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GSE64750
Mus musculus
22 Downloadable Samples
Description
Susceptible and Resistant mouse strain, e.g. DBA/2J and C57BL/6J respectively, were inoculated with a highly pathogenic H5N1 influenza A virus (A/Hong Kong/213/2003) for 72 hours.
Publication Title
Host genetic variation affects resistance to infection with a highly pathogenic H5N1 influenza A virus in mice.
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Sex
View Samples- Mus musculus
- 12 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia.
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Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
Description
To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo.
Publication Title
Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia.
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Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
Description
To find out genes regulated by geranylgeraniol (GGOH) treatment in peritoneal macrophage, we compared gene expression of cells treated with 200ng ml LPS and 250 micromolar compactin versus 200ng ml LPS, 250 micromolar compactin and 100micromolar GGOH.
Publication Title
Sufficient production of geranylgeraniol is required to maintain endotoxin tolerance in macrophages.
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Specimen part, Treatment
View Samples- Mus musculus
- 20 Downloadable Samples
Description
Triggering of B cell receptors (BCR) induces a massive synthesis of NFATc1 in splenic B cells. By inactivating the Nfatc1 gene and re-expressing NFATc1 we show that NFATc1 levels are critical for the survival of splenic B cells upon BCR stimulation. NFATc1 ablation led to decreased BCR-induced Ca++ flux and proliferation of splenic B cells, increased apoptosis and suppressed germinal centre formation and immunoglobulin class switch by T cell-independent antigens. By controlling IL-10 synthesis in B cells, NFATc1 supported the proliferation and IL-2 synthesis of T cells in vitro and appeared to contribute to the mild clinical course of Experimental Autoimmune Encephalomyelitis in mice bearing NFATc1-/- B cells. These data indicate NFATc1 as a key factor controlling B cell function.
Publication Title
NFATc1 affects mouse splenic B cell function by controlling the calcineurin--NFAT signaling network.
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Specimen part
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