differentiation.

74 e are hyperactivated and that they displayed hyperproliferation and increased production of interleuk

75 an skin condition characterized by epidermal hyperproliferation and infiltration of multiple leukocyt

76 Epidermal hyperproliferation and inflammation are hallmarks of the

77 nsic mechanism to limit injury-induced crypt hyperproliferation and inflammation-associated colon can

78 coid receptor knockout lung, suggesting that hyperproliferation and lack of maturation of the alveola

79 protein might be deterministic for beta-cell hyperproliferation and led us to hypothesize that Tag mi

80 oriasis-like phenotypes including epithelial hyperproliferation and leukocyte infiltration.

81 Blockade of any of these steps causes hyperproliferation and loss of arterial specification.

82 an oncogenic signaling program that leads to hyperproliferation and loss of polarity in three-dimensi

83 ic microabscess formation and contributes to hyperproliferation and markedly attenuated differentiati

84 ures of human AMKL, including megakaryoblast hyperproliferation and maturation block, thrombocytopeni

85 Full-length APC increases during epithelial hyperproliferation and may represent a homoeostatic resp

86 mmation, mdb3 deficiency resulted in colonic hyperproliferation and mbd3(DeltaG/DeltaG) mice showed m

87 gamma(null) mice, resulted in both thymocyte hyperproliferation and multiple pre- and post-beta-selec

88 ring early development resulted in transient hyperproliferation and overproduction of OPCs but genera

89 mice lacking neutrophils, NK cells displayed hyperproliferation and poor survival and were blocked at

90 short-term hematopoietic stem cells exhibit hyperproliferation and preferential susceptibility to mi

91 strin gene, has been shown to induce colonic hyperproliferation and promote colorectal cancer in mice

92 creased PDK4 is associated with PAH pericyte hyperproliferation and reduced endothelial-pericyte inte

93 This causes hyperproliferation and reduced sensitivity to chemothera

94 n mutants lacking functional Pten suppressed hyperproliferation and released the differentiation arre

95 This in turn leads to hyperproliferation and replication stress.

96 ETS2-overactivation in epidermal-SCs induces hyperproliferation and SCC super-enhancer-associated gen

97 ers (InvEE transgenics) results in epidermal hyperproliferation and skin inflammation.

98 ylphorbol-13-acetate (TPA)-induced epidermal hyperproliferation and skin tumor development.

99 T cells in primary infection resulting from hyperproliferation and stress induced signals, demonstra

100 intestine (Usp28(DeltaIEC)) ameliorated the hyperproliferation and the impaired goblet and Paneth ce

101 im-2 immunoglobulin [Ig]), results in T cell hyperproliferation and the production of Th2 cytokines.

102 nvironment is closely related to BPH stromal hyperproliferation and tissue remodeling with a local hy

103 to c-Myc protein and inhibits c-Myc-induced hyperproliferation and transformation with a concomitant

104 eracts with c-Myc and controls c-Myc-induced hyperproliferation and transformation.

105 ed NPM dramatically stimulates c-Myc-induced hyperproliferation and transformation.

106 dent proliferation signaling to prevent cell hyperproliferation and tumor initiation.

107 some cancers, most notably immortalization, hyperproliferation, and dissemination.

108 resulting in commensal dysbiosis, stem cell hyperproliferation, and epithelial dysplasia.

109 promoting cholangiocarcinoma cell anaplasia, hyperproliferation, and higher malignant grading in this

110 te-derived inflammatory mediators, epidermal hyperproliferation, and increased neutrophil infiltratio

111 ating hallmarks of ICD such as angiogenesis, hyperproliferation, and inflammation.

112 cant leukocytosis with neutrophilia, myeloid hyperproliferation, and myeloid cell infiltration into d

113 phosphorylation, supports ligand-independent hyperproliferation, and promotes promiscuous cooperation

114 stinal stem cell (ISC) signature, progenitor hyperproliferation, and transformation.

115 eads to constitutively active WNT signaling, hyperproliferation, and tumorigenesis.

