ライフサイエンスコーパス: D cell

1 receptors on the gastric SOM-secreting cell (D cell).

2 e gastrin or G cell, and the somatostatin or D cell.

3 he role of LR during KSHV infection of HMVEC-d cells.

4 gastrin from G cells, and somatostatin from D cells.

5 se new neurons through immature intermediate D cells.

6 stimulating the release of SOM from gastric D cells.

7 comitant decrease in somatostatin-expressing D cells.

8 ffin (EC) cells; neither was found in antral D cells.

9 gene expression differences between EVP and D cells.

10 o increase VEGF in the media of cultured T47-D cells.

11 ted by progesterone receptors present in T47-D cells.

12 decrease after cell cycle induction in COMMA D cells.

13 ginosa associated with plastic compared to 3-D cells.

14 their phenotype such that they resemble AhR-D cells.

15 s an exacerbated pathological condition in B-D cells.

16 itotic entry and catastrophe compared to DDR-D cells.

17 M2 cells, and is termed here displaced or M-d cells.

18 fically deglutathionylated by GSTO1-1 in T47-D cells.

19 hway, showed increased activities in beta1-k/d cells.

20 vbeta3-integrin was detected only in beta1-k/d cells.

21 vity and COL1A2 promoter activity in beta1-k/d cells.

22 enhanced COL1A2 promoter activity in beta1-k/d cells.

23 or the induction of apoptosis in infected M1-D cells.

24 e CLS for SSD1-V cells is twice that of ssd1-d cells.

25 ved by electron microscopy of infected HMVEC-d cells.

26 ssion of Bcl-2, which is not expressed in M1-D cells.

27 oxide synthase (nNOS) is present in gastric D-cells.

28 them engaged insulin production, like a- and d-cells.

29 lusive effect by AG-induced SST release from d-cells.

30 le for increased VSV replication in Dicer1(d/d) cells.

31 asin mutants and expressed them in 721.220-L(d) cells.

32 mote the hepatocyte differentiation of CD49f(D) cells.

33 NA levels and antral somatostatin-producing (D) cells.

34 intracellular Ca2+ release was decreased in DD cells.

35 bited lysosomal deficits similar to those in DS cells.

36 ight-evoked spike activity of neighboring ON DS cells.

37 actor in the enhanced metabolism of ara-C in DS cells.

38 n the cell cycle distributions of DS and non-DS cells.

39 a strong and specific RUNX1 dependency in ML-DS cells.

40 ly rescue the APP and PSD95 up-regulation in DS cells.

41 the suppression of mitochondrial function in DS cells.

42 classes ranging from LGN cells to V1 complex DS cells.

43 induced Hog1 activation was observed in Pbs2(DD) cells.

44 ntiation of WEHI-3B myelomonocytic leukemia (D(+)) cells.

45 by drifting sinusoidal gratings (negative OS/DS cells); (2) suppressed-by-contrast cells; (3) cells w

46 ck proteins (HSPs) in heat shock-treated T47-D cells, a human breast cancer cell line that expresses

47 promote terminal differentiation of WEHI-3B D(+) cells, a phenomenon accompanied by the recovery of

48 oylphorbol-13-acetate was added to the HMVEC-d cells after 48 h p.i.

49 the sequence of appearance of the different D cells after a 7-day treatment with anti-mitotics.

50 ntrol of a laptop computer and powered by 10 D-cell alkaline batteries.

51 of gamma interferon (IFN-gamma)-activated M1-D cells also resulted in apoptosis but with no evidence

52 alactose supplementation, NPC1-deficient ldl-D cells also transported more cholesterol from lysosomes

53 DS cells also exhibited slower proliferation rates.

54 electron-dense SGL cells, which we call type D cells and are derived from the astrocytes and probably

55 which reached a maximum at 2 h p.i. in HMVEC-d cells and at 8 h p.i. in HFF cells, and significantly

56 released mainly from gastric and pancreatic D cells and enteric neurons, inhibit peripheral cellular

57 ion very early during the infection of HMVEC-d cells and that ROS production was sustained over the o

