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1                                              DAI also interacts with RIP3 and this interaction potent
2                                              DAI at different brain regions was evaluated by neuropat
3                                              DAI binds to and colocalizes with endogenous RIP1 at cha
4                                              DAI has applications in the detection and identification
5                                              DAI is a novel application of biotin/streptavidin affini
6                                              DAI offers a new means of molecular profiling and monito
7                                              DAI was higher in Mdr1a (-/-) mice than in FVB mice, but
8                                              DAI-deficient mice fail to control IAV replication and s
9 ignificant upregulation of TLR-9 (P <0.006), DAI (P <0.001), and TLR-8 (P <0.01) in CP tissues compar
10 vage (BAL) eosinophilia observed at 7 and 14 DAI.
11 both control and ischemic animals, but at 30 DAI and afterward, the ischemic group maintained more th
12  and IL12p70 in plasma of infected pigs at 7 DAI and augmented bronchoalveolar lavage (BAL) eosinophi
13 and stained for amyloid precursor protein, a DAI marker.
14 restored in DAI(-/-) mice, consistent with a DAI-RIP3 complex being the natural target of vIRA.
15  significantly reduced the disease activity (DAI).
16  performed to determine mRNA levels of AIM2, DAI, and TLRs (TLR-1 through TLR-9).
17 nucleic acid surveillance proteins ADAR1 and DAI.
18           The expression of TLR-9, AIM2, and DAI in gingival tissues was further confirmed using immu
19 her confirmed expression of TLR-9, AIM2, and DAI in gingival tissues.
20 erferon-stimulated genes, such as CXCL10 and DAI.
21            These include ZBP1 (also known as DAI or DLM-1), which induces necroptosis, an inflammator
22 ZBP1 (Z-DNA binding protein 1; also known as DAI or DLM1) from activating RIPK3 upstream of MLKL.
23 e activity of mammalian cells (also known as DAI, P1-eIF-2, and p68 kinase).
24 " and "fast-action" mitigation to help avoid DAI and abrupt climate changes.
25 re found significantly increased, while both DAI and health transition on general health scores were
26  orchestrated by the sensing of infection by DAI/ZBP-1, engagement of the kinase RIPK3, and subsequen
27 related with DNA binding activity results by DAI.
28               Induction of class II genes by DAIs was accompanied by activation of a repressed class
29 s of climate change that might be considered DAI, authors of the Third Assessment Report (TAR) of the
30 rations of greenhouse gases would constitute DAI, a value judgment that would be policy prescriptive.
31              Cells lacking DAI or containing DAI mutants deficient in nucleic acid binding are resist
32 pendent activator of IFN-regulatory factors (DAI) that contain receptor-interacting protein (RIP) hom
33  activator of interferon-regulatory factors (DAI), and absent in melanoma 2 (AIM2) in chronic periodo
34  activator of interferon regulatory factors (DAI, also known as ZBP1 or DLM-1) sensitizes cells to vi
35 sting a spectrum of possible definitions for DAI.
36 istic global average temperature metrics for DAI with probability distributions of future climate cha
37              These studies unveil a role for DAI as the RIP3 partner mediating virus-induced necrosis
38 likelihood of avoiding a given threshold for DAI depends in part on uncertainty in the climate system
39 es are even more under-represented in global DAI than species-rich, developing countries in the tropi
40     SW MR imaging depicted 1,038 hemorrhagic DAI lesions with an apparent total hemorrhage volume of
41 The majority (59%) of individual hemorrhagic DAI lesions seen on SW MR images were small in area (<10
42                       These results identify DAI as a link between IAV replication and RIPK3 activati
43 we designed the DNA affinity immunoblotting (DAI) method to measure the activities of multiple sequen
44 plication and RIPK3 activation and implicate DAI as a sensor of RNA viruses.
45 vIRA mutant MCMV pathogenesis is restored in DAI(-/-) mice, consistent with a DAI-RIP3 complex being
46 reproduces human TBI consequences, including DAI and clinical sequelae such as memory impairment.
