ライフサイエンスコーパス: hyperproliferative

1 tes and lymphoma cells from MTA1-TG mice are hyperproliferative.

2 llicular proliferation, the epidermis became hyperproliferative.

3 AR+/+ cells, uPAR-/- kidney fibroblasts were hyperproliferative.

4 mmary epithelial cells were disregulated and hyperproliferative.

5 Hyperproliferative ACF had significantly increased mRNA

6 In hyperproliferative ACF, 44% possessed significant increa

7 COX-2 mRNA, the protein was not increased in hyperproliferative ACF.

8 Keratin 6 is a marker of hyperproliferative, activated keratinocytes, found in wo

9 that T(reg) from NIK-deficient mice display hyperproliferative activities upon GITR stimulation thro

10 These data suggest that epidermal hyperproliferative activity is accompanied by the upregu

11 This CD62(low) subset is responsible for the hyperproliferative activity upon GITR stimulation.

12 me a critical role of NF-kappaB in mediating hyperproliferative affects of PG on colonic crypts of Fa

13 However, the reentry of hyperproliferative alphaB-/- cells into S phase and mito

14 of chromosomes 1 and 9 demonstrated that the hyperproliferative alphaB-/- cells were 30% diploid and

15 of genomic instability was obtained when the hyperproliferative alphaB-/- cells were labeled with ant

16 ack of mutations in the p53 coding region of hyperproliferative alphaB-/- cells.

17 We now demonstrate that the hyperproliferative alphaB-/- lens epithelial cells under

18 Examination of the hyperproliferative alphaB-/- mitotic profiles revealed t

19 Hyperproliferative alphaB-crystallin-/- cells were shown

20 ted a critical role of NFkappaB in mediating hyperproliferative and anti-apoptotic effects of progast

21 muscle cells (PASMCs) from PAH patients are hyperproliferative and apoptosis-resistant and demonstra

22 monary arterial hypertension (IPAH) involves hyperproliferative and apoptosis-resistant pulmonary art

23 AnxA2 might therefore mediate the hyperproliferative and cocarcinogenic effects of progast

24 SMCs in elastin mutants, and these SMCs are hyperproliferative and dedifferentiated.

25 Similarly, formation of hyperproliferative and disorganized mammary acini induce

26 PASMCs from monocrotaline rats are hyperproliferative and display normoxic activation of hy

27 In aging men, the prostate gland becomes hyperproliferative and displays a propensity toward carc

28 ) keratinocytes expressing oncogenic RAS are hyperproliferative and fail to up-regulate proinflammato

29 neonatal megakaryocyte (MK) progenitors are hyperproliferative and give rise to MKs smaller and of l

30 ed therapy is feasible and may be useful for hyperproliferative and inflamed skin diseases.

31 cinomas is largely through the creation of a hyperproliferative and inflammatory niche that facilitat

32 Psoriasis is a chronic hyperproliferative and inflammatory skin disease caused

33 s strongly upregulated in human psoriasis, a hyperproliferative and inflammatory skin disease.

34 We show that these hyperproliferative and invasive Drosophila phenotypes ar

35 milar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express

36 Null epidermis is hyperproliferative and overexpresses keratins 6 and 16,

37 the recovery period the progenitor cells are hyperproliferative and potentially more radiosensitive)

38 T cells from untreated Sphk2(-/-) mice were hyperproliferative and produced more IFN-gamma than did

39 Instead, their T cells were hyperproliferative and relatively, but not completely, r

40 and ASM cells from patients with asthma are hyperproliferative and release more IL-6 and CXCL8.

41 signaling, Smad2/3-deficient podocytes were hyperproliferative and resistant to TGF-beta-induced gro

42 Thus, ST14 hypomorphic mice developed hyperproliferative and retention ichthyosis with impaire

43 Golli-deficient T cells were hyperproliferative and showed enhanced calcium entry upo

44 (-/-) mammary lesions contain cells that are hyperproliferative and stain positively with nucleolar (

45 CD43(-/-) T cells are hyperproliferative and the cytoplasmic tail of CD43 has

46 fic deletion of Pten in mice causes multiple hyperproliferative and tumor lesions that strikingly res

47 Ikkalpha(-/-) mice present with a hyperproliferative and undifferentiated epidermis charac

48 elective antibody rendered endothelial cells hyperproliferative, and caused defective cell fate speci

49 res derived from LMP2A-expressing cells were hyperproliferative, and epithelial differentiation was i