58 uman dermal microvascular endothelial (HMVEC-d) cells and human foreskin fibroblast (HFF) cells in vi

59 uman dermal microvascular endothelial (HMVEC-d) cells and human foreskin fibroblast (HFF) cells is ch

60 ide the first description of the negative OS/DS cells and demonstrate that the SC segregates cells wi

61 nalysis shows that GEDDs are present both in DS cells and in Dp1Tyb mouse fibroblasts and hippocampus

62 were 2.6-fold higher in DS compared with non-DS cells and may be a factor in the enhanced metabolism

63 inducing AKR1C1-mediated P4 inactivation in DS cells and that inhibiting and/or bypassing of AKR1C1-

64 eas the dSC is enriched with the negative OS/DS cells and with cells with large RFs, low evoked FRs,

65 lls interact with maternal decidual stromal (DS) cells and maternal immune cells in the decidua (endo

66 ), and have reduced numbers of somatostatin (D-cells) and peptide YY-expressing cells (L-cells).

67 addition to their direction selectivity (OMS-DS cells) and thereby combine sensitivity to two distinc

68 t one blastomere at the four-cell stage, the D cell, and its direct descendants play an important rol

69 focal adhesion significantly more in beta1-k/d cells, and activated alphavbeta3-integrin was detected

70 on secreting A-cells, somatostatin secreting D-cells, and gastrin secreting G-cells are absent from t

71 ON DS cells are coupled indirectly via gap junctions made w

72 The OMS-DS cells are further distinct from standard (non-OMS) DS

73 We propose that OFF inputs to ON DS cells are normally masked by a GABAergic inhibition,

74 Furthermore, although the salamander DS cells are OFF-type, there is a strong analogy to the

75 ationship with DP and found that a subset of DS cells are retained following each hair cycle, exhibit

76 BP-delta gene expression is induced in COMMA D cells arrested in G0 by serum and growth factor withdr

77 cell-cycle determined default polarity site (DS), cells assemble a gradient tracking machine (GTM) co

78 nally, we identify OS and two populations of DS cells at the superficial border of the tectal neuropi

79 In MMR-d cells, ATRi stimulates the accumulation of nascent DNA

80 raft blocked viral gene expression in HMVEC-d cells but not in HUVEC or HFF cells.

81 d mutant FA-D (Fanconi complementation group D) cells but not in mutant FA-A cells.

82 ith the early endosome marker EEA-1 in HMVEC-d cells, but rather with the late endosome marker LAMP1,

83 or (ATRi) imposes synthetic lethality on MMR-d cells by inducing DNA damage in a replication- and MUS

84 Introduction of AhR cDNA into AhR-D cells by stable transfection alters these characterist

85 at this is mediated by inactivation of P4 in DS cells by aldo-keto reductase family 1 member C1 (AKR1

86 are further distinct from standard (non-OMS) DS cells by their smaller receptive fields and different

87 In contrast to COMMA D cells, C/EBP-beta and C/EBP-delta mRNA levels remain r

88 l effect of cell contacts is to position the D cell cleavage furrow closer to the animal pole, and th

89 ti-biofilm peptide DJK-5 were evaluated on 3-D cells compared to a plastic surface, in medium with an

90 The CEs of 7-d cells contain significant amounts of the protein loric

91 , and the enhanced division asymmetry of the D cell contributes to the suppression of eye development

92 oclonal antibodies to hK2, we found that T47-D cells could be induced with androgens, mineralocortico

93 By contrast, two-dimensional (2-D) cell-counting methods are said to be 'assumption-base

94 icelles were evaluated in vitro in 2-D and 3-D cell culture and in vivo in xenograft models of ovaria

95 lles were not significantly more potent in 2-D cell culture in comparison to paclitaxel; however, the

96 DOX) efficacy were evaluated using 2-D and 3-D cell culture models.

97 idely developed for efficient and reliable 3-D cell culture research.

98 etection and demonstrated its utility in a 3-D cell culture system.

99 -derived breast tumoroids corroborated the 2-D cell culture-based findings.

