ライフサイエンスコーパス: RID

1 RID also abolished IL-8 secretion induced by heat-killed

2 RID also down-regulates certain tyrosine kinase cell sur

3 RID also downregulates other death receptors, such as FA

4 RID also mediates internalization of the receptor for ep

5 RID induces the internalization of TRAIL-R1 from the cel

6 RID inhibits TRAIL-induced apoptosis when cells are sens

7 RID is thus a dual function initiator of both RIP and th

8 RID mediates clearance from the cell surface and lysosom

9 RID was also shown previously to internalize and degrade

10 RID was performed before and after the intervention to q

11 RID was shown previously to force the internalization an

12 RID-mediated Fas and EGFR down-regulation occurs via end

13 The paired 13C-RID test was used to measure TBSs.

14 he seven E3 products, E3-10.4K and E3-14.5K (RID alpha/beta).

15 outcome of RID, cutaneous microbiomes of 78 RID patients and 20 healthy subjects were characterized

16 utation of this residue to alanine abolished RID function.

17 In addition, RID inhibits signaling induced by LPS without affecting

18 Here we show that the adenovirus RID (for receptor internalization and degradation) prote

19 genotypes, whereas the 5mC MTases DIM-2 and RID are more recently derived, and that 5mC levels are c

20 Both the ACD and RID independently disrupted polarized epithelial tight j

21 ified a polycistronic mRNA for RID-alpha and RID-beta.

22 cation of rpgrip1 and deletion of its C2 and RID domains.

23 Hence, RID(D1114G) and RID(DeltaE1279) constitute loss- and gain-of-function mu

24 The RID(D1114G) and RID(DeltaE1279) mutations exhibit strong cis-acting and

25 kingly, coexistence of diabetes mellitus and RID was remarkably correlated with a significant overrep

26 In contrast to RID(WT) and RID(D1114G), chemical genetics shows that the interactio

27 erotrimer complex 10.4K/14.5K, also known as RID (for "receptor internalization and degradation"), is

28 ermined by the radial immunodiffusion assay (RID).

29 and Candida albicans was determined for both RID-MyC and panfungal PCR across 3 different media: nucl

30 nhibition of TNF alpha-induced chemokines by RID.

31 that regulation of TNFR1 and that of FAS by RID are mechanistically different.

32 signaling pathways are strongly inhibited by RID, the chemokines up-regulated by IL-1beta stimulation

33 rated that surface TNFR1 was internalized by RID by a clathrin-dependent process involving mu2 and dy

34 VA status was previously measured by RID-estimated total body VA stores (TBSs) and total live

35 crosstalk and transport pathway regulated by RID, and hence by RPGR, emerges with implications in the

36 to estimate total liver retinol reserves by RID with a follow-up 14-d blood sample.

37 Although in some cases, RID causes loss of only a fraction of surface Fas, the p

38 In contrast to conventional RID/RIT where the radionuclides and oncotropic vector mo

39 and organic acids were evaluated by HPLC-DAD-RID during fermentation, and phenolic compounds were ana

40 e performed with LC-DAD-ESI-MS/MS and LC-DAD-RID was used for the sugar analyses.

41 everse phase liquid chromatography (HPLC-DAD/RID).

42 eral regulators of interferon-induced death (RIDs).

43 A palmitoylation-defective RID-alpha mutant deregulates cholesterol homeostasis and

44 E3 receptor internalization and degradation (RID) complex.

45 ed receptor internalization and degradation (RID) protein (previously named E3-10.4K/14.5K), which is

46 he receptor internalization and degradation (RID) protein complex, which is composed of the RIDalpha

47 ilizing combined relative indentation depth (RID) and viscoelastic response distance (VRD) data obtai

48 Radiotherapy-induced dermatitis (RID) is an inflammatory cutaneous disorder that is acqui

49 C) coupled with a refractive index detector (RID) and LC coupled with a mass spectrometry (MS), and t

50 Retinol isotope dilution (RID) is a more sensitive technique than serum retinol to

51 The retinol isotope dilution (RID) test can sensitively characterize VA status and int

52 ng women using the retinol isotope dilution (RID) test.

53 osis A assessed by retinol isotope dilution (RID) with measures of growth and bone turnover in this c

54 etermined by using retinol isotope dilution (RID).

55 wn as the Reduced Interference Distribution (RID)-Rihaczek distribution, to estimate both the phase a

56 of MARTX(Vc) is the Rho inactivation domain (RID(Vc)) known to cause cell rounding through inactivati

57 ng domain (ACD) and Rho-inactivation domain (RID) are found to cross-link actin and inactivate RhoA,

58 The Rho-inactivation domain (RID) of MARTX(Vc) is responsible for inactivating the Rh

59 ing domain (ACD), a Rho inactivation domain (RID), and an alpha/beta hydrolase domain (ABH)-to suppre

60 the RHD and TAD as a REL inhibitory domain (RID) because deletion of these sequences increases both

61 and D1114G, in the RPGR-interacting domain (RID) of RPGRIP1, enhance and abolish, respectively, its

62 ning the functional RPGR-interacting domain (RID) of the protein.