50 ultured from PRKO mouse aortae were markedly hyperproliferative, and their growth was not affected by

51 Hyperproliferative apoptosis-resistant cells were also g

52 RVX208 normalized the hyperproliferative, apoptosis-resistant, and inflammator

53 ave previously demonstrated the existence of hyperproliferative, apoptosis-resistant, proinflammatory

54 Because all lesions are hyperproliferative, are associated with inflammation, an

55 gamma-secretase inhibitor (GSI) rescued the hyperproliferative baseline phenotype in the Mtgr1(-/-)

56 Additionally, loss of Dab2 protein occurs in hyperproliferative, but histological benign ovarian epit

57 Px44-TRAIL caused apoptosis of the hyperproliferative, but not differentiating, cultured ke

58 sorders have an elevated risk to progress to hyperproliferative cancer at a later stage.

59 Hyperproliferative cancer cells face increased replicati

60 This contributes to the hyperproliferative capacity of T cells from c-FLIP(L)-tr

61 fect of reconstituting CD43 mutants into the hyperproliferative CD43(-/-) T cells.

62 nfirm that the mature SMC can give rise to a hyperproliferative cell which appears to promote inflamm

63 pertranscription and transgene expression in hyperproliferative cells early in reprogramming is criti

64 35 samples revealed the presence of foci of hyperproliferative cells in the bronchiolar epithelium,

65 become activated: they turn into migratory, hyperproliferative cells that produce and secrete extrac

66 hway and that the dead cells are replaced by hyperproliferative cells, leading to epidermal hyperplas

67 few stratified foci/microadenomas containing hyperproliferative cells, resembling precursors of papil

68 l tumor suppressor mechanism for eliminating hyperproliferative cells.

69 hether inflammatory events occur pre or post hyperproliferative changes.

70 ived from alphaB-crystallin-/- mice produced hyperproliferative clones at a frequency of 7.6 x 10(-2)

71 d with cytomegalovirus (CMV) infection and a hyperproliferative CMV-specific T-cell response.

72 ollicular epidermis and sebaceous glands are hyperproliferative, coincident with expanded nuclear Yap

73 d only in keratinocytes and the keratinocyte hyperproliferative component of the TGFbeta1 -/- phenoty

74 asymmetric cell divisions were increased in hyperproliferative conditions and decreased under hypopr

75 t targets of Nrf2, which are activated under hyperproliferative conditions in the liver.

76 However, many squamous hyperproliferative conditions, including HPV-induced war

77 proliferation by triggering cell death under hyperproliferative conditions.

78 y, characterized by increased IEC apoptosis, hyperproliferative crypts, epithelial barrier dysfunctio

79 e ARF tumor suppressor is a potent sensor of hyperproliferative cues emanating from oncogenic signali

80 Notably, the hyperproliferative Cxcr4(-/-) HSCs are able to maintain

81 CYP4F expression is up-regulated in situ in hyperproliferative dermatoses-an innate mechanism to rep

82 ch as anemia, patients have elevated risk of hyperproliferative disease (cancer) by midlife.

83 and low-risk HPVs (e.g., HPV-6) cause benign hyperproliferative disease.

84 S100A7 is highly expressed in epidermal hyperproliferative disease; however, its function is not

85 d as important drug targets for treatment of hyperproliferative diseases and inflammation.

86 tor (EGFR) has frequently been implicated in hyperproliferative diseases of renal tubule epithelia.

87 unt for their beneficial effects in treating hyperproliferative diseases such as psoriasis, actinic k

88 o mTOR activation that plays a major role in hyperproliferative diseases, in some cases rapamycin doe

89 TIG3 level is reduced in hyperproliferative diseases, including psoriasis and ski

90 anism of retinoid action in the treatment of hyperproliferative diseases, we used a long-range differ

91 a major role in non-malignant and malignant hyperproliferative diseases.

92 (ROS) and may underlie certain therapies for hyperproliferative diseases.

93 Surprisingly, rather than a hyperproliferative disorder expected from the loss of a

94 used to diagnose lymphangioleiomyomatosis, a hyperproliferative disorder of lung smooth muscle cells

95 However, in epidermal hyperproliferative disorders and tumors, integrins are a

96 or 1alpha,25-dihydroxyvitamin D(3)) to treat hyperproliferative disorders is hampered by calcemic eff

97 However, in certain hyperproliferative disorders of the skin, including psor

98 gastrointestinal stromal tumors (GISTs) are hyperproliferative disorders of the stomach caused by dy

99 oint that can be therapeutically targeted in hyperproliferative disorders such as PAH.

