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

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

5 xeroderma pigmentosum complementation group G cells.

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

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

8 in defective maturation of nascent GCase in GD cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 G cells are luminal sampling chemomechanosensory cells w

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

27 60-G cells, but are reduced relative to HL60-G cells arrested by 96 h treatment with 1,25D3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 FA-G cells demonstrate distorted mitochondrial structures,

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

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

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

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

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

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

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

56 .022 +/- 0.001, and 0.0077 +/- 0.0003 mL/min/g cells for FIAU, FHBG, and FHPG, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 = 16.44 g cell/mol ATP and m = 3.27 mmol ATP/g cell per hour, were obtained from cellobiose-grown che

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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