63 profile of NCoR receptor interaction domain (RID) binding to REV-ERBB ligand-binding domain (LBD).

64 mutation in the receptor interaction domain (RID) of SMRT (SMRT(mRID)) that solely disrupts its inter

65 on of the first receptor interaction domain (RID) of the nuclear corepressor SMRT disrupts interactio

66 ent on the SMRT receptor interaction domain (RID), and Flt3-ITD enhances the binding of nuclear-cytop

67 lpha) with the receptor interacting domains (RIDs) of three cofactors (SRC1, SRC2, SRC3) in living ce

68 rminal nuclear receptor interacting domains (RIDs) present in NCoR.

69 receptors and receptor interaction domains (RIDs) in the middle and C-terminus of coactivators and c

70 x via specific receptor interaction domains (RIDs).

71 Ectopic RID-alpha regulates intracellular cholesterol traffickin

72 face of adenovirus-infected cells expressing RID may allow infected cells to resist Fas-mediated cell

73 Using a retrovirus expressing RID to infect six human lymphocyte cell lines, we found

74 We also identified a polycistronic mRNA for RID-alpha and RID-beta.

75 A GFP fusion to this subdomain from RID colocalized with a plasma membrane marker when trans

76 ing activity does not depend on a functional RID(Vc), demonstrating that these domains function indep

77 defective vectors that express all E3 genes, RID plus E3-14.7K only, RID only, or E3-14.7K only.

78 Hence, RID(D1114G) and RID(DeltaE1279) constitute loss- and gai

79 However, RID and ABH, which are naturally delivered together with

80 However, RID-alpha also induces a novel cellular phenotype, sugge

81 HPLC-RID analysis allowed quantification of maltodextrins wit

82 two chromatographic methods (GC-FID and HPLC-RID) for the quantification of carbohydrates present in

83 upled with a refractive index detector (HPLC-RID) was applied to determine the carbohydrates profile

84 gh-throughput (FIA-HESI-HRMS; HT-GC-MS; HPLC-RID) and pattern recognition techniques (PLS-DA).

85 The results of HPLC-RID were subjected to multivariate statistical analysis,

86 as amino acid (UPLC-ESI-MS/MS), sugar (HPLC-RID), and aroma (SPME-GC/MS) profiles, of four varieties

87 graphy with refractive index detector (HPSEC-RID) and gas chromatography with mass detector (GC-MS).

88 , and Cys-3022, were identified as impacting RID(Vc) function in depolymerization of the actin cytosk

89 -based sorting signal in RID plays a role in RID's ability to down-regulate receptors.

90 n which the tyrosine-based sorting signal in RID plays a role in RID's ability to down-regulate recep

91 s modified to carry a catalytically inactive RID(Vc) show that the rate and efficiency of MARTX(Vc) a

92 -linking mass spectrometry reveals a 2:1 LBD:RID stoichiometry, consistent with cellular studies show

93 ained elaborating data deriving from NARP-LC-RID analysis.

94 t are localized to late endosomes/lysosomes, RID-alpha induces the accumulation of autophagy-like ves

95 novirus type 5 encodes three proteins, named RID (previously named E3-10.4K/14.5K), E3-14.7K, and E1B

96 s that encode proteins with alterations near RID: one lacking exon 9 sequences (aa 308-330; RELDelta9

97 that the more amino-terminal RID#1, but not RID#2, is necessary for binding to both GR and PR agonis

98 Nonetheless, the ability of RID to block Fas signaling is independent of the Fas sig

99 Here, we test the ability of RID to protect human lymphocytes from apoptosis induced

100 genomic repeats are RIPed in the absence of RID, showing that eu- and hetero- chromatic repeats are

101 e analyze the immunoregulatory activities of RID on lipopolysaccharide (LPS) and interleukin-1 beta (

102 Based on a deletion analysis of RID to determine the minimal functional domain, we have

103 required for several but not all aspects of RID motor neuron differentiation and that the lim-6 Lhx

104 Deletion of RID does not affect REL's ability to transform chicken s

105 Moreover, deletion of RID or exon 9 sequences increases transactivation by ful

106 Deletion of RID or exon 9-encoded sequences increases transactivatio

107 ur data demonstrate the inhibitory effect of RID on two additional cell surface receptor-mediated sig

108 It is possible that the expression of RID facilitates long-term infection by preventing Fas-me

109 lar interactions underlying this function of RID are unknown.

110 henylalanine did not abolish the function of RID, arguing that phosphorylation of the tyrosine is not

111 a but did not affect any of the functions of RID that were examined.

112 markedly associated with delayed healing of RID.

113 mical genetics shows that the interaction of RID(DeltaE1279) with RPGR is resistant to various stress

114 ial diversity was detected in microbiomes of RID in comparison to controls.

115 To explore the skin microbiota of RID and deduce their underlying impact on the outcome of

116 ce their underlying impact on the outcome of RID, cutaneous microbiomes of 78 RID patients and 20 hea

117 their potential roles in the pathogenesis of RID.

118 ecovery or tendency toward the permanence of RID (Kruskal Wallis: P = 2.66 x 10(-4)).

