ライフサイエンスコーパス: HBP

1 HBP and pre-HBP in children and adolescents are on the r

2 HBP ascertainment was based on age-, gender-, and height

3 HBP genes were overexpressed in human prostate cancers a

4 HBP is a strong chemoattractant for monocytes that also

5 HBP was administered to mice at different concentrations

6 In addition, HBP had an additive effect on LPS-induced production of

7 D32w expression in PECs did not change after HBP or CLP.

8 BP and HBP reversed their downward trends 10 years after the in

9 Pre-HBP and HBP increased 2.3% (P=0.0003) and 1% (P=0.17), respectiv

10 The BP, pre-HBP, and HBP trends were downward from 1963 to 1988 and upward th

11 ent call for early prevention of obesity and HBP and illustrate racial/ethnic disparities in this age

12 determinant for washout of gadoxetic acid at HBP (P < .001).

13 , which included the retention or washout at HBP and degree of transporter expression.

14 e LKB1-AMPK and the hexosamine biosynthesis (HBP)-OGT pathways, which coordinate together for the sen

15 The crystal structure of a histamine-bound HBP, determined at 1.25 A resolution, reveals a lipocali

16 lts suggest that altered nutrient sensing by HBP with age may be the link among nutrients, insulin re

17 pothesized that altered nutrient sensing (by HBP) with age may provide a link among aging, nutrient f

18 Azurocidin/CAP37/HBP is an antimicrobial and chemotactic protein that is

19 that with glucosamine alone without changing HBP product levels.

20 ing of fluorescein isothiocyanate-conjugated HBP to human monocytes in the presence of EDTA and the p

21 ) significantly reduced the affinity of FITC-HBP for CD14-positive monocytes.

22 appeared in 1988 for pre-HBP and in 1999 for HBP; non-Hispanic blacks and Mexican Americans had a gre

23 s In a multivariable Cox model adjusting for HBP as a time-varying covariate, comparing those on PCB

24 he data we obtained in the present study for HBP enables a comparison of the driving forces for bindi

25 between the low affinity binding site of FS-HBP and monomine, suggesting that histamine binding has

26 imilar to the lower, low affinity site of FS-HBP.

27 emale-specific histamine-binding protein (FS-HBP), the histamine-binding lipocalin of the tick Rhipic

28 As soluble receptors of histamine, HBPs offer a new strategy for controlling histamine-base

29 However, HBP is not a biologically inactive molecule but rather a

30 man monocytes activated by recombinant human HBP and LPS and their interaction with the LPS receptor

31 ability to convert DBT to 2-hydroxybiphenyl (HBP) with the release of inorganic sulfur.

32 Our findings identify HBP as a modulator of prostate cancer growth and c-MYC a

33 was accompanied by absolutely no increase in HBP product levels in all of the muscles examined.

34 nding of structure-function relationships in HBP.

35 ral obesity, partially explained the rise in HBP and pre-HBP from 1988 to 1999.

36 nce is additive to that induced by increased HBP flux via glucosamine infusion and, if so, whether su

37 Here, we observed increased HBP flux and hyper-O-GlcNAcylation in human pancreatic d

38 pheral insulin resistance without increasing HBP product levels in skeletal muscle.

39 microscopy showed that monocytes internalize HBP within 30 min.

40 nstrated that administration of 10 microg ip HBP alone did not enhance phagocytosis of fluorescent Es

41 dministration of 10 microg and 100 microg ip HBP demonstrated a 1.7-fold increase in the total number

42 ice that received cefoxitin and 50 microg ip HBP immediately after CLP, followed by continuous admini

43 4 was clearly differentiated from the 95 kDa HBP by two-dimensional electrophoretic mobility.

44 We conclude that the 95 kDa HBP is a new HDL receptor candidate widely expressed in

45 not affect either HDL binding to the 95 kDa HBP or its size, while in contrast it affected the molec

46 The association of HDL(3) with the 95 kDa HBP plateaued in 15-30 min while dissociation was comple

47 The HDL binding with the 95 kDa HBP plateaus at 2.5-5 microg/mL under reducing and nonre

48 The 95 kDa HBP predominantly resides on the surface of cells since

49 I, and apoA-II were recognized by the 95 kDa HBP while low density lipoproteins (LDL) and tetranitrom

50 d with four- to fivefold increases in muscle HBP product levels.

