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GSE22448
Mus musculus
6 Downloadable Samples
Description
Nlrc5 is encoding a Nod-like receptor protein NLRC5/NOD27. To check the involvement of Nlrc5 in antiviral response, we examined gene expression profile in wild-type and Nlrc5 knockout GM-CSF bone marrow macrophage with using microarrays.
Publication Title
NLRC5 deficiency does not influence cytokine induction by virus and bacteria infections.
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Specimen part, Time
View Samples- Mus musculus
- 12 Downloadable Samples
Description
IL-1R-associated kinases (IRAKs) participate in Toll-like receptor (TLR) signal transduction. MALP-2 is a TLR2 ligand, and stimulation of macrophages with MALP-2 activates expression of various genes including proinflammatory cytokines.
Publication Title
Sequential control of Toll-like receptor-dependent responses by IRAK1 and IRAK2.
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No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Polarization of macrophages to M1 or M2 cells is important for mounting responses against bacterial and helminth infection respectively. Jumonji domain containing 3 (JMJD3), a histone 3 K27 demethylase, has been implicated in the activation of macrophages. Here we show that JMJD3 is essential for M2 macrophage polarization to helminth infection and chitin, though JMJD3 is dispensable for M1 responses. Furthermore, Jmjd3 is critical for proper bone marrow macrophage differentiation in a demethylase activity-dependent manner. Jmjd3 deficiency affected trimethylation of H3K27 in only a limited numbers of genes. Among them, we identified Irf4 as the target transcription factor critical for controlling M2 macrophage polarization. Collectively, these results show that JMJD3-mediated H3K27 demethylation is critical for regulating M2 macrophage development leading to anti-helminth host responses.
Publication Title
The Jmjd3-Irf4 axis regulates M2 macrophage polarization and host responses against helminth infection.
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Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus, Homo sapiens
- 1 Downloadable Sample
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.
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No sample metadata fields
View Samples- Mus musculus
- 1 Downloadable Sample
Description
Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here we examine BCL11A as a potential regulator of HbF expression. The high HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders.
Publication Title
Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 9 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Direct recruitment of polycomb repressive complex 1 to chromatin by core binding transcription factors.
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Specimen part, Cell line
View Samples- Mus musculus
- 24 Downloadable Samples
Description
Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury.
Publication Title
Dietary quercetin alleviates diabetic symptoms and reduces streptozotocin-induced disturbance of hepatic gene expression in mice.
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Sex, Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
Description
To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet.
Publication Title
Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice.
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Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 37 Downloadable Samples
Description
The glucocorticoid receptor overexpression in early life is sufficient to alter gene expression patterns for the rest of the animal's life.
Publication Title
Early-life forebrain glucocorticoid receptor overexpression increases anxiety behavior and cocaine sensitization.
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Sex, Specimen part
View Samples- Mus musculus
- 2 Downloadable Samples
Description
The glomerular filtration barrier prevents large serum proteins from being lost into the urine. It is not known, however, why the filter does not routinely clog with large proteins that enter the glomerular basement membrane (GBM). Here we provide evidence that an active transport mechanism exists to remove immunoglobulins that accumulate at the filtration barrier. We found that FcRn, an IgG and albumin transport receptor, is expressed in podocytes and functions to internalize IgG from the GBM. Mice lacking FcRn accumulated IgG in the GBM as they aged and tracer studies showed delayed clearance of IgG from the kidneys of FcRn deficient mice. Supporting a role for this pathway in disease, saturating the clearance mechanism potentiated the pathogenicity of nephrotoxic sera. These studies support the idea that podocytes play an active role in removing proteins from the GBM and suggest that genetic or acquired impairment of the clearance machinery is likely to be a common mechanism promoting glomerular diseases.
Publication Title
Podocytes use FcRn to clear IgG from the glomerular basement membrane.
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Specimen part
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