100 are typically grown using two-dimensional (2-D) cell culture approaches, where the native tumor micro

101 raphy techniques to produce 3 dimensional (3-D) cell culture substrates decorated with micron sized p

102 In 2-D cell cultures, irradiation with NIR light at low power

103 er, IL-4 stimulated SOM release from primary D cell cultures.

104 The latter population may underlie the type D cell current.

105 Type D cell currents had more hyperpolarized availability and

106 lasses of doublecortin and PSA-NCAM-positive D cells (D1, D2, D3) were observed.

107 The data suggest that IFN-gamma-activated M1-D cell death receptors become susceptible to their ligan

108 osylation, we used Chinese hamster ovary ldl-D cells defective in UDP-Gal/UDP-GalNAc 4-epimerase in w

109 Although the DS cell dendrite received the majority of its synaptic i

110 tly observed synaptic profile consisted of a DS cell dendrite receiving synapses from a cluster of se

111 make a putative inhibitory synapse with the DS cell dendrite.

112 offset of the direct inhibitory input to the DS cell dendrites.

113 nor apoptosis, whereas differentiated M1 (M1-D) cells developed a restricted virus infection and chan

114 Only in H2d/d cells did Ly49C/I dominantly inhibit Ly49D-Dd stimulat

115 majority of genes after UV, whereas pure XP-D cells did not.

116 Although Pbs2(DD) cells did not exhibit high basal levels of Hog1 phos

117 Increased OLIG2 expression in DS cells directly upregulates interneuron lineage-determ

118 Significantly, both Pbs2(AA) and Pbs2(DD) cells displayed impaired stress resistance and atten

119 Fluorescence microscopy reveals that AhR-D cells do not exhibit an increased rate of death.

120 s provides a secondary mechanism by which ON DS cell ensembles can signal direction of stimulus motio

121 pears key to the direction selectivity of ON DS cells, evoking both an attenuation of spike frequency

122 Our results reveal that AhR-D cells exhibit a different morphology, decreased albumi

123 ntermediate step to bridge the gap between 2-D cell experiments and in-vivo studies.

124 Because ldl-D cells express endogenous cell surface CD44, the effect

125 Both unactivated and activated M1-D cells expressed TRAIL receptors (R1 and R2), but only

126 Growth arrest is markedly delayed in COMMA D cells expressing a C/EBP-delta antisense construct.

127 appear to interact closely with clusters of D cells forming radial proliferative units.

128 Therefore, we investigated the role of NO in D-cell function and the effects of prolonged exposure of

129 Compared with 2-D, cells grown in 3-D had increased numbers of KSHV late

130 Type D cells had little or no current in 0.3 microM TTX at a

131 Only EVP cells and not TA and D cells had self-renewal capacity as demonstrated by col

132 Although COMMA-D cells harbor mutations in both alleles of p53, they ar

133 trol (Bmal1-wildtype) and Bmal1-disrupted (B-D) cells having their molecular clock impaired.

134 Conversely, D cells highly expressed genes related to differentiated

135 uman dermal microvascular endothelial (HMVEC-d) cells, human B (BJAB) cells, and Chinese hamster ovar

136 in FA-A cells but also in FA-B, FA-C and FA-D cells (i.e. in all FA cell lines tested), suggesting a

137 ECs but stimulates PTHrP production by Comma-D cells (immortalized murine mammary cells) and MCF-7 hu

138 at Salmonella established infection of the 3-D cells in a much different manner than that observed fo

139 ic acid increased differentiation of WEHI-3B D(+) cells in a manner that was analogous to the combina

140 d a severe reduction in recipient type (H-2b,d) cells in mice with active GVHD, whereas in protected

141 rong analogy to the systems of ON and ON-OFF DS cells in the mammalian retina.

