ライフサイエンスコーパス: G cell

1 e microtubule/Golgi organization in clone II/G cells.

2 he G1 phase as compared to the parental HL60-G cells.

3 by the hormone gastrin released from gastric G cells.

4 e E1A reporter in NIH 3T3 cells but not in L-G cells.

5 ms of the FANCA and FANCC proteins in the FA-G cells.

6 xeroderma pigmentosum complementation group G cells.

7 tic differentiation of GM-CSF-dependent ECoM-G cells.

8 ells while histamine would stimulate that of G-cells.

9 signaling from gastrin-expressing endocrine (G) cells.

10 nduced the lncRNA-KMT2E tandem in hypoxic (G/G) cells.

11 in defective maturation of nascent GCase in GD cells.

12 eased to a maximum level of 8.0 +/- 0.9 nmol/g cell 30 s after hypoxia.

13 ll subpopulations corresponding to an SOH (e.g. cell activation status), isolating it from other SOH

14 the addition of material functionalities (e.g., cell adhesion ligands).

15 are critical for many cellular processes (e.g., cell adhesion, migration, and invasion), we examined

16 tain highly purified G cells by culture (64% G cells) after flow cytometry on elutriated fractions of

17 The G/G cells also exhibited increased norepinephrine-stimulat

18 re was a threefold increase in the number of G cells and a doubling in the number of parietal cells.

19 ot VMAT2, was localized to subpopulations of G cells and enterochromaffin (EC) cells; neither was fou

20 ylori, such as ammonia, release gastrin from G cells and might be responsible.

21 Depletion of Ly6-G(+) cells and use of C5aR1(-/-) bone marrow chimeras su

22 t here the presence of VMAT1 in rat gastrin (G) cells and the relevance of VMAT1 function for the mod

23 ns of precursor cells to produce the coupled G-cells and ECL cells.

24 It is proposed that the G-cells and the ECL cells are coupled by the couplet mol

25 r high-throughput imaging applications in, e.g., cell and developmental biology.

26 ns in the analysis of biological entities (e.g., cells and molecules).

27 nd applies to various biological entities (e.g., cells and virus particles).

28 rochromaffin-like (ECL) cell, the gastrin or G cell, and the somatostatin or D cell.

29 om enterochromaffin-like cells, gastrin from G cells, and somatostatin from D cells.

30 Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL)

31 tation group C, and XP complementation group G cells are deficient in ODD repair and ODD induces a hi

32 G cells are luminal sampling chemomechanosensory cells w

33 cells while for lateral loading even at 1400 g cells are modestly affected.

34 tin secreting D-cells, and gastrin secreting G-cells are absent from the epithelium of the glandular

35 60-G cells, but are reduced relative to HL60-G cells arrested by 96 h treatment with 1,25D3.

36 Both 28 and 29 displayed good potency in GS cell-based assay.

37 phaoGS/GS and nearly abolished in Galphai2GS/GS cells because of enhanced signaling via a pertussis t

38 p27 cells compared with transfectant control G cells but not at 4-h ATP depletion.

39 gene driven by glycoprotein IX promoter in L-G cells but not in NIH 3T3 cells, the fusion protein was

40 vAc(64-) formed plaques on Sf9(VSV-G) cells but not on Sf9 cells, and plaques formed on Sf9

41 nt sublines as compared to the parental HL60-G cells, but are reduced relative to HL60-G cells arrest

42 A method to obtain highly purified G cells by culture (64% G cells) after flow cytometry on

43 Thus rat antral G cells can express VMAT1; transport of biogenic amines

44 n-actin binding) and cellular functioning (e.g. cell-cell adhesion and differentiation).

45 (e.g. cortical mark) or an extrinsic cue (e.g. cell-cell signal).

46 ss numerous fields, including fundamental (e.g., cell-cell communication) and applied (e.g., drug dis

47 hose with more recently evolved functions (e.g., cell-cell communication).

