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1 pha/Akt signaling, promoting cell growth and proliferation.
2 tant p53, significantly inhibited tumor cell proliferation.
3 ently reversed E1S- and E1-induced T47D cell proliferation.
4 , was a very effective compound induced SSCs proliferation.
5 for effects of CDK4/CDK6 inhibitors on cell proliferation.
6 chemokines and controlling cell survival and proliferation.
7 Teff cells, was required for selective Treg proliferation.
8 ular smooth muscle cell (VSMC) migration and proliferation.
9 and flow cytometry assays for apoptosis and proliferation.
10 together drove their suppression of TH2 cell proliferation.
11 ide, further enhancing stimulation of T-cell proliferation.
12 connected with human cancer development and proliferation.
13 ) play a critical role in cell signaling and proliferation.
14 ared to be compensated for by increased MPP4 proliferation.
15 lular differentiation to aggressive cellular proliferation.
16 proliferation, but did stimulate VDR KO cell proliferation.
17 ging metrics using (18)F-FLT to assess tumor proliferation.
18 ms by which these GFs regulate the survival, proliferation.
19 ellular functions, including metabolisms and proliferation.
20 nutrients required for continued growth and proliferation.
21 ilitate cell-cycle progression and stem cell proliferation.
22 sion of KLF5; a high level of KLF5 increased proliferation.
23 uencing compensatory signaling and expanding proliferation.
24 s that regulate cellular differentiation and proliferation.
25 associated with differentiation rather than proliferation.
26 ide led to reverse CD8+ T cell-enhanced BECs proliferation.
27 n cancer cells to promote their survival and proliferation.
28 lactate production and increased SHH-driven proliferation.
29 regulate cell migration, cell adhesion, and proliferation.
30 iron and an augmented dependence on iron for proliferation.
31 is one pathway that suppresses local T cell proliferation.
32 centration, hormone secretion/expression and proliferation.
33 lation over genes associated with progenitor proliferation.
34 itive and negative signals that control cell proliferation.
35 lts from altered cell cycle and reduced cell proliferation.
36 fferentiation and taste stem/progenitor cell proliferation.
37 ator of cell differentiation, migration, and proliferation.
38 ive regions, is dominated by microstructural proliferation.
39 tween organellar genome maintenance and cell proliferation.
40 lation, c-Myc up-regulation and reduced cell proliferation.
41 individual kinases in agonist-induced P-UAEC proliferation.
44 FN1, olaratumab specifically reduced HHSteC proliferation (AlamarBlue assay) and cell migration (tra
47 red to be due to blood infiltration or local proliferation, although the presence of resident hematop
49 moyl}amino)hexadecanoic acid (13b) decreased proliferation and activated apoptosis in MDA-MB-231 brea
50 Foxp1-Shq1 and Pten deletion show increased proliferation and anaplastic dedifferentiation, as well
51 gastric cancer cells leads to increased cell proliferation and angiogenesis, which may, in turn, cont
52 he expression of well characterized cellular proliferation and apoptosis guards (NF-kappaB, Bcl-2 and
53 e epithelial cell turnover and expression of proliferation and apoptosis-related genes in gastric can
56 genes identified converge on aspects of cell proliferation and cell cycle regulation, including DNA s
57 lls with the equivalent human IFPs increased proliferation and cytokine production in response to CD2
59 l processes such as autophagy, inflammation, proliferation and differentiation of stem cell, cell sur
60 expression, which is required for osteoblast proliferation and differentiation through transcriptiona
61 eling enzymes, is required for both myoblast proliferation and differentiation, and the control of Br
66 ate induced a time-dependent increase in LPC proliferation and expression of genes associated with ch
70 osis patients, mTORC1 activation, macrophage proliferation and glycolysis were identified as hallmark
75 ed by quantifying the dose-dependent drop in proliferation and increase in differentiation in etoposi
76 ne silencing of KIND1 decreased keratinocyte proliferation and increased apoptosis in vitro and in sk
