ライフサイエンスコーパス: GC-C

1 GC-C activity can regulate colonic cell proliferation by

2 GC-C and GC-CD853A showed similar Bmax and Kd values for

3 GC-C is also expressed in neurons, where it plays a role

4 GC-C is glycosylated in the extracellular domain, and di

5 GC-C is primarily expressed in the gastrointestinal trac

6 GC-C is targeted by the enterotoxigenic Escherichia coli

7 GC-C mRNA and protein were ectopically expressed in appr

8 GC-C mRNA was detected in blood mononuclear cells from a

9 GC-C null mice contained no detectable GC-C protein.

10 GC-C signaling regulated proliferation by restricting th

11 GC-C+/+ control mice or those having GC-C genetically ab

12 GC-C-/- mice had an increase in C. rodentium bacterial l

13 GC-C-deficient mice given the lactose diet reacted with

14 olon carcinoma cell (approximately 20 to 200 GC-C transcripts/cell) in 10(6) to 10(7) mononuclear blo

15 this model of osmotic diarrhea results in a GC-C-independent increase in intestinal fluid accumulati

16 ce or those having GC-C genetically ablated (GC-C-/-) were administered C. rodentium by orogastric ga

17 gesic mechanism of linaclotide: it activates GC-C expressed on mucosal epithelial cells, resulting in

18 n glycosylation at the same sites that allow GC-C to fold and bind ligand.

19 on isotope ratio mass spectrometry analysis (GC-C-IRMS).

20 By immunoblot analysis, GC-C protein appeared as early as 4 h after partial hepa

21 were characterized in uninfected GC-C+/+ and GC-C-/- mice using 16S rRNA PCR analysis.

22 Using 0.5 microg of total RNA and GC-C-specific primers, nested RT-PCR detected a single h

23 These results suggest the utility of STa and GC-C for the development of novel targeted imaging and t

24 ine the levels of guanylin, uroguanylin, and GC-C in mice with osmotic diarrhea.

25 to predict the primary interactions between GC-C agonists and their receptor.

26 nduction of guanylin and uroguanylin in both GC-C heterozygous and null animals.

27 ells were assayed for the expression of both GC-C and other epithelial cell-specific markers.

28 Immunoblot confirmed that both GC-C and GC-CD853A formed similar higher order oligomers

29 ild-type and heterozygous suckling mice, but GC-C null animals were resistant.

30 ' stage D colorectal cancer were analyzed by GC-C-specific nested RT-PCR using 1 microg of total RNA.

31 , purification, and halogenation followed by GC-C-IRMS analysis.

32 inoma cells that express guanylyl cyclase C (GC-C) and SW480 human colon carcinoma cells that do not

33 Guanylyl cyclase C (GC-C) has been shown to be the primary receptor involved

34 Guanylyl cyclase C (GC-C) is a multidomain, membrane-associated receptor gua

35 Guanylyl cyclase C (GC-C) is a transmembrane receptor expressed by human int

36 Guanylate cyclase C (GC-C) is a transmembrane receptor that is expressed prim

37 Guanylate Cyclase C (GC-C) is an apically-oriented transmembrane receptor tha

38 Guanylyl cyclase C (GC-C) is expressed in intestinal epithelial cells and se

39 Guanylyl cyclase C (GC-C) is the receptor for the heat-stable enterotoxin pr

40 uenced GUCY2C, encoding guanylate cyclase C (GC-C), an intestinal receptor for bacterial heat-stable

41 Guanylyl cyclase C (GC-C), an intestine-specific tumor suppressor, may repre

42 STaR, also known as guanylyl cyclase C (GC-C), is a member of the transmembrane guanylyl cyclase

43 n binds to and activates guanylyl cyclase C (GC-C), regulating fluid and electrolyte secretion in int

44 in intestinal receptor guanylate cyclase C (GC-C), the genetic cause for the majority of CSD is stil

45 Guanylyl cyclase C (GC-C), the receptor for diarrheagenic enterotoxins and t

46 me intestinal receptor, guanylate cyclase C (GC-C).

47 nd bind to the receptor guanylate cyclase C (GC-C).

48 heir actions through the guanylyl cyclase-C (GC-C) receptor.

49 activates the receptor guanylate cyclase-C (GC-C) to reduce food intake and prevent obesity.

50 alytic domain (D853A) of guanylyl cyclase-C (GC-C), the heat-stable enterotoxin (STa) receptor, rende

51 umably by activation of guanylate cyclase-C (GC-C), which stimulates production and release of cyclic

52 the intestinal receptor guanylate cyclase-C (GC-C).

53 tinal brush border, guanylyl cyclase type C (GC-C).

54 cose homeostasis are not mediated by central GC-C receptors.