100 ue new approach for the topical treatment of hyperproliferative disorders such as psoriasis and skin

101 ation of MEF cultures in vitro and, in vivo, hyperproliferative disorders that progress to cancer.

102 eful for developmental studies, for treating hyperproliferative disorders, and for developing animal

103 eases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.

104 In contrast, in other hyperproliferative disorders, such as basal cell carcino

105 S100A7 is markedly increased in epidermal hyperproliferative disorders.

106 ed antitumor drug, also for the treatment of hyperproliferative disorders.

107 oth RB(-/-) and RB(+/+) tumors as well as in hyperproliferative disorders.

108 lymph node T cells from PKR:(-/-) mice were hyperproliferative during Con A-mediated stimulation.

109 mors present without an obvious premalignant hyperproliferative dysplastic lesion.

110 The hyperproliferative ECs of human pulmonary arterial hyper

111 ur generations of clonal expansion to enrich hyperproliferative ECs.

112 both necessary and sufficient to mediate the hyperproliferative effect of a gain-of-function mutation

113 eta/NFkappaB pathway, may be integral to the hyperproliferative effects of progastrin on proximal col

114 d formation of plexiform lesions composed of hyperproliferative endothelial and vascular smooth-muscl

115 ir in all the three tissues, indicative of a hyperproliferative environment.

116 lar growth in keratinocytes, carcinomas, and hyperproliferative epidermal disorders, including psoria

117 der psoriasis vulgaris is characterized by a hyperproliferative epidermis and aberrant immune activit

118 K5 Myc transgenic mice have hyperplastic and hyperproliferative epidermis and develop spontaneous tum

119 liferating epidermis, we produced a model of hyperproliferative epidermis by topical application of d

120 The hyperproliferative epidermis from the affected regions e

121 e and Wy-14,643, activators of PPARalpha, on hyperproliferative epidermis in hairless mice, induced e

122 ome and popliteal pterygium syndrome, have a hyperproliferative epidermis that fails to undergo termi

123 In hyperproliferative epidermis there was decreased express

124 The hyperproliferative epidermis was characterized by an inc

125 Finally, treatment of hyperproliferative epidermis with oxysterols restored ep

126 ealing, prolonged secretion of chemokines, a hyperproliferative epidermis, and neutrophil infiltratio

127 with wild-type littermates consistent with a hyperproliferative epidermis.

128 with a lentiviral miR vector, resulted in a hyperproliferative epidermis.

129 and are lined by abnormally functioning and hyperproliferative epithelial cells.

130 rapy was associated with a more well defined hyperproliferative epithelial region, higher cell densit

131 e as a consequence of persistent exposure of hyperproliferative epithelial stem cells to an inflammat

132 Similarly, in the hyperproliferative epithelium of regenerating murine ski

133 DeltaK5-M2SMO mouse epidermis is hyperproliferative, ex presses BCC protein markers and g

134 types: dysplastic sessile ear papillomas and hyperproliferative follicular/interfollicular chest dysp

135 Development of these hyperproliferative gammadelta T cells was not dependent

136 These data point to hyperproliferative glial progenitors as the source of th

137 cation mutants from these patients transduce hyperproliferative growth responses.

138 t often transition from hypoproliferative to hyperproliferative growth.

139 kening of skin after treatment, illustrating hyperproliferative growth.

140 associated with pigmented melanocytes in the hyperproliferative hair follicles in the Tyr-MIP-2 trans

141 72 show enhanced Ca(2+) mobilization and are hyperproliferative in response to BCR ligation.

142 Unexpectedly, cells expressing Y559F were hyperproliferative in response to CSF-1.

143 s expressing mutant human (h)IL-4Ralpha were hyperproliferative in response to IL-4 compared with cel

144 verexpressing wild type SHIP are found to be hyperproliferative in response to IL-4 in comparison to

145 PTEN-deficient B cells were hyperproliferative in response to mitogenic stimuli, and

146 f B cell activation, as CD72-/- B cells were hyperproliferative in response to various stimuli and sh

147 tudy that murine Treg are prone to death but hyperproliferative in vitro and in vivo, which is differ

148 ferentiated with interleukin-12 present, are hyperproliferative in vitro, compared with CTLA-4(+/+)Tc

149 Cav-1-/- mammary epithelia were hyperproliferative in vivo, with dramatic increases in t

150 not CD44(low) T cells, are hyperreactive and hyperproliferative in vivo.