48 ion manifest at scales ranging from local (e.g., cell-cell interactions) to global (e.g., body axis p

49 transducing cells, particularly the gastrin (G) cell, co-ordinate gastric acid secretion with the arr

50 The higher PPARGC1B expression in G/G cells coincided with greater accumulation of triglycer

51 r in genes involved in specific processes, e.g., cell communication, transcription, regulation of tra

52 that the perturbed insulin secretion of high-G cells could not be accounted for by increased proton l

53 amine in a variety of biological settings (e.g., cell culture experiments and in vivo mouse labelling

54 f cells and cell debris, a 0.50 mL sample (e.g., cell culture medium) is incubated with CM-Dil dye to

55 wofold; whereas bombesin treatment of antral G cell cultures stimulated gastrin release but not gene

56 not inhibit thioredoxin reductase or cause a G cell cycle arrest.

57 we have examined the expression of specific G, cell cycle regulators.

58 s cell types and identifies both expected (e.g. cell cycle and hypoxia) and novel activity programs,

59 the niche, exhibit sex-specific behaviors (e.g. cell cycle length) and therefore have acquired sexual

60 s, thereby triggering cell fate decisions (e.g., cell cycle arrest, apoptosis).

61 e to intracellular Ca2+ than other events, e.g., cell cycle resumption.

62 ce, revealed Tyr-specific sex differences (e.g., cell cycle), accentuated in females (with significan

63 The rate of k (g COD/g Cells.d) in ASM 1 was 2.69% and, 22.79% higher than AS

64 ly contribute to radiation-induced damage (e.g. cell death, genomic instability, carcinogenesis), par

65 udying plaque-related pathological events (e.g., cell death and neuron dysfunction).

66 consequences that affect cell phenotypes (e.g., cell death) in unanticipated ways.

67 FA-G cells demonstrate distorted mitochondrial structures,

68 GalphaoG184S homozygous knock-in (GalphaoGS/GS) cells demonstrated enhanced adenosine A1 and muscari

69 of 24.7% in the number of gastrin-producing G cells detected.

70 After 2 h at 2.8 mm glucose, high-G cells did not retain increased levels of glycolytic or

71 that control critical cell-fate decisions (e.g., cell division and apoptosis) can function with such

72 ablished up to a concentration of 700 microg/g cell dry weight for each analyte.

73 PC12-G cells express sufficient levels of PAC1 receptors to p

74 In addition, PC12-G cells expressing bPAC1hop acquired the ability to rele

75 Notably, ordinal and nominal (e.g., cell fate observations) non-quantitative data synerg

76 .022 +/- 0.001, and 0.0077 +/- 0.0003 mL/min/g cells for FIAU, FHBG, and FHPG, respectively.

77 ry transitions, in which biological units (e.g., cells) form groups that evolve into new units of bio

78 nger-associated molecular patterns (DAMPs; e.g. cell-free DNA and ATP) and cytokines (e.g. IL-1beta a

79 n and mortality, whereas other NET assays (e.g., cell-free DNA, myeloperoxidase, and myeloperoxidase-

80 These studies of nutrient-regulated G-cell gastrin secretion and growth provide definitive e

81 -CSF production) and tumor cell behaviors (e.g. cell growth, survival, and invasion).

82 s describing various stochastic phenomena (e.g., cell growth, cell division), and even identify and a

83 Furthermore, G/G cells had improved basal- and norepinephrine-stimulate

84 Isolated canine G cells in primary culture have been used to study calci

85 Gastrin, produced by G cells in the gastric antrum, has been identified as th

86 The expression of CaR on gastrin-secreting G cells in the stomach and their shared activation by Ca

87 gastrin mRNA, many fewer gastrin-producing (G) cells in the stomach antrum, hypogastrinemia, and inc

88 Gastrin is a hormone produced by G-cells in the normal gastric antrum.

89 is of the stomach is associated with loss of G cells, increased symmetric stem cell division, glandul

90 The G cell is activated by acetylcholine and gastrin-releasi

91 bombesin-induced gastrin release from canine G cells is stimulated by Ca2+ but not by PKC, and is enh

92 The feedback modulation by G cells is thought to also provide the mechanism for obj

93 ase from the antral gastrin-expressing cell (G cell) is regulated by bombesin and luminal factors.