55 A gas chromatograph-combustion (GC-C) system is described for the introduction of sample

56 However, under the same conditions, GC-C mRNA was detected in mononuclear cells from all 24

57 Relative to wild-type controls, GC-C(-/-) and Gn(-/-) mice had reduced apoptosis and inc

58 a-stimulated cGMP accumulation by decreasing GC-C activation in intact T84 human colorectal carcinoma

59 GC-C null mice contained no detectable GC-C protein.

60 Although they did not develop diarrhea, GC-C-sufficient and -deficient mice on the lactose diet

61 Here, eliminating GC-C expression in mice increased crypt length along a d

62 not into normal tissues that do not express GC-C.

63 lung tumor xenografts, which do not express GC-C.

64 o human colon cancer xenografts that express GC-C but not into normal tissues that do not express GC-

65 P production in those transiently expressing GC-C but not GC-CD853A.

66 ells infected with vaccinia virus-expressing GC-C and GC-CD853A (VVGC-CD853A) had [125I]STa-binding c

67 ependent manner in vaccinia virus-expressing GC-C-infected cells but not in those infected with VVGC-

68 Familial GC-C mutations demonstrate that epithelial cGMP signalin

69 therefore, identify downstream effectors for GC-C that contribute to regulating intestinal cell proli

70 of Cdx2, a transcription factor required for GC-C expression.

71 ss of ligand expression, suggests a role for GC-C in organizing the crypt-villus axis.

72 These findings demonstrate a novel role for GC-C signaling in facilitating mucosal wounding and infl

73 were performed with intestinal mucosae from GC-C knockout (KO) and wild type (WT) mice.

74 mammals, the pressure to retain a functional GC-C in the face of diarrhea-inflicted mortality remains

75 GC-C+/+ control mice or those having GC-C genetically ablated (GC-C-/-) were administered C.

76 When glycosylation of human GC-C was prevented, either by pharmacological interventi

77 Our aim was to determine if GC-C is required for host defense during infection by th

78 dependence showed that (125)I-STa-binding in GC-C KO mice involved a receptor distinct from that of W

79 stimulated a significant increase in DBS in GC-C KO mice.

80 ated duodenal bicarbonate secretion (DBS) in GC-C KO mice in vitro and in vivo.

81 C+/+ mice and, to an even greater degree, in GC-C-/- animals.

82 in contrast, continued to cause diarrhea in GC-C null mice, demonstrating that the cAMP signaling pa

83 a (RELMbeta) was substantially diminished in GC-C(-/-) mice.

84 Moreover, crypt expansion in GC-C(-/-) mice was associated with adaptive increases in

85 on strongly decreased guanylin expression in GC-C+/+ mice and, to an even greater degree, in GC-C-/-

86 of each of the 10 sites of glycosylation in GC-C, either singly or in combination, identified two si

87 n led to significant liver histopathology in GC-C-/- mice as well as lymphocyte infiltration and elev

88 ell apoptosis was significantly increased in GC-C-/- mice following 10 days of infection and this was

89 lpha and IFN-gamma production was minimal in GC-C(-/-) animals.

90 nic mucosa were significantly less severe in GC-C(-/-) mice and moderately reduced in Gn(-/-) animals

91 Increased GC-C signaling disturbs normal bowel function and appear

92 e thought to be restricted to the intestine, GC-C mRNA has recently been detected in other tissues.

93 lation of recombinant RELMbeta by enema into GC-C(-/-) mice restores sensitivity to DSS-mediated muco

94 We showed that 131- and 140-kDa GC-C isoforms represented immature and mature GC-C glyco

95 inducing cell cycle arrest, and mice lacking GC-C display increased cell proliferation in colonic cry

96 t tracer studies indicated that mice lacking GC-C, unlike GC-C+/+ animals, had a substantial loss of

97 C-C isoforms represented immature and mature GC-C glycoforms on the basis of endoglycosidase H and PN

98 and [(2)H5]phenylalanine tracers, and GC-MS/GC-C-IRMS we studied the effect of HMB or Leu alone on M

99 enerating liver contained four times as much GC-C as purified hepatocytes.