116 mouse skin led to severe alopecia, epidermal hyperproliferation, and ulceration, without obvious effe

117 in HFK caused inhibition of differentiation, hyperproliferation, and up-regulation of AKT activity in

118 ce of this pathway, the role of NF-kappaB in hyperproliferation appears rooted in its impact on epide

119 that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the patho

120 lation, mTOR-Stat3 signaling, and epithelial hyperproliferation are integrated and simultaneously lin

121 We show that epidermal hyperproliferation arising from p120 loss can be abrogat

122 -jun reverted physiological and pathological hyperproliferation, as well as the increased tumorigenes

123 xide was confirmed in the keratinocyte-based hyperproliferation assay.

124 ) from E47-deficient mice exhibit a striking hyperproliferation associated with a loss of cell cycle

125 m may be important for regulating epithelial hyperproliferation associated with increased SFK activit

126 n Lyn-deficient BMMCs not only represses the hyperproliferation associated with the loss of Lyn but a

127 stitution models, depletion of STRA6 induced hyperproliferation-associated differentiation, resulting

128 By its influence on hyperproliferation-associated differentiation, STRA6 cou

129 , molecules with antimicrobial activity, and hyperproliferation-associated keratins.

130 f inflammatory cells and a reduced epidermal hyperproliferation at lesional skin sites.

131 .6+/-2.8%), whereas gefitinib inhibited this hyperproliferation (BrdUrd, 6.2+/-4.0%; <0.005).

132 T cell hyperproliferation, but not other autoimmune symptoms, w

133 mouse head and neck epithelia gives rise to hyperproliferation, but only a few lesions progress to H

134 entiating MYC to promote G1-S transition and hyperproliferation by downregulating cyclin-dependent ki

135 etween scrib(-) and wild-type cells prevents hyperproliferation by suppressing Yki activity in scrib(

136 Hyperproliferation can initiate dysplastic growth, resul

137 s displayed both basal and GM-CSF-stimulated hyperproliferation compared with cells transduced with v

138 architectural irregularities and epithelial hyperproliferation compared with wild-type mice.

139 cy of miR-31 in keratinocytes inhibits their hyperproliferation, decreases acanthosis and reduces the

140 TEC hyperproliferation development is accelerated in mice gi

141 have marked megakaryocytic progenitor (MkP) hyperproliferation during early fetal liver (FL) hematop

142 utophagy was also critical to maintain early hyperproliferation during metabolic stress.

143 iasis include keratinocyte dysregulation and hyperproliferation, elongated rete ridges, and inflammat

144 In contrast, PTPRF silencing led to cell hyperproliferation, enhanced tumor colony formation in s

145 Exogenous IFN-alpha markedly reduced the hyperproliferation FL-derived MkPs of GATA1s mice in vit

146 nd maintenance of intestinal stem cell (ISC) hyperproliferation following Apc1 loss.

147 nificant increase in epidermal thickness and hyperproliferation following exposure to the tumor promo

148 c-Cbl(-/-) mice exhibit augmented pool size, hyperproliferation, greater competence, and enhanced lon

149 ty of vitamin D analogs in causing epidermal hyperproliferation has been distinguished from that resu

150 e, including in intestinal epithelium, where hyperproliferation has been reported, and in skin epithe

151 mmunoblot analyses of these regions revealed hyperproliferation, impaired terminal differentiation, a

152 s(G12D) in the colonic epithelium stimulated hyperproliferation in a Mek-dependent manner.

153 dation were significantly reduced and caused hyperproliferation in cell lines expressing these mutate

154 h the loss of polarity genes associated with hyperproliferation in Drosophila melanogaster.

155 to abnormal keratinocyte differentiation and hyperproliferation in EKV patient skin.

156 ng that the up-regulation of EGFR stimulates hyperproliferation in epithelia of mice with genetic red

157 y reported that loss of Cbl functions caused hyperproliferation in lymphoid and hematopoietic systems

158 We observed epidermal hyperproliferation in newborn transgenic mice, as eviden

159 ute to excessive Epo signaling and erythroid hyperproliferation in PFCP.

160 ow activated NF-kappaB promotes keratinocyte hyperproliferation in psoriasis is largely unknown.

161 a greater uterine weight gain and epithelial hyperproliferation in response to estradiol (E2) and a s

162 and wound healing and may be a mechanism for hyperproliferation in skin disorders such as psoriasis.