94 Parietal and G cells, Ki67, TUNEL, villin and MUC2 expression were an

95 Correction of an FA-G cell line with the FANCG complementary DNA (cDNA) resu

96 correct the mitomycin C sensitivity of an FA-G cell line.

97 n, visualization and statistical analysis, e.g. cell line mutation or drug class/target pathway.

98 genization and solubilization of a source (e.g., cell line) followed by immobilization on either the

99 human mast cells with chymase and cathepsin G cells may be grossly underestimated.

100 esults suggest that modulatory feedback from G-cells may underlie both spatial and object-based atten

101 so deepened our knowledge of other topics (e.g. cell mechanosensing, motility, and bacterial aging),

102 omolecules, lipid membranes, and proteins (e.g. cell membrane receptors, ion channels) are presented.

103 es that do not interact with cell borders (e.g., cell membrane or nucleus).

104 actions of water molecules with obstacles (e.g., cell membranes), the observed changes point to a dyn

105 were found to contain significant numbers of GS+ cells (microglia) at the time of grafting.

106 involve physical interactions among them, e.g. cell migration and proliferation.

107 al tissues are regulated by cell fluidity, e.g., cell migration and intercalation, lacking in plant t

108 in processes important for vasculogenesis (e.g., cell migration, adhesion, extracellular matrix organ

109 This GD cell model was amenable to lead discovery via titrati

110 maintenance parameters, Y(X/ATP)True = 16.44 g cell/mol ATP and m = 3.27 mmol ATP/g cell per hour, we

111 or of metastatic tumor cells are indirect, e.g., cell motility is examined in vitro and the results a

112 actin are key to many cellular functions, e.g., cell motility, endocytosis, cell:cell adhesion, and

113 n growth and developmental functions of CaR, G-cell number was progressively reduced between 30 and 9

114 maffin cells resulted in acquisition by PC12-G cells of PACAP-dependent [Ca2+]i increase and extracel

115 lecular level in a biological environment, e.g. cells or cell components.

116 articular features of inhibitory networks (e.g., cell or input type) contribute to their synchronizin

117 ples on their native transparent surfaces, e.g., cells or tissue sections on slides.

118 a 1-L culture of E. coli ( approximately 2.3 g cell paste).

119 = 16.44 g cell/mol ATP and m = 3.27 mmol ATP/g cell per hour, were obtained from cellobiose-grown che

120 affinity for reduced nitrogen (68,700 l per g cells per h) of SCM1 suggests that Nitrosopumilus-like

121 ed more sensitive for microscopic studies (e.g., cell physiology).

122 Pure G-cell preparations (>97%) were isolated.

123 um velocities of 4.62 and 14.2 ng/min/ micro g cell protein, respectively.

124 Thus, MO7e-G cells provide a powerful system in which the molecular

125 functionally active, and the resultant MO7e-G cells recapitulate the proliferative synergy between S

126 This study unravels a mode of G cell regulation that is functionally important in gast

127 ellular insulin content was depleted in high-G cells, relative to low-G and high-P cells, cellular fu

128 hat the antral innervation normally inhibits G-cell responses to non-nutrient distension of the stoma

129 age and amplification of vAc(64-) on Sf9(VSV-G) cells resulted in pseudotyped virus particles that co

130 nges in gastric acidity to the regulation of G-cell secretion of gastrin.

131 ed with a loss of the electron-dense core of G cell secretory vesicles.

132 a wide range of repair construct designs (e.g. cell-seeding strategy, sheath material, culture condi

133 High-G cells showed decreased responsiveness, relative to low

134 In contrast, Galphai2GS/GS cells showed enhanced responses to M2 but not A1 rece

135 Pr) at the promoters of upregulated genes (e.g., cell signaling and extracellular matrix genes) and a

136 ection and alter true biological features (e.g. cell size) due to our limited ability to interpret th

137 sms of RBP specificity have been proposed (e.g., cell-specific expression of RBPs and secondary struc

138 pes and physiologically relevant contexts (e.g., cell spheroids, ex vivo tissues, in vivo tissues).