78 ought to identify cytokines that can promote proliferation and induce or maintain IL-22 production by
80 Tnrc6a was previously reported to promote proliferation and inhibit differentiation of myoblast ce
82 known molecular target of ABHD5, impeded the proliferation and invasion, suggesting an ATGL-independe
87 scavenged reactive oxygen species, inhibited proliferation and migration of smooth muscle cells (SMCs
91 results suggest that carbofuran inhibits NSC proliferation and neuronal differentiation by altering T
95 t Dengue virus (DENV)-NS2A, leads to reduced proliferation and premature differentiation of radial gl
96 d BRD7389, for their ability to inhibit both proliferation and protein synthesis in patient-derived m
101 rgy homeostasis to influencing hepatoma cell proliferation and suggest a potential role of SLC13A5 in
102 sizes during the early months, with reduced proliferation and suppression of AKT, S6, ERK, and STAT3
104 ons within the ERK pathway can regulate cell proliferation and transformation, and suggest oncogene-s
106 l proliferative cells by inhibiting neuronal proliferation and triggering the formation of microglial
107 as OP9 preadipocytes were assessed for cell proliferation and triglyceride accumulation following di
109 ription of downstream genes and promote cell proliferation and tumor growth in vivo Taken together, o
111 exerts its effect on OPCs by inducing their proliferation and, at a late stage, by modulating OPC ma
112 han 10% naive T cells, reduced/absent T-cell proliferation, and at least 1 significant clinical event
113 cultures or in the SGZ induces increased NSC proliferation, and CD44-null as well as HA-disrupted wil
114 nse to Wnt stimuli and immunohistochemistry, proliferation, and cell death assays to identify new neu
117 ore, low-dose DAC preserved HSPC-NK killing, proliferation, and interferon gamma production capacity,
118 bosome-related gene sets, promoted excessive proliferation, and led to retinoblastoma with anaplastic
119 -cycle-related genes are a characteristic of proliferation, and likely tumor evolution, rather than o
120 ctate levels strongly correlated with T cell proliferation, and measuring lactate compared favorably
121 m and progenitor cells displayed compromised proliferation, and replication stress that could be resc
123 cer cell phenotypes, including angiogenesis, proliferation, and stemness, and a minor subpopulation (
124 erves as a molecular switch from invasion to proliferation, and suggest that targeting both receptors
127 NSF1), and functional effects on viability, proliferation, apoptosis, and cytotoxicity were monitore
129 cells underpin synovial hyperplasia through proliferation, are recruited to a Nestin-GFP(high) periv
131 Here, we performed marker analysis, cell proliferation assays, and genetic lineage tracing to def
133 estines, but caused no defects in epithelial proliferation, barrier integrity, or ultrastructure.
136 p3 activation had no effect on cholangiocyte proliferation but significantly decreased the expression
140 gly, however, only LECs showed enhanced cell proliferation by regulating the vascular endothelial gro
141 triac) and 3-iodothyronamine (T1AM), on cell proliferation, cell death and DNA damage was studied in
143 ines that expressed MAN2A1-FER had increased proliferation, colony formation, and invasiveness and fo
144 median survival with reduced tumor size and proliferation compared with control Pten-mutant mice, th
145 Ag mice had an unexpected increase in villus proliferation compared with unmanipulated littermates, w
146 biting unique changes in pathways related to proliferation, cytoskeletal organization, and apoptosis.
147 In this report, we demonstrate enhanced proliferation, decreased apoptosis and increased cytotox
148 , CDK20-depleted cells display impaired cell proliferation, defective G2/M arrest and increased radio
150 This response is cell type- rather than proliferation-dependent and does not appear to be driven
151 sion analysis revealed a major defect in the proliferation, differentiation and mineralization abilit
152 dies showing its involvement in keratinocyte proliferation, differentiation, and migration and in epi
153 -related processes by controlling a neuronal proliferation/differentiation switch of ID-bHLH factors.