163 ive epidermal acanthosis and inflammatory KC hyperproliferation in the effector phase of CHS.

164 nt response in the absence of FRK-1 leads to hyperproliferation in the endoderm, as is also seen when

165 s after birth, accompanied by blistering and hyperproliferation in the epithelia, similar to the cons

166 years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

167 BPalpha(-/-) FL cells, indicating progenitor hyperproliferation in vitro and in vivo.

168 e absence of ABCG1 in CD4 T cells results in hyperproliferation in vitro, but only when cells are sti

169 nt epidermal changes, including keratinocyte hyperproliferation, incomplete differentiation, and impa

170 condition of haploinsufficiency that led to hyperproliferation, increased adhesion to collagen type

171 EGF) receptor blockade, which resulted in EC hyperproliferation, increased IL-32 three-fold.

172 Cell hyperproliferation, inflammation, and angiogenesis are b

173 vivo model to study the pathogenesis of cell hyperproliferation, inflammation, and angiogenesis.

174 results in the rescue of the epithelial cell hyperproliferation, inflammation, and neovascularization

175 No difference in TPA-induced hyperproliferation, inflammation, or Erk activation was

176 ssociated with inflammation, carcinogenesis, hyperproliferation, invasion, and angiogenesis, we hypot

177 lacking only one of these subunits, and thus hyperproliferation is independent of either reduced MHC

178 cancers, in the majority of sporadic cancers hyperproliferation is likely to play a permissive role i

179 curs at an age (11 weeks) at which epidermal hyperproliferation is most visible and is spatially cont

180 se cells in vitro, suggesting that epidermis hyperproliferation is not epidermal cell-autonomous but

181 Yet at the same time, cellular hyperproliferation is the fundamental pathological condi

182 Hyperproliferation is TNFR1-dependent because Tnfr1 dele

183 cient increased mTOR signaling and astrocyte hyperproliferation is unaffected by Rheb shRNA silencing

184 d elicits epithelial damage and compensatory hyperproliferation, leading to hyperplasia.

185 kin wounds, the K5.CtBP1 epidermis displayed hyperproliferation, loss of E-cadherin, and failed termi

186 oth craniofacial and skin defects, including hyperproliferation, loss of spinous and granular keratin

187 f p85 alpha or Rac2 corrects the promiscuous hyperproliferation observed in response to multiple cyto

188 that the dominant action of GATA1s leads to hyperproliferation of a unique, previously unrecognized

189 ystemic toxicity of IL-15 SA was mediated by hyperproliferation of activated NK cells.

190 Notably, hyperproliferation of ALPS DNT cells is associated with

191 demonstrate a key role of LMP2A in promoting hyperproliferation of B cells by enhancing MYC expressio

192 sence of PTEN, p110beta is important for the hyperproliferation of basal cells in PHTS.

193 lor, a polarized distribution of melanin and hyperproliferation of basal keratinocytes.

194 Hyperproliferation of bile duct epithelial cells due to

195 We observe hyperproliferation of both CD4(+) and CD8(+) T cell subs

196 at the genetic ablation of the Casr leads to hyperproliferation of colonic epithelial cells, expansio

197 or antisense aldose reductase mRNA prevented hyperproliferation of cultured rat aortic SMCs induced b

198 Hyperproliferation of cystic cholangiocytes is linked to

199 lel to natural T1D development, potentiating hyperproliferation of diabetogenic T cells.

200 somatic deletion of Foxo1 is associated with hyperproliferation of ECs.

201 haracterized by abnormal differentiation and hyperproliferation of epidermal keratinocytes.

202 s target, ppp6c, as critical factors for the hyperproliferation of epidermis in psoriasis.

203 lomavirus (HPV) infection frequently induces hyperproliferation of epithelial cells, leading to both

204 in any core PRC1 component cause pronounced hyperproliferation of eye imaginal tissue, accompanied b

205 pamycin complex 1 (mTORC1), which results in hyperproliferation of hepatocytes.