142 d the kinetics of BeAn virus infection in M1-D cells, in order to temporally relate virus replication

143 ymetrix 430 2.0 arrays) revealed that WT and D(-) cells incubated with 8-CPT-cAMP have similar, but n

144 e in extramitochondrial Ccp1 isolated from 7-d cells, indicating that heme labilization results from

145 1(H) MKPs produced a partial effect on CD49f(D) cells, inducing the formation of hepatoepithelial lay

146 The D cell is activated by either gastrin or CCK and appears

147 One role of PRs in T47-D cells is regulating expression of vascular endothelial

148 ssion of mitochondrial electron transport in DS cells is due to high expression of cystathionine-beta

149 uman microvascular dermal endothelial (HMVEC-d) cells, Kaposi's sarcoma-associated herpesvirus (KSHV)

150 Similar to the results for HMVEC-d cells, KSHV infection of HUVEC cells also resulted in

151 strocytes form baskets that hold clusters of D cells, largely insulating them from the hilus.

152 ith normal extracts, but extracts from an XP-D cell line exhibit twice the activity.

153 In a human DS cell line and in explant cultures of term human fetal

154 te Nkx6.3 as a selective regulator of G- and D-cell lineages, which are believed to derive from a com

155 DS cell lines also generated higher levels of ara-CTP co

156 In model B, injection of a anti-b/tol-d cells markedly reduced, but did not deplete, periphera

157 ption factor Ngn3 that were positive for the d cell marker somatostatin and occasionally co-expressed

158 ell locomotion within a three-dimensional (3-D) cell mass, we have undertaken a systematic 3-D analys

159 othesis that enhanced metabolism of ara-C in DS cells may be a contributing factor to the superior su

160 Implanted QNR/D cells migrate only to the retinal ganglion and amacrin

161 normal forces play important roles even in 2-D cell migration.

162 inoglycosides were more efficacious in the 3-D cell model.

163 FBS, colistin was less efficacious in the 3-D cell model.

164 atostatin, released respectively from a- and d-cells, modulate the secretion of insulin by B-cells.

165 helial cell line Int-407 revealed that the 3-D cells more accurately modeled human in vivo differenti

166 hibition that temporally shifts firing of ON DS cell neighbors, resulting in a desynchronization of s

167 Kit(D)CD45(-)Ter119(-)), the remaining CD49f(D) cells neither differentiated nor survived in vitro.

168 ded on tissue culture-treated surfaces, by 4 d cell numbers and proliferation rates were significantl

169 A threefold decrease in the number of D cells occurred in H. pylori- and A. lwoffii-infected m

170 oreactivity were often in close proximity to D cells of the gastric and intestinal mucosa.

171 array system has the potential to improve 3-D cell oncology models and allow for better-controlled s

172 tional dysregulation compared with "pure" XP-D cells or WT cells.

173 of time, and typically involve engineered 3-D cell organization.

174 minimum phase differences needed to generate DS cells overlaps that exhibited by non-DS simple cells.

175 However, we find that ON DS cell pairs show robust synchrony for all directions o

176 e distribution of viral capsids at the HMVEC-d cell periphery, and capsids did not associate with mic

177 In DS cells, pharmacological inhibition of CBS activity wit

178 DS cells produced significantly more H(2)S and polysulfi

179 cromeres in the establishment of the dorsal (D) cell quadrant was examined in C. lacteus by removing

180 logous to the typical spiralian A, B, C, and D cell quadrants.

181 The sustained, uncoupled ON DS cell ramifies completely within the lower cholinergic

182 wever, analysis of cell pairs indicates that DS cells receive cortical input from non-DS simple cells

183 From light micrographic 3-D cell reconstructions, the absolute volume, number, and

184 rythroid precursors and knockdown (KD) in ML-DS cells reduced their erythroid phenotype.

185 ses imply that the slowed growth rate of AhR-D cells reflects prolongation of G1.

186 tely 1100 transcripts were changed in WT and D(-) cells, respectively.