51 ipid infusion also failed to increase muscle HBP product levels.

52 such additive effects correlate with muscle HBP product levels.

53 The activation of HBP induces an aberrant cell surface glycosylation and O

54 ats, we show that experimental activation of HBP, through the systemic infusion of glucosamine, induc

55 The addition of HBP imaging did not affect interreader agreement but sig

56 Intravenous administration of HBP (0.1, 1, and 10 microg) at the time of CLP showed an

57 LP, followed by continuous administration of HBP (12 microg/24 hrs).

58 erformance liquid chromatography analyses of HBP metabolic activity, short term exposure to an exogen

59 onocytes was mediated by specific binding of HBP to monocytes, which resulted in an up-regulation of

60 microM) significantly reduced the effect of HBP (10 microg/ml) to enhance LPS (10 ng/ml)-induced TNF

61 an and EDTA abrogate the enhancing effect of HBP on LPS-induced TNF-alpha production.

62 hypothesized that the stimulatory effect of HBP on the LPS-induced release of proinflammatory mediat

63 nduced by CLP is important for the effect of HBP to enhance phagocytosis.

64 Expression of HBP enzyme glucosamine-phosphate N-acetyltransferase 1 (

65 findings demonstrate that internalization of HBP in monocytes is essential for the enhancement of LPS

66 anterior) were taken for the measurement of HBP product levels.

67 Pretreatment with 10 microg of HBP did not further enhance CD11b/CD18 expression in PEC

68 owever, 24-hr pretreatment with 10 microg of HBP followed by CLP increased phagocytosis in PECs 1.8-f

69 s before CLP with 10 microg or 100 microg of HBP without cefoxitin (p = .01, Cox-Mantel log-rank test

70 ON Data from ECOG 4599 suggest that onset of HBP during treatment with PCB may be associated with imp

71 exican Americans had a greater prevalence of HBP and pre-HBP than non-Hispanic whites, and males had

72 To assess the role of HBP in the induction of TRIB3, we demonstrated that the

73 In this study, we investigated the role of HBP on HG-stimulated fibronectin protein synthesis, a ma

74 Transport of HBP to an activating compartment depends on intact F-act

75 role of the hexosamine biosynthesis pathway (HBP) in fat-induced insulin resistance, we examined whet

76 ated by the hexosamine biosynthesis pathway (HBP) in response to metabolic nutrients.

77 through the hexosamine biosynthesis pathway (HBP) induces insulin resistance and facilitates lipid st

78 whether the hexosamine biosynthesis pathway (HBP) mediates glucose regulation of mRNA expression, we

79 The hexosamine biosynthesis pathway (HBP) regulates the post-translational modification of nu

80 The hexosamine biosynthesis pathway (HBP) serves as a nutrient sensor and has been implicated

81 athway, the hexosamine biosynthesis pathway (HBP) via regulation of expression of glutamine:fructose-

82 sis through Hexosamine Biosynthesis Pathway (HBP), as well as cellular redox homeostasis, resulting i

83 ated by the hexosamine biosynthesis pathway (HBP), in which fructose-6-phosphate is converted to gluc

84 athway, the hexosamine biosynthesis pathway (HBP), rapidly decreased the expression of a cluster of n

85 through the hexosamine biosynthesis pathway (HBP).

86 duct of the hexosamine biosynthesis pathway (HBP).

87 lism is the hexosamine biosynthesis pathway (HBP).

88 ctivate the hexosamine biosynthetic pathway (HBP) and promote the O-glycosylation of proteins by O-gl

89 The hexosamine biosynthetic pathway (HBP) generates uridine diphosphate N-acetylglucosamine (

90 Hexosamine biosynthetic pathway (HBP) is a candidate nutrient-sensing pathway.

91 The hexosamine biosynthetic pathway (HBP) is highly dependent on multiple metabolic nutrients

92 through the hexosamine biosynthetic pathway (HBP) is implicated in the development of insulin resista

93 ent-sensing hexosamine biosynthetic pathway (HBP) known to mediate glucose toxicity in diabetes.