206 c T cell progenitors results in compensatory hyperproliferation of immature thymocytes and developmen

207 Deletion of MED1 also caused hyperproliferation of interfollicular epidermal KCs, and

208 tion, but a dermal inflammatory response and hyperproliferation of interfollicular epidermis accompan

209 in reversed the excessive mTOR signaling and hyperproliferation of Itpkb(-/-) HSC without rescuing co

210 Since psoriasis is marked by hyperproliferation of keratinocytes and loss of epiderma

211 ization in wound healing and is critical for hyperproliferation of keratinocytes in atopic dermatitis

212 Blocking MED1/MED21 expression caused hyperproliferation of keratinocytes, accompanied by incr

213 while deletion of GRP94 in the liver led to hyperproliferation of liver progenitor cells, deletion o

214 These benign tumors represent clonal hyperproliferation of melanocytes that are in a senescen

215 xpression is induced in association with the hyperproliferation of mitochondria.

216 ve compounds that could effectively suppress hyperproliferation of mouse brain primary astrocytes def

217 rived metabolites such as butyrate that fuel hyperproliferation of MSH2(-/-) colon epithelial cells.

218 rant activation of Notch signaling underlies hyperproliferation of mutant cardiomyocytes, and forced

219 These mice exhibit immune dysfunction, hyperproliferation of myeloid cells, and regenerative an

220 opoietic stem cell disorders associated with hyperproliferation of myeloid cells.

221 GSK-3 deletion resulted in massive hyperproliferation of neural progenitors along the entir

222 revealed that SOX5/6/21 prevent detrimental hyperproliferation of oncogene expressing SVZ cells by f

223 Hyperproliferation of PCK cholangiocytes in response to

224 we report here that loss of CARM1 results in hyperproliferation of pulmonary epithelial cells during

225 Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients

226 blast number that was likely to be driven by hyperproliferation of Sp7(+) preosteoblasts.

227 vitro lends support to the concept that the hyperproliferation of splenocytes is not a result of the

228 ased expression of Indian Hedgehog (Ihh) and hyperproliferation of surface mucous cells.

229 signal-regulated kinase 1/2 is required for hyperproliferation of SVAS iPSC-SMCs.

230 suppressed synovial recruitment of EPCs and hyperproliferation of synovial cells.

231 molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts.

232 s expressed Foxp3 and efficiently controlled hyperproliferation of T cells and rescued the IL-2(-/-)

233 In summary, this novel phenotype of hyperproliferation of T cells lacking both MECL-1 and LM

234 We do not observe hyperproliferation of T cells lacking only one of these

235 otein or TIM-4-Ig fusion protein resulted in hyperproliferation of T cells, and TIM-4-Ig costimulated

236 es characterized by clonal hematopoiesis and hyperproliferation of terminally differentiated myeloid

237 Hyperproliferation of the colonic epithelium, leading to

238 more, the homozygous affected mice exhibited hyperproliferation of the epidermis, disturbed cornifica

239 Interestingly, hyperproliferation of the external granule layer (EGL) w

240 Mice exposed to desiccating stress showed hyperproliferation of the meibomian gland and ductal dil

241 nding of the molecular mechanisms underlying hyperproliferation of the palmoplantar epidermis in both

242 genesis without affecting TPA- or E7-induced hyperproliferation of the skin.

243 Mice lacking Crebbp in GC B cells exhibited hyperproliferation of their GC compartment upon immuniza

244 mor stem cells can paradoxically promote the hyperproliferation of their wild-type counterparts.

245 y and EZH1 mutations cooperate to induce the hyperproliferation of thyroid cells.

246 e-specific deletion of VHL led to dysplastic hyperproliferation of tubular epithelial cells, confirmi

247 ice lacking TSC2 in developing SCs displayed hyperproliferation of undifferentiated SCs incompatible

248 These findings are accompanied by hyperproliferation of WASp-deficient follicular and germ

249 activation of Notch signaling recapitulates hyperproliferation of working myocytes but not the condu

250 Increased stratification and hyperproliferation only happened in the limbal, but not

251 hanisms, as IL-4 deficiency does not prevent hyperproliferation or elevated mTORC1 signalling in Ndfi

252 No hyperproliferation or hyperplasia was observed, suggesti

253 , however, does the distal RPE show signs of hyperproliferation or respecification, likely due to loc

254 radic cases, AR-DLBCL demonstrated increased hyperproliferation (P < .001) and c-Myc rearrangements,