187 stochemistry of junctional markers on A549 3-D cells revealed that these cells formed tight junctions

188 including microfluidic device fabrication (2 d), cell seeding (1 d), and progressive development of t

189 promising profile regarding activity in T47-D cells, selectivity toward ERalpha and ERbeta, inhibiti

190 We conclude that 3-D cell shape information, transduced through tension-ind

191 A recent study reported that DS cells show genome-wide transcriptional changes in whi

192 Moreover, conditioned medium from PC3 PDGF-D cells significantly increased the tube formation of hu

193 Our results suggest that the two classes of DS cells specialize to encode motion direction of local

194 e found that the hK2 in androgen-induced T47-D cell spent media appears to be the pro-form of hK2 rat

195 CRISPR generated, NPC1-deficient ldl-D cells supplemented with galactose accumulated more cho

196 uman microvascular dermal endothelial (HMVEC-d) cell surface heparan sulfate (HS), integrins alpha3be

197 irus was highly restricted, BeAn-infected M1-D cells synthesized and appropriately processed virus ca

198 partment concentrations and N-SS flux in the D-Cell tests and, at 500 rpm, the FDM-determined D(Gel)

199 In 72 D-Cell tests with nitrate, 63 met this threshold, but th

200 rst law from two-compartment diffusion cell (D-Cell) tests.

201 strate that the expression of GSTO1-1 in T47-D cells that are devoid of endogenous GSTO1-1 resulted i

202 osis in A-cells, and trans-acting factors in D-cells that can overcome this protection, resulting in

203 specifically on the mechanical properties of Dd cells, the results suggest that this behavior will be

204 ilar to the characteristic ON response of ON DS cells, the masked OFF response is also direction sele

205 ted cells suggests that susceptibility of M1-D cells to apoptosis may be controlled, in part, by expr

206 Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduc

207 e considerably more responsive than parental D(+) cells to ATRA as a single agent, supporting the con

208 ion and the effects of prolonged exposure of D-cells to NO.

209 g the mechanisms of increased sensitivity of DS cells to ara-C related to the CBS gene may lead to th

210 apping of adult hair follicle dermal sheath (DS) cells to determine their lineage relationship with D

211 D(+) cells transfected with an expression plasmid contai

212 Unirradiated COMMA-D cells transplanted to mammary fat pads cleared previou

213 ments against an elastic cantilever, and a 2-d cell undergoing wave-like protrusion dynamics.

214 necessary for its efficient entry into HMVEC-d cells via macropinocytosis.

215 le, plausible neuronal circuits that produce DS cells via different mechanisms and tested these circu

216 d a H(2) production rate of 72 +/- 2 LH(2)/L-d (cell voltage of 0.79 +/- 0.00 V).

217 ) and a H(2) production rate of 72 2 LH(2)/L-d (cell voltage of 0.79 0.00 V).

218 he mass balance model predicted D(FBS/w) and D(cell/w) within a factor of 3 and 3.4, respectively, in

219 (FBS/w)) and cell-water distribution ratios (D(cell/w)) for four different cells lines were determine

220 chemicals was used to calculate D(FBS/w) and D(cell/w).

221 Androgen induction of hK2 in T47-D cells was dose dependent.

222 PACAP action on D cells was measured by [Ca(2+)](i) and radioimmunoassay

223 howed differential expression between WT and D(-) cells, we found differences in cAMP-mediated regula

224 polymyxins) showed enhanced efficacy when 3-D cells were present.

225 Elevated ara-CTP levels in the DS cells were accompanied by slightly lower levels of en

226 as, thus unresponsive to DBA/2 (a anti-b/tol-d cells), were injected into (B6 x D2)F(1) --> B10.A mix

227 ntly inhibited both mTOR and Akt in PC3 PDGF-D cells, which were correlated with decreased cell proli

228 c or oxidative stress, activate Spc1 in wis1-DD cells, which express Wis1 protein that has the MEKK c

229 al ganglion cell is the direction selective (DS) cell, which responds vigorously to stimulus movement

230 cium signaling and somatostatin release from D cells with almost equal efficacy.

231 ubpopulation of weakly melanopsin-positive M-d cells with similarities to M2 cells.

232 Pretreatment of HMVEC-d cells with the antioxidant N-acetylcysteine (NAC) sign

233 antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosi

234 ing: (1) orientation/direction-selective (OS/DS) cells with a firing rate that is suppressed by drift

235 sa formed antibiotic resistant biofilms on 3-D cells without affecting cell viability.