94 The hexosamine biosynthetic pathway (HBP) senses metabolic status and produces an essential s

95 ions in the hexosamine biosynthetic pathway (HBP) to be critical for CRPC.

96 ment of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization.

97 olysis, the hexosamine biosynthetic pathway (HBP), to increase uridine diphosphate-N-acetylglucosamin

98 enters the hexosamine biosynthetic pathway (HBP), which regulates levels of O-linked beta-N-acetylgl

99 h enter the hexosamine biosynthetic pathway (HBP).

100 Comparing the PCB HBP group with PC gave an adjusted PFS HR of 0.54 (95% C

101 without and set 2 with hepatobiliary phase [HBP] images).

102 Hyperbranched polymers (HBPs) with decorated donor and acceptor chromophores in

103 Pre-HBP and HBP increased 2.3% (P=0.0003) and 1% (P=0.17), r

104 partially explained the rise in HBP and pre-HBP from 1988 to 1999.

105 HBP and pre-HBP in children and adolescents are on the rise.

106 cans had a greater prevalence of HBP and pre-HBP than non-Hispanic whites, and males had a greater pr

107 The BP, pre-HBP, and HBP trends were downward from 1963 to 1988 and

108 hnic and gender gap appeared in 1988 for pre-HBP and in 1999 for HBP; non-Hispanic blacks and Mexican

109 High blood pressure (HBP) by the end of cycle 1 was defined as blood pressure

110 g) for the diagnosis of high blood pressure (HBP) in adolescents.

111 ty, we sought to assess high blood pressure (HBP) secular trends in children and adolescents enrolled

112 Before this proposal, HBP had been defined as BP at or above the 95th percenti

113 he binding of the neutrophil-derived protein HBP to monocytes is inhibited in the presence of EDTA an

114 h density lipoprotein (HDL)-binding protein (HBP) corresponding to a high affinity HDL-binding site w

115 e lipoprotein-anchored heme binding protein (HBP) of this transporter is SiaA (HtsA).

116 neutrophil-derived heparin-binding protein (HBP), also known as CAP37 or azurocidin, potentiates the

117 Heparin-binding protein (HBP), also known as CAP37, is a proteolytically inactive

118 leukocytes release heparin-binding protein (HBP; also known as CAP37 or azurocidin) from azurophilic

119 High-affinity histamine-binding proteins (HBPs) were discovered in the saliva of Rhipicephalus app

120 Recombinant HBP increases survival in murine fecal peritonitis.

121 puncture (CLP) and treated with recombinant HBP and 60 mg/kg cefoxitin twice a day.

122 ate a greater activation of nutrient-sensing HBP with age in both old ad libitum-fed and calorie-rest

123 monstrate the therapeutic value of targeting HBP in CRPC.

124 We used flow cytometry to demonstrate that HBP had a high affinity to monocytes but not to the LPS

125 Our results demonstrated that HBP alone (10 microg/ml) stimulated the production of TN

126 We have previously demonstrated that HBP is internalized in monocytes.

127 These data provide supporting evidence that HBP binds to a receptor expressed on monocytes.

128 In the current study, we hypothesize that HBP is internalized in monocytes via endocytosis, and th

129 The HBP end product UDP-N-acetylglucosamine (UDP-GlcNAc) is

130 The HBP is a branch of the glucose metabolic pathway that co

131 The HBP may be involved in retinal neurodegeneration in diab

132 ata provide the mechanistic link between the HBP flux and insulin resistance and point to TRIB3 as a

133 Conversely, blocking the HBP with a GFA inhibitor reduced AMPK activity, ACC phos

134 nthesis in the mesangium are mediated by the HBP possibly via hexosamine regulation of CREB and PKC/P

135 demonstrating that AMPK is regulated by the HBP, we found that AMPK was recognized by succinylated w

136 into adipocytes where it directly enters the HBP.