154 ase in APC function for allergen-specific TC proliferation during allergic inflammation is largely du
155 two independent systems to impair hepatocyte proliferation during liver injury to evaluate the contri
159 cancer model systems, was required for cell proliferation, enhanced AR's transcriptional activity, a
162 complex preferentially interacted with anti-proliferation gene transcripts in a Cnot3-dependent mann
163 were associated with unrestrained fibroblast proliferation, impaired scar remodeling, reduced fibrobl
164 ll tumours, caused a significant decrease in proliferation in 5/23 (22%) tumours, and that KRAS/BRAF
166 r homeostatic conditions was low, microglial proliferation in a mouse model of Alzheimer's beta-amylo
168 sides, all compounds inhibit the trophozoite proliferation in amoebic liver abscess induced in hamste
169 e calcitriol treatment did not decrease cell proliferation in BVE(Cyp24a1-null) cells, it strengthene
171 low concentrations of 20E support prolonged proliferation in explanted wing discs in the absence of
175 show that USP36 down-regulation alters cell proliferation in human cancer cells by inducing both apo
178 P2 deletion in mouse skin results in reduced proliferation in neonatal and wounded adult epidermis.
180 thelial cells (ECs) coordinate migration and proliferation in response to growth factor activation to
181 omosome segregation, p53 regulation and cell proliferation in somatic cells, but its role in embryoni
182 we do not find evidence implicating altered proliferation in the rescue, we observe a significant in
184 found no significant change in prostate cell proliferation in treated mice when compared to controls.
185 suppression results in a modest reduction of proliferation in vascular smooth muscle cells, but given
186 Finally, we show that CCAR2 is required for proliferation in vitro and in established SCC tumors in
187 icantly abolished platelet-induced EOMA cell proliferation in vitro and tumor development in vivo.
188 , EPO directly inhibited conventional T cell proliferation in vitro via tyrosine phosphatase SHP-1-de
190 ificantly inhibited ductal branching and MEC proliferation in vivo, which corroborated the in vitro a
191 -dependent activation of gene expression and proliferation, in the absence of ligand or presence of 4
192 suffering from recurrent EBV-induced B cell proliferations including Hodgkin's lymphoma because of a
193 mice, intestinal epithelial permeability and proliferation increase; this led to the concept that gli
198 tive tissues, providing evidence of how cell proliferation is controlled in an identity-specific mann
200 the embryonal theory for cancer cell growth/proliferation is overly simplistic, as meiotic factors a
203 cle, we show that CXCL8 expression, prior to proliferation, is common in newly arising T cells (so-ca
204 n of new taste bud cells, but not progenitor proliferation, is interrupted in mice treated with a hed
205 brate ribonuclease, is known to promote cell proliferation, leading to neovascularization as well as
206 survival times) were processed for DCX, cell proliferation markers (Ki-67, BrdU), pallial/subpallial
207 - and catecholamine-induced endothelial cell proliferation may be indicative of unappreciated evoluti
208 t and maturation and by suppressing aberrant proliferation mediated by the T cell antigen receptor (T
212 onstrated that RGC32 overexpression promoted proliferation, migration and tumorigenic growth of human
213 s is known to alter cell behaviors including proliferation, migration, and cell-cell adhesion, which
214 lays diverse roles in the regulation of cell proliferation, migration, and differentiation, these dat
216 and 24R,25(OH)2D3 on corneal epithelial cell proliferation, migration, and on the vitamin D activatin
217 L-deficient (lal(-/-)) mice possess enhanced proliferation, migration, and permeability of inflammato
218 elanoma tumor models decreased the levels of proliferation more than pancreatic cancer derived MDSC.
220 complete Foxc1 loss leads to aberrations in proliferation, neuronal differentiation and migration in
222 en-dependent signals delivered in the LZ, DZ proliferation occurs in the absence of such signals.
