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PMID |
Sentence |
1 |
10331639
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The RT6 (Art2) family of ADP-ribosyltransferases in rat and mouse.
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2 |
10331639
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Recent evidence suggests that a new member of the mono-ADP-ribosyltransferase/NAD glycohydrolase family, RT6, may be important in immune regulation.
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3 |
10331639
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RT6-expressing T cells in the rat may have a regulatory role, a conclusion based on their ability to prevent autoimmune diabetes in the BB rat model of insulin-dependent diabetes mellitus.
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4 |
10331639
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RT6, like many GPI-linked proteins, can mediate cell signal transduction events associated with T cell activation, and is also present in a soluble form in the circulation.
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5 |
11292261
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The majority of cells were CD8+ART2+ T-cells.
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6 |
11292261
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In contrast, BBDP rat FTOC yielded 60% fewer cells (approximately 0.3 x 10(5)/lobe), a smaller percentage of CD8+ and TcRalphabeta+ T-cells, and almost no detectable ART2+ T-cells.
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7 |
11292261
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Addition of anti-ICAM-1 (CD54) antibody reduced T-cell number in BBDR rat FTOC by approximately 70%, but addition of IL-7 or IL-1beta had no effect.
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8 |
11292261
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The majority of cells were CD8+ART2+ T-cells.
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9 |
11292261
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In contrast, BBDP rat FTOC yielded 60% fewer cells (approximately 0.3 x 10(5)/lobe), a smaller percentage of CD8+ and TcRalphabeta+ T-cells, and almost no detectable ART2+ T-cells.
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10 |
11292261
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Addition of anti-ICAM-1 (CD54) antibody reduced T-cell number in BBDR rat FTOC by approximately 70%, but addition of IL-7 or IL-1beta had no effect.
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11 |
16585549
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Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
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12 |
16585549
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Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
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13 |
16585549
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ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
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14 |
16585549
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Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
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15 |
16585549
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However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
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16 |
16585549
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Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
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17 |
16585549
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These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
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18 |
16585549
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Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
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19 |
16585549
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Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
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20 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
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21 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
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22 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
23 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
24 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
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25 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
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26 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
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27 |
16585549
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Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
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28 |
16585549
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Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
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29 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
30 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
31 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
32 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
33 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
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34 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
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35 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
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36 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
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37 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
38 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
39 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
40 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
41 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
42 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
43 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
44 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
45 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
46 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
47 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
48 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
49 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
50 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
51 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
52 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
53 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
54 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
55 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
56 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
57 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
58 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
59 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
60 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
61 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
62 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
63 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
64 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
65 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
66 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
67 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
68 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
69 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
70 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
71 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
72 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
73 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
74 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
75 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
76 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
77 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
78 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
79 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
80 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
81 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
82 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
|
83 |
16585549
|
Targeted disruption of CD38 accelerates autoimmune diabetes in NOD/Lt mice by enhancing autoimmunity in an ADP-ribosyltransferase 2-dependent fashion.
|
84 |
16585549
|
Ubiquitously expressed CD38 and T cell-expressed ADP-ribosyltransferase 2 (ART2) are ectoenzymes competing for NAD substrate.
|
85 |
16585549
|
ART2 is an ADP-ribosyltransferase on naive CD4+ and CD8+ T cells.
|
86 |
16585549
|
Transfer of a genetically disrupted CD38 allele into the autoimmune diabetes-prone NOD/Lt background accelerated diabetes onset in both sexes, whereas transfer of a disrupted ART2 complex had no effect.
|
87 |
16585549
|
However, the fact that the accelerated pathogenesis mediated by CD38 deficiency required ART2 activity was demonstrated by combining both ART2 and CD38 deficiencies.
|
88 |
16585549
|
Rather, the balance between T-effectors and T-regulatory cells was disturbed in CD38-deficient but ART2-intact NOD mice.
|
89 |
16585549
|
These changes were corrected when CD38 deficiency was combined with ART2 deficiency.
|
90 |
16585549
|
Both ART2-deficient and CD38/ART2 combined deficient T cells were resistant to NAD-induced killing in vitro, whereas CD38-deficient but ART2-intact T cells showed increased sensitivity, particularly the CD4+ CD25+ subset.
|
91 |
16585549
|
Unexpectedly, diabetes development in the combined CD38/ART2 stock was strongly suppressed, possibly through epistatic interactions between genes linked to the targeted CD38 on Chromosome 5 and the ART2 complex on Chromosome 7.
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92 |
16920929
|
CD38 is required for the peripheral survival of immunotolerogenic CD4+ invariant NK T cells in nonobese diabetic mice.
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93 |
16920929
|
Unlike in standard NOD mice, alpha-galactosylceramide pretreatment did not protect the CD38-deficient stock from T1D induced by an adoptively transferred pancreatic beta cell-autoreactive CD8 T cell clone (AI4).
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94 |
16920929
|
We found that in the absence of CD38, ADP-ribosyltransferase 2 preferentially activates apoptotic deletion of peripheral iNKT cells, especially the CD4+ subset.
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