151 role of alpha(E)beta(7) in a murine model of hyperproliferative inflammatory skin disorders that is i

152 al role for SRF as the master regulator of a hyperproliferative, inflammatory phenotype accompanied b

153 at has been shown to play a role in numerous hyperproliferative/inflammatory diseases.

154 kin epidermis systematically transforms to a hyperproliferative, invasive tissue replete with inflamm

155 nic inflammatory dermatosis characterized by hyperproliferative keratinocytes (KC).

156 lays an epidermal phenotype characterized by hyperproliferative keratinocytes and undifferentiated ep

157 ctivated lymphocytes and causes apoptosis of hyperproliferative keratinocytes, features of various sk

158 These hyperproliferative lesions appeared to progress through

159 ta-catenin led to the formation of localized hyperproliferative lesions by 3 months, which did not pr

160 All SRF-VP16iHep mice develop hyperproliferative liver nodules that progresses to leth

161 nd in epithelial layers of dilated ducts and hyperproliferative lobular regions in the mammary glands

162 Hyperproliferative mammary epithelia contained increased

163 Loss of CD177 leads to hyperproliferative mammary epithelium and contributes to

164 y stem cells resulted in the regeneration of hyperproliferative mammary glands in vivo.

165 reepithelialization of skin wounds to become hyperproliferative, migratory, and invasive.

166 espond to injury by becoming activated, i.e. hyperproliferative, migratory, and proinflammatory.

167 or no difference in JNK and ERK activity in hyperproliferative mucosa from DMH-treated animals compa

168 ic factors, consistent with the inflammatory hyperproliferative nature of KS lesions.

169 therapeutic strategy has been to target the hyperproliferative nature of the disease.

170 ed from these mice became hypermigratory and hyperproliferative on overexpression of CTGF.

171 ent checkpoint that safeguards cells against hyperproliferative, oncogenic signals.

172 se subunits could be beneficial for treating hyperproliferative or fibrogenic diseases of the skin.

173 enzoic acid) porphyrin (MnTBAP) reverses the hyperproliferative PAH phenotype.

174 een implicated in numerous human cancers and hyperproliferative pathological processes.

175 xazoles was synthesized for the treatment of hyperproliferative pathologies, including neoplasms.

176 EAD inhibitors for treating cancer and other hyperproliferative pathologies.

177 ulmonary hypertension through suppression of hyperproliferative pathways, including STAT3-mediated si

178 ol cells) whereas the surviving cells became hyperproliferative (PCNA positive).

179 At the protein level, 46% of ACF were hyperproliferative (PCNA, 3.2 +/- 1.2-fold).

180 tutive activation of oncoprotein Stat3 and a hyperproliferative phenotype characterized by increased

181 Resolution of the hyperproliferative phenotype correlated with reduced Fyn

182 This ACA11-driven hyperproliferative phenotype depended on increased ROS l

183 een documented, the molecular basis for this hyperproliferative phenotype has not been fully characte

184 asthma that contributes to its secretory and hyperproliferative phenotype in asthma, and which may pl

185 Here, the mechanism underlying the hyperproliferative phenotype in RPE was investigated.

186 BrdU labeling similarly failed to identify a hyperproliferative phenotype in T cells lacking IL-16.

187 l mononuclear cells recapitulated the B-cell hyperproliferative phenotype in vitro.

188 the TGFbeta1 transgene, suggesting that the hyperproliferative phenotype may result in part from dev

189 ession increased apoptosis and abrogated the hyperproliferative phenotype of blood-outgrowth ECs from

190 E cells, providing a molecular basis for the hyperproliferative phenotype of Hfe(-/-) and Hjv(-/-) RP

191 ologic activation of Trpv4 might reverse the hyperproliferative phenotype of PCK cholangiocytes.

192 NAs are consistent with the inflammatory and hyperproliferative phenotype of psoriatic lesions.

193 ed with mCTLA4Ig reverses the activation and hyperproliferative phenotype of the CTLA-4-deficient T c

194 ing mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf(-/-) and p53(

195 The hyperproliferative phenotype of these transgenic mice wa

196 s also effective in suppressing the cellular hyperproliferative phenotype seen in Apc defective intes

197 ll-differentiated epidermal layer, exhibit a hyperproliferative phenotype similar to wounded native s

198 expression of keratin 6 associated with the hyperproliferative phenotype was observed in transgenic

199 cer, and a novel murine model demonstrated a hyperproliferative phenotype with prostate-specific USP2

200 CR-stimulated Abcg1(-/-) T cells rescues the hyperproliferative phenotype.

201 ion by the d715 G-CSFR may contribute to its hyperproliferative phenotype.