223 ic T cells are important to control HSV, and proliferation of activated T cells requires increased me
224 r MDS/EVI in regulating the formation and/or proliferation of adult intestinal adult stem cells durin
225 o inform on/off treatment cycles, suppresses proliferation of androgen-independent cells and lowers c
230 3 and CFB expression inhibited migration and proliferation of cSCC cells and resulted in potent inhib
232 hese data suggest that zinc may inhibit cell proliferation of esophageal cancer cells through Orai1-m
234 of STN NMDA receptors, which also suppresses proliferation of GABAergic pallido-STN inputs in PD mice
235 novel SOCE/Ca(2+)/beta-catenin-mediated anti-proliferation of GC cells, which is different from the c
237 ciated with reduced liver injury, diminished proliferation of hepatocytes and leukocytes, and attenua
239 th an ILC3 survival factor, IL-15, to induce proliferation of human ILC3s, as well as induce and main
240 brafish synergizes with MYCN to increase the proliferation of hyperplastic sympathoadrenal precursor
242 osed mice treated with celecoxib reduced the proliferation of LLC1 naive cells, while the opposite oc
245 ompartment and how wild-type cells limit the proliferation of mutant cells to maintain proper tissue
246 importance of these diseases as well as the proliferation of new diseases on a wider host range is l
248 resent antigen was examined by assessment of proliferation of ovalbumin-specific T cells in rat insul
249 growth factor, PDGF-AA, results in increased proliferation of PDGFRalpha+ cells via PI3K/Akt signalin
254 e assembly is essential for the survival and proliferation of SMARCA4/BRG1 mutant but not of SMARCA4/
255 mice induced endogenous CcnE1 expression and proliferation of surviving hepatocytes and nonparenchyma
256 ed that EBI3 activates STAT3 and induces the proliferation of the IL-6-dependent B9 mouse plasmacytom
258 instead a crucial role for SHH in promoting proliferation of these RP progenitors and for differenti
259 n of sensors of apoptotic cells impaired the proliferation of tissue-resident macrophages and the ind
261 essed the Hh-dependent growth events and the proliferation of tumor cells with aberrant activation of
263 ures and assigned them to categories such as proliferation-progenitor, proliferation-transforming gro
265 ll intrinsic MyD88 signaling is required for proliferation, protection from apoptosis and expression
266 that I-PTH plays a critical role in cellular proliferation, proteoglycan distribution, and mineraliza
267 staining in human organ-cultured corneas and proliferation rate in cultured corneal epithelial cells.
269 n of ACTRT1 reduced the in vitro and in vivo proliferation rates of cell lines with aberrant activati
270 d jaw bones of Cdc73(+/-) mice had increased proliferation rates that were 2-fold higher than in Cdc7
271 is required for fueling B cells prior to DZ proliferation rather than for allowing cell-cycle progre
272 12 to 18 mg/L, significantly inhibited cell proliferation, reduced cell viability, and was directly
275 (PH3) staining to assess apoptosis and cell proliferation, respectively, showed a significant increa
276 ith CMV antigens, induce a recall CD4(+) TH1 proliferation response only in CMV-seropositive donors.
277 Cas9 gene editing resulted in a halt of cell proliferation, severely impaired EGFR signaling and the
280 pression of various proteins involved in the proliferation, survival, migration and epithelial-to-mes
281 mutant models more effectively inhibited ALL proliferation than either inhibitor alone (P < .001) and
282 ependent energy signals alone stimulate cell proliferation, the development of a normal leaf lamina r
283 ector T cells (Teffs) rely on glycolysis for proliferation, the distinct metabolic features of regula
284 interaction could potentially suppress virus proliferation, this approach could offer a new strategy
285 S treatment significantly decreased PCa cell proliferation through down-regulation of GR and up-regul
286 uperoxide and inhibited cyst epithelial cell proliferation through extracellular signal-related kinas
288 by increasing apoptosis and decreasing cell proliferation through initiation of cell cycle arrest.
289 categories such as proliferation-progenitor, proliferation-transforming growth factor beta, and Wnt-c
291 found that a PKA inhibitor impaired ES cell proliferation, tumor growth and metastasis, which was re
292 itro and in vivo by inhibiting leukemia cell proliferation/viability and by promoting cell-cycle arre
294 fic peripheral blood mononuclear cell (PBMC) proliferation was evident, while decreased mitogen-stimu
297 oli cells prevents Kras (G12D) -induced cell proliferation, which leads to reduced tumor formation.
298 ssion level is critical for lung cancer cell proliferation, which may serve as a prognostic marker fo
300 e concentration-dependent inhibition of cell proliferation, yielding an IC50 value of 356 +/- 21 nM i
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