100 We carried out functional studies of mutant GC-C using HEK293T cells.

101 Relative to naive GC-C+/+ mice, the commensal microflora load in uninfecte

102 f this study were to determine whether a non-GC-C receptor exists for STa and what is the functional

103 r, our results suggest that alternative, non-GC-C, receptors likely exist for STa, uroguanylin, and g

104 aimed to determine the genetic cause for non-GC-C non-syndromic CSD in 18 patients from 16 unrelated

105 Activation of GC-C by administration of ST to wild type, but not Gucy2

106 We investigated whether activation of GC-C by the endogenous agonist uroguanylin or the primar

107 Activation of GC-C by the endogenous ligands guanylin or uroguanylin e

108 Ligand activation of GC-C causes it to produce cyclic GMP inside target cells

109 Activation of GC-C elevates intracellular cGMP, which modulates intest

110 ese data suggest that endogenous agonists of GC-C, such as uroguanylin, may play a role in regulating

111 Chronic deregulation of GC-C activity in early life increases susceptibility to

112 to < or = 0.8 microg eliminated detection of GC-C and other tissue-specific transcripts in blood of h

113 ctively binds to the extracellular domain of GC-C with subnanomolar affinity.

114 The downstream effector of GC-C, cGMP, was released after administration of linaclo

115 The cytostatic effects of GC-C agonists were associated with accumulation of intra

116 The exuberant expression of GC-C by nonparenchymal cells and, to a lesser extent, he

117 Virus-mediated expression of GC-C in H295R cells revealed concentration-dependent STa

118 he present studies examine the expression of GC-C in normal tissues and tumors from esophagus and sto

119 deoxycholate and acid induced expression of GC-C.

120 estinal metaplasia and ectopic expression of GC-C.

121 urrent work on the physiological function of GC-C in the intestine.

122 dine-2,4,6-trione; BPIPP} as an inhibitor of GC-C that can suppress STa-stimulated cGMP accumulation

123 Ala(15) comprise the primary interactions of GC-C agonists with the receptor surface.

124 ivity and/or glycan-mediated interactions of GC-C may have a crucial role to play in its functions in

125 occurred in the proximal small intestines of GC-C KO and WT mice.

126 In the context of uniform loss of GC-C signaling during tumorigenesis, dysregulation of th

127 ve mutations in NHE3, a downstream target of GC-C, as a cause of CSD and implies primary basal NHE3 m

128 reflected low-level ectopic transcription of GC-C in CD34+ progenitor cells.

129 Guanylate cyclase C (GUCY2C or GC-C) and its ligands, guanylin (GUCA2A or Gn) and urogu

130 ed agonist of guanylate cyclase-C (GUCY2C or GC-C) that reduces symptoms associated with irritable bo

131 in membranes from COS7 cells overexpressing GC-C but not GC-CD853A.

132 fied as a target of E. coli enterotoxin STa, GC-C is an important regulator of physiological salt and

133 , was found to express linaclotide's target, GC-C.

134 his work demonstrates the novel finding that GC-C signaling is an essential component of host defense

135 Given that GC-C is a major intestinal receptor in all mammals, the

136 Murine models indicate that GC-C regulates the composition of intestinal commensal m

137 We also show that GC-C is the first identified receptor client of the lect

138 These results suggest that GC-C agonists like linaclotide alleviate colorectal pain

139 nses in migration and apoptosis suggest that GC-C coordinates component processes maintaining homeost

140 These data suggest that GC-C may be useful for detecting circulating colorectal

141 The GC-C gene was disrupted by insertion of neo into exon 1

142 relevance of genetic variants affecting the GC-C-CFTR pathway to conditions such as Crohn's disease

143 16-fold higher in wild-type mice than in the GC-C null mice, and STa-stimulable guanylyl cyclase acti

144 e also carefully phenotyped mice lacking the GC-C receptor and found them to have normal body weight,

145 Therapeutic GC-C ligands are used to successfully treat constipation

146 Therefore, GC-C ligands may be novel therapeutic agents for the tre

147 Therefore, GC-C likely provides a protective effect against stresso

148 Thus, GC-C agonists regulate the proliferation of intestinal c

149 Thus, GC-C is the major cyclase activity present in the intest

150 the related peptide ligand guanylin bind to GC-C and stimulate an increase in cyclic GMP, inducing c

151 88, an inactive analog that does not bind to GC-C, did not selectively accumulate in cancer xenograft

152 colon cancer xenografts reflected binding to GC-C because (99m)Tc-NC100588, an inactive analog that d

153 (5--18) selectively recognizes and binds to GC-C expressed by human colon cancer cells in vivo.

154 odentium bacterial load in stool relative to GC-C+/+.

155 ing the regenerative period, we detected two GC-C isoforms that differed in their size, temporal expr

156 central nervous system administration of two GC-C agonists and found no significant reduction of food

157 al bacteria were characterized in uninfected GC-C+/+ and GC-C-/- mice using 16S rRNA PCR analysis.

158 the commensal microflora load in uninfected GC-C-/- mice was decreased and bacterial composition was

159 ies indicated that mice lacking GC-C, unlike GC-C+/+ animals, had a substantial loss of intestinal ba

160 e aim of this study was to determine whether GC-C and its ligands direct the course of intestinal inf