ライフサイエンスコーパス: RID

1 RID also down-regulates certain tyrosine kinase cell sur

2 RID also downregulates other death receptors, such as FA

3 RID also mediates internalization of the receptor for ep

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

5 RID inhibits TRAIL-induced apoptosis when cells are sens

6 RID mediates clearance from the cell surface and lysosom

7 RID was also shown previously to internalize and degrade

8 RID was shown previously to force the internalization an

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

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

11 utation of this residue to alanine abolished RID function.

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

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

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

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

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

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

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

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

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

21 ermined by the radial immunodiffusion assay (RID).

22 nhibition of TNF alpha-induced chemokines by RID.

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

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

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

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

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

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

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

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

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

32 E3 receptor internalization and degradation (RID) complex.

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

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

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

36 etermined by using retinol isotope dilution (RID).

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

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

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

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

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

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

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

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

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

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

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

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

49 x via specific receptor interaction domains (RIDs).

50 Ectopic RID-alpha regulates intracellular cholesterol traffickin

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

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

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

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

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

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

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

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

59 HPLC-RID analysis allowed quantification of maltodextrins wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 lar interactions underlying this function of RID are unknown.

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

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

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

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

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

86 with RPGR without affecting the stability of RID.

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

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

89 eraction motifs had no discernible effect on RID function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 The RID complex prevents death of infected cells by blocking

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

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

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

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

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

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

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

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

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

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

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

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

122 re analyzed quantitatively for TBSs by using RID.

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

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

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

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

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