119 y a fraction of surface Fas, the presence of RID completely blocks the immediate events downstream of

120 of ACD but strong selection for retention of RID and ABH suggests these two domains may primarily fun

121 with RPGR without affecting the stability of RID.

122 microbiome profiling at the early stages of RID could be indicative of prospective clinical outcomes

123 ing mutagenesis in the activity subdomain of RID(Vc), four residues, His-2782, Leu-2851, Asp-2854, an

124 identified a subdomain at the N terminus of RID that is homologous to the membrane targeting C1 doma

125 eraction motifs had no discernible effect on RID function.

126 xpress all E3 genes, RID plus E3-14.7K only, RID only, or E3-14.7K only.

127 d sugar composition were studied by HPLC-PDA-RID.The main amino acids were glutamic acid (6.24-12.96

128 y induced by the adenovirus membrane protein RID-alpha that also subverts the cellular autophagy path

129 th non-invasive cancer radioimmunodetection (RID) and radioimmunotherapy (RIT).

130 eat-Linker-Repeat (R-L-R) constructs require RID alone for RIP, while genomic repeats are RIPed in th

131 m the Vibrio vulnificus MARTX toxin restored RID activity, indicating that there is functional overla

132 tion, we have characterized one of the RIDs, RID-2.

133 graphy with refractometric detection (HP-SEC-RID).

134 lectively, our results demonstrate that SMRT-RID-dependent repression is a key determinant of the adi

135 xes containing two ER alphas at low free SRC-RID concentrations (<2 nm) to lower affinity complexes w

136 lexes with an ER alpha monomer at higher SRC-RID concentrations (approximately 10 nm).

137 was available to form complexes with the SRC-RIDs in the cell.

138 interactions of ER alpha with all three SRC-RIDs, measured throughout the cell nucleus, transitioned

139 NCoR establish that the more amino-terminal RID#1, but not RID#2, is necessary for binding to both G

140 stingly, among the four T-cell lines tested, RID caused loss of Fas in the two T-cell lines bearing a

141 tor Toll-like receptor 4, demonstrating that RID need not target degradation of the receptor to alter

142 x human lymphocyte cell lines, we found that RID functions in the absence of other viral proteins to

143 Sequence analysis revealed that RID-2 was identical to human inositol hexakisphosphate k

144 omatin status affects RIP, we also show that RID, when tethered with LexA, acts as a nucleation cente

145 We recently showed that RID expression correlates with down-regulation of the ce

146 Collectively, these data suggest that RID functions to prevent apoptosis of some human lymphoc

147 The data suggest that RID has intracellular targets that impair signal transdu

148 The RID complex prevents death of infected cells by blocking

149 The RID test was repeated after the intervention.

150 The RID(D1114G) and RID(DeltaE1279) mutations exhibit strong

151 The RID-MyC assay demonstrated a sensitivity of 88.24% (95%

152 The RID-MyC assay may advance the rapid and precise diagnosi

153 The RID-MyC assay was 10- to 1000-fold more sensitive than p

154 000 IU VA capsule was administered after the RID test.

155 This study evaluated the RID-MyC (Rapid Identification of Mycoses using clustered

156 K) and RIDbeta (formerly E3-14.5K), form the RID (receptor internalization and degradation) complex (

157 lytic triad is essential for function of the RID effector domain family shared by MARTX toxins produc

158 addition, we found that substitution of the RID MLD with the MLDs from two different effector domain

159 mpetent mutants that lack one or more of the RID, E3-14.7K, and E1B-19K genes, and adenovirus E1-minu

160 value, and negative predictive value of the RID-MyC assay against panfungal PCR and culture.

161 ion and degradation of TR2, whereas only the RID protein is required for TRAIL receptor 1 downregulat

162 ions that span E3 were used to show that the RID and E3-6.7K proteins are both necessary for the inte

163 E3 proteins were used to establish that the RID and E3-6.7K proteins are sufficient to clear TR2.

164 strate, which can be directly related to the RID and VRD results.

165 The time to diagnosis with the RID-MyC assay was consistently <2 hours.

166 estigation, we have characterized one of the RIDs, RID-2.

167 In contrast to RID(WT) and RID(D1114G), chemical genetics shows that th

168 Wild-type RID-alpha rescues lipid-sorting defects in cells from pa

169 unds were identified and quantified by UHPLC-RID/PDA and HS-SPME/GC-MS, respectively.

170 of total-body retinol stores (TBSs) by using RID, tests included analyses of serum carotenoids, retin

171 re analyzed quantitatively for TBSs by using RID.

172 h-performance liquid chromatography (HPLC-UV/RID).

173 C42, although the effect is ameliorated when RID is also present.

174 s with TNFR1 on the plasma membrane, whereas RID probably associates with FAS in a cytoplasmic compar

175 ifferential effects support a model in which RID associates with TNFR1 on the plasma membrane, wherea

176 contrast, the mutants did not affect the WT RID-induced downregulation of FAS.

177 n the mixing experiments, the wild-type (WT) RID-mediated TNFR1 downregulation was partially inhibite