137 T), which is the rate-limiting enzyme in the HBP pathway.

138 retention and washout, respectively, in the HBP.

139 Inhibiting the HBP through genetic and chemical methods reverses p53 st

140 N concentrations, unrestricted flux into the HBP greatly exceeds the biosynthetic capacity of the pat

141 eful in exploring the functional role of the HBP and in avoiding the potential pitfalls in the pharma

142 Thus, the activation of the HBP by nutrients represents a biochemical link between n

143 mechanism and functional significance of the HBP in directly linking extracellular glucose signal to

144 of the discrepant reports on the role of the HBP in glycogen metabolism.

145 Despite the established role of the HBP in metabolism and multiple diseases, regulation of t

146 genesis, demonstrating the importance of the HBP in the development of glucose intolerance.

147 Strikingly, addition of the HBP metabolite UDP-N-acetylglucosamine (UDP-GlcNAc) to C

148 ism and multiple diseases, regulation of the HBP remains largely undefined.

149 We now identify a regulatory arm of the HBP that involves rapid allosteric activation of glycoge

150 rm exposure to an exogenous substrate of the HBP, glucosamine (GlcNH(2)), leads to increased GlcNH(2)

151 tes, wherein the rate-limiting enzyme of the HBP, glutamine:fructose-6-phosphate amidotransferase (GF

152 exosamines (UDP-HexNAc), end products of the HBP, were increased approximately 2- and 15-fold after a

153 To explore the molecular mechanism of the HBP-induced fatty acid oxidation in adipocytes, we studi

154 e 1 (GFAT1), the rate-limiting enzyme of the HBP.

155 oprotection in part through induction of the HBP.

156 is a direct transcriptional activator of the HBP.

157 hese results support the hypothesis that the HBP is a sensor and regulator of the actions of glucose

158 Here, we report that the HBP is activated in prostate cancer cells and that OGT i

159 e data to mean that glucose flux through the HBP is linked to regulation of lipogenesis through contr

160 that the excessive glucose flux through the HBP may direct retinal neurons to undergo apoptosis in a

161 d whether increased glucose flux through the HBP perturbs insulin action and induces apoptosis in ret

162 g factor, excessive glucose flux through the HBP.

163 pathway, the glucose is shunted through the HBP.

164 ies reveal that Xbp1s couples the UPR to the HBP to protect cells under stress.

165 ered that breast cancer cells upregulate the HBP, including increased O-GlcNAcation and elevated expr

166 ational surveys and to determine whether the HBP trend reversed its course with the rise in obesity.

167 merization, two structural parameters in the HBPs, for example, the molar ratio of the acceptor Couma

168 Increased flux through HBP leads to elevated post-translational addition of bet

169 Thus, HBP links the altered metabolism with aberrant glycosyla

170 The conversion of DBT to HBP is catalyzed by a multienzyme pathway consisting of

171 release of TNF-alpha or PGE2 in response to HBP and LPS.

172 We demonstrate that the UPR triggers HBP activation via Xbp1s-dependent transcription of gene

173 could be overcome by the risk of undiagnosed HBP.

174 e demonstrate a physiologic role for the UPR-HBP axis by showing that acute stimulation of Xbp1s in h

175 ablish that this previously unrecognized UPR-HBP axis is triggered in a variety of stress conditions.

176 been elucidated, and it is not known whether HBP also increases the LPS-induced production of other b

177 To date, the mechanisms by which HBP enhances LPS-induced monocyte activation have not be

178 alization is an important mechanism by which HBP enhances LPS-induced TNF-alpha release.

179 The mechanisms by which HBP reduces septic death are not fully understood, but t

180 rying covariate, comparing those on PCB with HBP with those on PC gave an OS hazard ratio (HR) of 0.6

181 < .0001) and comparing those on PCB without HBP to those on PC, the HR was 0.72 (95% CI, 0.62 to 0.8

182 1; P = .001); comparing those on PCB without HBP with those on PC alone, the OS HR was 0.86 (95% CI,