202 /Srcasm transgenic mice did not manifest the hyperproliferative phenotype.

203 osphorylatable Srcasm mutant, maintained the hyperproliferative phenotype.

204 d PCNA overexpression, consistent with their hyperproliferative phenotype.

205 orescein isothiocyanate-albumin; and (iii) a hyperproliferative phenotype.

206 t outflow tract explant cultures rescued the hyperproliferative phenotype.

207 valves, providing a molecular basis for the hyperproliferative phenotype.

208 testis, pancreas, kidney, and adrenal gland, hyperproliferative phenotypes associated with p18 loss w

209 e retinoblastoma-dependent pathway, yielding hyperproliferative phenotypes in pupae and adult flies.

210 ll proliferation, it is not required for the hyperproliferative pituitary phenotype caused by p19 los

211 istrafficked EREG form significantly larger, hyperproliferative, poorly differentiated, and locally i

212 ependent elevation of Mmp1 expression, and a hyperproliferative population lacking elevated JNK signa

213 CD4 T cells from Apc(Min/+) mice showed hyperproliferative potential in vitro and in vivo and in

214 Although this hyperproliferative process has been proposed to represen

215 ased chimeras to recipient nude mice produce hyperproliferative psoriasiform epidermal keratinocytes

216 Hyperproliferative pulmonary vascular fibroblasts isolat

217 formation, starting with rapid but transient hyperproliferative reactivation, followed by a long peri

218 flammatory responses and ultraviolet-induced hyperproliferative rebound.

219 tate tissue that was less differentiated and hyperproliferative relative to WT littermates.

220 ions when the epidermis becomes "activated" (hyperproliferative), remains unclear.

221 The hyperproliferative response can be reversed by reintrodu

222 Mice deficient for the VDR display a hyperproliferative response in the hair follicle and epi

223 reversed the potentially tumor-predisposing hyperproliferative response of BLNK(-/-) pre-B cells to

224 or deficiency of SHP-1 activity results in a hyperproliferative response of myelomonocytic cell popul

225 autoreactive B cells lacking CD11b exhibit a hyperproliferative response to B cell receptor (BCR) cro

226 Despite this evidence for a hyperproliferative response to G-CSF, no cases of AML ha

227 GF-I stimulation of VSMC proliferation and a hyperproliferative response to vascular injury.

228 This hyperproliferative response was due, at least in part, t

229 to the stratum corneum elicits an epidermal hyperproliferative response, a pathogenic feature in man

230 tained matrix adhesion and provoked a strong hyperproliferative response.

231 ry low minimal erythemal dose and a dramatic hyperproliferative response.

232 leads to increased sensitivity to VEGF and a hyperproliferative response.

233 atin 14, which reflect the antimicrobial and hyperproliferative responses of keratinocytes.

234 attenuated induction of Klf5 expression, and hyperproliferative responses to C rodentium were reduced

235 se mutations affect one allele and result in hyperproliferative responses to G-CSF, presumably throug

236 on of the endogenous phosphatase and induces hyperproliferative responses to interleukin-3 (IL-3) and

237 and seborrheic dermatitis (D/SD) are common hyperproliferative scalp disorders with a similar etiolo

238 Palpha(-/-) fetal liver (FL) progenitors are hyperproliferative, show decreased differentiation poten

239 t excessive telomerase activity may act as a hyperproliferative signal in cells and induce a senescen

240 DNA damage and/or hyperproliferative signals activate the wild-type p53 tu

241 induced in response to potentially oncogenic hyperproliferative signals and activates p53 by interfer

242 ropose that nucleolin, like ARF, responds to hyperproliferative signals by upregulation of p53 throug

243 m of nucleophosmin induction and showed that hyperproliferative signals emanating from oncogenic H-Ra

244 r limits ribosome biogenesis and responds to hyperproliferative signals to activate the p53 checkpoin

245 In response to hyperproliferative signals, ARF is upregulated, resultin

246 rucial component of the cellular response to hyperproliferative signals, including oncogene activatio

247 In response to hyperproliferative signals, p14(Arf) stabilizes p53 by b

248 ut is induced by high thresholds of aberrant hyperproliferative signals, thereby activating p53 in in

249 limits cell cycle progression in response to hyperproliferative signals.