255 We further show that the hyperproliferation phenotype of NHERF-2-silenced EC is b

256 This transition from hypo- to hyperproliferation presents an intriguing paradox in the

257 TGFbeta signaling in epithelial cells causes hyperproliferation, reduced apoptosis and increased geno

258 and growth associated with hypermutation and hyperproliferation, respectively, in conjunction with at

259 a contrived compensatory non-cell-autonomous hyperproliferation response when cell-autonomous apoptos

260 ification, it is not apparently required for hyperproliferation resulting from excessive Wnt signalin

261 Epidermal hyperproliferation resulting in acanthosis is an importa

262 ts polarity and tight junctions and promotes hyperproliferation, resulting in large, filled structure

263 for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts.

264 Strikingly, hyperproliferation, self-renewal, and autophagy defects

265 FVB mice developed epithelial cell hyperproliferation, severe inflammation with erosions an

266 ties in the cornea including epithelial cell hyperproliferation, stromal inflammation, and neovascula

267 expression was induced only during epidermal hyperproliferation, such as in psoriasis and in murine w

268 by reduced BMPR2 expression and endothelial hyperproliferation, supporting the relevance of this mec

269 ting that in spite of extensive keratinocyte hyperproliferation, susceptibility to carcinogen-depende

270 oimmune thyroid disease characterized by TEC hyperproliferation that develops spontaneously in IFN-ga

271 infection, EBV induces a transient period of hyperproliferation that is suppressed by the activation

272 malities, as well as growth factor-dependent hyperproliferation that underlies PH.

273 s includes host predisposition to epithelial hyperproliferation; therefore, a possible association of

274 arization-scrambling RPE layer, ranging from hyperproliferation to focal atrophy.

275 d IL-17(+) gammadelta T cells, and epidermal hyperproliferation to levels similar to a Rag1-/- backgr

276 Expansion, in part, involved E1 cell hyperproliferation together with rapid E2 conversion plu

277 atenin expression in an established model of hyperproliferation, transmissible murine colonic hyperpl

278 he hESC-derived RPE cells showed no signs of hyperproliferation, tumorigenicity, ectopic tissue forma

279 from c-FLIP(L)-transgenic (Tg) mice manifest hyperproliferation upon activation, although it was not

280 T lymphocytes showed normal development but hyperproliferation upon stimulation, which correlates wi

281 role of CXCR4 in IL-23-induced keratinocyte hyperproliferation using an epidermal-specific knockout

282 d for their ability to suppress keratinocyte hyperproliferation using HaCaT cells as the primary test

283 sis, we found that Myc-mediated keratinocyte hyperproliferation was abolished by the loss of Skp2.

284 the presence of the gut microbiota, because hyperproliferation was completely eliminated by antibiot

285 Hyperproliferation was explored using Ki67 and cell cycl

286 vidence of canonical hedgehog signaling, and hyperproliferation was not blocked by smoothened (SMO) i

287 In contrast, CD43(-/-) T cell hyperproliferation was reversed by an intracellular-only

288 Heme-induced hyperproliferation was shown to depend on the presence o

289 he most potent analogue against keratinocyte hyperproliferation was the 1,2,4-oxadiazole 18, the pote

290 oxide synthase expression, and keratinocyte hyperproliferation were suppressed.

291 in the differentiating layers, resulting in hyperproliferation when the receptors are activated.

292 a by Helicobacter pylori leads to epithelial hyperproliferation, which increases the risk for gastric

293 n and organization, express RANK and undergo hyperproliferation, which is abrogated by RANKL neutrali

294 heir potency for suppression of keratinocyte hyperproliferation, which was evaluated using HaCaT cell

295 They undergo moderate hyperproliferation with increased self-renewal.

296 We speculate that B cell hyperproliferation within parotid glands of pSS patients

297 Immunohistochemistry showed hyperproliferation within the punctate lesions.

298 trophic myopathy was caused by cardiomyocyte hyperproliferation without hypertrophy and was associate

299 haviours such as differentiation defects and hyperproliferation, yet fail to produce macroscopically

300 IL-15 administration, followed by influx and hyperproliferation yielding 10-fold expansions of NK cel