139 f events following postreceptor occupancy (e.g., cell spreading).

140 The gastrin (from G-cells) stimulates the ECL cells to produce and secrete

141 o showed increased parietal cells and lacked G cells, suggesting loss of antral identity.

142 n of pseudotyped vAc(64-) virions in Sf9(VSV-G) cells suggests that the VSV-G protein may either poss

143 esting an effect on the up-regulation of HLA-G cell surface expression.

144 rved mainly in certain types of molecules (e.g. cell surface receptors) and systemic functions, parti

145 The sorting of transmembrane proteins (e.g., cell surface receptors) into the multivesicular body

146 tivalent proteins and multivalent ligands (e.g., cell surfaces).

147 l as functional pathways of breast cancer (e.g. cell survival, proliferation, and colony formation).

148 ting calibration of biological dosimeters (e.g., cell survival, chromosome aberrations), which can be

149 of buffers, reagents, reaction conditions (e.g., cell suspension concentration, lysis time, lysis tem

150 activity in FA-A, FA-C, FA-D2, FA-F, and FA-G cells that could account for the deficiency in alphaII

151 nted by a population of dedicated grouping ("G") cells that integrate the activity of the distributed

152 postulate the existence of a second type of G-cell that represents spatial attention by modulating t

153 g cells (that also lack subunit e) do not show PTP chann

154 in FA complementation group B, C, D2, F, and G cells there is also a deficiency in production of thes

155 zation of and extended growth on surfaces (e.g., cell tissue) and increases antibiotic resistance.

156 is essential to understanding a matrix's (e.g. cell, tissue, or biofluid) metabolic state.

157 on of PRDX3 suppresses the sensitivity of FA-G cells to H2O2, and decreased PRDX3 expression increase

158 We aimed to isolate pure G cells to identify the mechanistic basis of luminal- an

159 n signaling pathway that operates in gastric G cells to inhibit gastrin expression on a transcription

160 s histamine (from ECL cells), stimulates the G-cells to produce and secrete gastrin.

161 logies, and stabilizing mechanical forces, e.g., cell-to-cell and cell-to-matrix adhesion.

162 orm retained surface CD19 and immunoglobulin G, cells transduced with the short TACI isoform complete

163 tion status), isolating it from other SOH (e.g. cell type, cell cycle phase).

164 r, symmetry, organ number) and microscale (e.g. cell type, tissue patterning) features often lead to

165 le statements following a fixed structure (e.g., "cell type, signal, response, behavior").

166 mechanisms of these therapies may differ (e.g., cell type-specificity, N-methyl-D-aspartate receptor

167 into microcosms with specialist functions, e.g. cell types.

168 AK1, and PTK2B), and downstream functions (e.g. cell viability, protein quality control), and metabol

169 Cell toxicity characterisation (e.g., cell viability assays using 3-(4, 5-dimethylthiazol-

170 By monitoring multiple system quantities (e.g., cell volume, Hog1, glycerol) and using varied input

171 enzymes for sucrose and starch hydrolysis (e.g. cell wall invertase, alpha-amylase, and starch phosph

172 se, when present in complex carbohydrates, e.g., cell wall, glycoproteins, and glycolipids, is specif

173 and fluorescence-activated cell sorting, rat G cells were prepared and luminal, neural, hormonal, and

174 on Sf9 cells, and plaques formed on Sf9(VSV-G) cells were observed only after prolonged intervals.

175 eic and allogeneic grafts, intensely labeled GS+ cells were localized in the centers of rosettes in s

176 ifferent microtubule distributions: clone II/G cells, which gradually reorganize a PN-type distributi

177 This notwithstanding, titration of low-G cells with low protonophore concentrations, monitoring

178 Pretreatment of G cells with thapsigargin (10(-8)-10(-6) M) and release

179 ase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-exp

180 le to maintain a hyperpolarized potential (e.g. cells with a large inwardly rectifying or Ca(2+)-acti

181 ed decreased responsiveness, relative to low-G cells, with respect to mitochondrial membrane hyperpol