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Items: 3

1.

In vitro responses of PBMC and fibroblasts from patients with TRIF deficiency after TRIF dependent and independent stimuli

(Submitter supplied) We report here unrelated HSE patients with autosomal recessive (AR) or autosomal dominant (AD) TRIF deficiency. The AR form of the disease is due to a homozygous nonsense mutation, resulting in a complete absence of the TRIF protein. Both the TLR3 and the TRIF-dependent TLR4 signaling pathways are abolished. The AD form of TRIF deficiency is due to a heterozygous missense mutation resulting in a dysfunctional protein. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS4539 GDS4540
Platform:
GPL10558
27 Samples
Download data: TXT
Series
Accession:
GSE32390
ID:
200032390
2.
Full record GDS4540

TRIF-deficient Herpes simplex encephalitis patient: peripheral blood mononuclear cell response to TLR agonists LPS and R-848

Analysis of PBMCs collected from an HSV1 encephalitis (HSE) patient with TRIF deficiency (homozygous TRIF nonsense mutation) and stimulated with LPS or resiquimod hydrochloride R-848. TRIF is the sole adaptor protein for TLR3. Results provide insight into the role of the TLR3 pathway in HSE.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 agent, 2 disease state, 3 genotype/variation sets
Platform:
GPL10558
Series:
GSE32390
9 Samples
Download data
3.
Full record GDS4539

TRIF-deficient Herpes simplex encephalitis patient: fibroblast response to interleukin-1β and TLR3 agonist poly (I:C)

Analysis of SV40 skin fibroblasts collected from an HSV1 encephalitis (HSE) patient with TRIF deficiency (homozygous TRIF nonsense mutation) and stimulated with IL-1β or poly I:C . TRIF is the sole adaptor protein for TLR3. Results provide insight into the role of the TLR3 pathway in HSE.
Organism:
Homo sapiens
Type:
Expression profiling by array, transformed count, 3 agent, 2 disease state, 4 genotype/variation sets
Platform:
GPL10558
Series:
GSE32390
18 Samples
Download data
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