250 Most of these hyperproliferative skin changes improve when a MEK inhib

251 a, with the main toxicity being a variety of hyperproliferative skin conditions due to paradoxical ac

252 elafin and SLPI, has been related to several hyperproliferative skin conditions.

253 ye discrete epidermal hyperplasia (WEH) is a hyperproliferative skin disease that is prevalent on adu

254 Psoriasis is a common inflammatory and hyperproliferative skin disease with a multifactorial ge

255 vulgaris (PsV) is a common inflammatory and hyperproliferative skin disease.

256 epidermis, the importance of amphiregulin in hyperproliferative skin diseases has been further suppor

257 LML3 localization in normal epidermis and in hyperproliferative skin diseases including actinic kerat

258 ytes has been implicated in inflammatory and hyperproliferative skin diseases.

259 be an effective strategy in the treatment of hyperproliferative skin diseases.

260 Although psoriasis is a hyperproliferative skin disorder, the possible role of a

261 epithelial malignancies and in psoriasis, a hyperproliferative skin disorder.

262 regulating the expression of ErbB ligands in hyperproliferative skin disorders and wound healing.

263 y play a role in the pathogenesis of certain hyperproliferative skin disorders via modulation of gene

264 d tissue sections from normal human skin and hyperproliferative skin disorders were examined by immun

265 ound effects on epidermal gene expression in hyperproliferative skin disorders.

266 The hyperproliferative skin inflammation in this novel murin

267 itions, such as the psoriasis, a nonallergic hyperproliferative skin inflammatory disorder with a neu

268 d WEHV2, respectively) are associated with a hyperproliferative skin lesion on walleyes that appears

269 native skin, including genes associated with hyperproliferative skin or activated keratinocytes.

270 and S100A8/A9, were also up-regulated in the hyperproliferative skin.

271 culturing C/EBPalpha(-/-) FL cells in vitro Hyperproliferative spleen colonies and myelodysplastic s

272 We previously proposed that the keratinocyte hyperproliferative state in psoriatic skin results from

273 , and establishment of a TGF-beta-resistant, hyperproliferative state in the colonic epithelium.

274 minution of p21 and p27 levels resulted in a hyperproliferative state in VHL-negative cells, leading

275 This hyperproliferative state is thought to represent the pre

276 an essential process that helps maintain the hyperproliferative state of most cancer cells.

277 ose obtained from healthy volunteers and the hyperproliferative state of the lesions was characterize

278 s from untreated HIV(+) individuals are in a hyperproliferative state that is modulated by type I int

279 Cx26 expression kept wounded epidermis in a hyperproliferative state, blocked the transition to remo

280 It can be induced in hyperproliferative states such as wound healing, inflamm

281 ich Connexin 26 is up-regulated in epidermal hyperproliferative states).

282 times (T2) in magnetic resonance imaging of hyperproliferative states, for example, malignancy.

283 DDR limits keratinocyte multiplication upon hyperproliferative stimuli.

284 ein ARF provides a defence mechanism against hyperproliferative stresses that can result from the abe

285 two distinct types of 3D structures: large, hyperproliferative structures and small, growth-arrested

286 opels disease by nourishing the inflamed and hyperproliferative synovium.

287 d show that loss of TIGIT in mice results in hyperproliferative T cell responses and increased suscep

288 memory T cells but remain as long-lived and hyperproliferative T cells.

289 rker, CD151 in humans thus marks and enables hyperproliferative T cells.

290 intrahepatic Treg numbers were increased and hyperproliferative, the intrahepatic CD4/CD8 ratio was d

291 n ureteric morphogenesis, including dilated, hyperproliferative tips and decreased branching.

292 This phenotype was hyperproliferative to serum and platelet-derived growth

293 indicative of spontaneous activation and are hyperproliferative upon in vitro stimulation.

294 ink in the emergence of apoptosis-resistant, hyperproliferative vascular cells after EC apoptosis.

295 Pulmonary arterial hypertension (PAH) is a hyperproliferative vascular disorder observed predominan

296 Obese ZSF1 rats developed hyperproliferative vascular foci in the subendocardium,

297 ll adult vascular beds produced CNS-specific hyperproliferative vascular malformations.

298 dvancement with lesions at early stage being hyperproliferative, whereas lesions at late stage are cl

299 At the RNA level, 38% of ACF were hyperproliferative, with proliferating cell nuclear anti

300 ts in injury-resistant enterocytes, that are hyperproliferative, yet have regenerative deficits and a