47 TO-curcumin improved disease activity index (DAI) dose-dependently, while the anti-inflammatory effic
48 ht, food intake, and disease activity index (DAI) were assessed throughout the study, and at 21 or 24
49 -Ex reduced colitis, disease activity index (DAI), and histological colitis scores, and increased the
50  with MCIBDQ, SF-36, disease activity index (DAI), marriage, employment and economic burden questionn
51                              Upon infection, DAI recognizes IAV genomic RNA, associates with RIPK3, a
52      Gaps in digital accessible information (DAI) on species distributions hamper prospects of safegu
53 we show that histone deacetylase inhibitors (DAIs) that alter the acetylation of histones in chromati
54                       Diffuse axonal injury (DAI) is one of the most common and important pathologies
55           It produces diffuse axonal injury (DAI), which contributes to cognitive impairment, but eff
56 s, most likely due to diffuse axonal injury (DAI).
57 TBI) characterized by diffuse axonal injury (DAI).
58 aumatic brain damage [diffuse axonal injury (DAI)] occurs in such children has not yet been reliably
59  oil alone per os on days after inoculation (DAI) -1, +1, and +3 with infective eggs.
60 on of "dangerous anthropogenic interference (DAI) with the climate system." However, success will be
61 revent dangerous anthropogenic interference (DAI) with the climate system." In an effort to provide s
62 e of "dangerous anthropogenic interference" (DAI).
63    Knockdown of DNA Activator of Interferon (DAI) and p204, the murine ortholog to IFI16, had minimal
64 nt activator of IFN regulatory factors (IRF; DAI, also known as ZBP1 or DLM-1) is a cytosolic DNA sen
65 , MDA5, and DNA-dependent activator of IRFs (DAI), use TBK1/IKKe as the terminal kinases to activate
66 ker expression up to 60 days after ischemia (DAI).
67 ion (DAE) and differential allelic isoforms (DAI) from the phased full-length isoform reads.
68                                Cells lacking DAI or containing DAI mutants deficient in nucleic acid
69 y young is diffuse hypoxic brain damage, not DAI, can be explained in one of two ways: either the unm
70 letal breakdown as a possible contributor of DAI after repeated blast exposure.
71 re has the potential to improve diagnosis of DAI.
72 ogical analysis showed significant levels of DAI at the frontal cortex and cerebellum at multiple tim
73 amyloid precursor protein (APP), a marker of DAI.
74 plays a major role in the pathophysiology of DAI.
75                                  The role of DAI in activation of NF-kappaB in response to immunostim
76 e genes cannot be explained by the effect of DAIs on the cell cycle or enhanced apoptosis.
77 eep modulation after trauma has an impact on DAI and memory outcome.
78 thogenicity was restored in either RIPK3- or DAI-deficient mice.
79 s with its upstream adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death recep
80 s with RIP3 and this interaction potentiates DAI-mediated activation of NF-kappaB, implicating RIP3 i
81 ith regard to their potential for preventing DAI.
82 e N terminus of the VACV E3 protein prevents DAI-mediated induction of necroptosis.
83 t exposed to the forces necessary to produce DAI.
84 s more potent than that with MSC in reducing DAI, the histological score, and nitrite levels.
85 ind that outside a few well-sampled regions, DAI on point occurrences provides very limited and spati
86  RIP3 binding to one of three partners-RIP1, DAI, or TRIF-via a common RIP homotypic interaction moti
87 in programmed necrosis induced by RIP1-RIP3, DAI-RIP3, and TRIF-RIP3 complexes.
88 encoded Zalpha domain-containing DNA sensor, DAI.
89                    A variety of DNA sensors (DAI, AIM2, DDx41, RNA polymerase [Pol] III, and IFI16 [p
90 zes cells to virus-induced necrosis and that DAI knockdown or knockout cells are resistant to this de
91                               We report that DAI (ZBP1/DLM-1), previously implicated as a cytoplasmic
92                                          The DAI method is largely independent of the distance betwee
93                                        Thus, DAI interacts with RIP3 to mediate virus-induced necrosi
94 volve the previously described sensors TLR9, DAI, RNA polymerase-III or IFI16/p204.
95 toskeletal proteins in the brain can lead to DAI, and evaluated alpha-II spectrin degradation in the
96 tion motif (RHIM)-dependent interaction with DAI.
97  inactivation of RIPK1, RIPK3, TRIF and ZBP1/DAI and inhibition of tumour necrosis factor (TNF), lipo
98 taining proteins RIPK1, RIPK3, TRIF and ZBP1/DAI during infection.

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