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GSE112449
Mus musculus
6 Downloadable Samples
Description
The 24R,25-dihydroxyvitamin D metabolite (24R,25D) has long been suspected of participating to bone fracture repair. We used Cyp24a1-deficient mice, unable to produce 24R25D, to observe gene expression in callus tissue compared to that of control littermates.
Publication Title
Optimal bone fracture repair requires 24R,25-dihydroxyvitamin D3 and its effector molecule FAM57B2.
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Age, Specimen part, Treatment, Time
View Samples- Mus musculus
- 9 Downloadable Samples
Description
This study revealed pathogenic role of pre-BCR-independent SYK activation in high-risk B-ALL.
Publication Title
Therapeutic potential of spleen tyrosine kinase inhibition for treating high-risk precursor B cell acute lymphoblastic leukemia.
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Specimen part
View Samples- Mus musculus
- 42 Downloadable Samples
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Activity-dependent regulation of inhibitory synapse development by Npas4.
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No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
Description
we performed a DNA microarray experiment to identify activity-regulated genes that are misregulated in the absence of Npas4.
Publication Title
No associated publication
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Description
Histone deacetylases (Hdac) remove acetyl groups from proteins, influencing global and specific gene expression. Hdacs control inflammation, as shown by Hdac inhibitor-dependent protection from DSS-induced murine colitis. While tissue-specific Hdac knockouts show redundant and specific functions, little is known of their intestinal epithelial cell (IEC) role. We have shown previously that dual Hdac1/Hdac2 IEC-specific loss disrupts cell proliferation and determination, with decreased secretory cell numbers and altered barrier function. We thus investigated how compound Hdac1/Hdac2 or Hdac2 IEC-specific deficiency alters the inflammatory response. Floxed Hdac1 and Hdac2 and villin-Cre mice were interbred. Compound Hdac1/Hdac2 IEC-deficient mice showed chronic basal inflammation, with increased basal Disease Activity Index (DAI) and deregulated Reg gene colonic expression. DSS-treated dual Hdac1/Hdac2 IEC-deficient mice displayed increased DAI, histological score, intestinal permeability and inflammatory gene expression. In contrast to double knockouts, Hdac2 IEC-specific loss did not affect IEC determination and growth, nor result in chronic inflammation. However, Hdac2 disruption protected against DSS colitis, as shown by decreased DAI, intestinal permeability and caspase-3 cleavage. Hdac2 IEC-specific deficient mice displayed increased expression of IEC gene subsets, such as colonic antimicrobial Reg3b and Reg3g mRNAs, and decreased expression of immune cell function-related genes. Our data show that Hdac1 and Hdac2 are essential IEC homeostasis regulators. IEC-specific Hdac1 and Hdac2 may act as epigenetic sensors and transmitters of environmental cues and regulate IEC-mediated mucosal homeostatic and inflammatory responses. Different levels of IEC Hdac activity may lead to positive or negative outcomes on intestinal homeostasis during inflammation
Publication Title
The acetylome regulators Hdac1 and Hdac2 differently modulate intestinal epithelial cell dependent homeostatic responses in experimental colitis.
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Specimen part
View Samples- Mus musculus
- 3 Downloadable Samples
Description
TLR ligands consistently induce expression of two Hes family members Hes1 and Hey1 in macrophages.To evaluate the effects of these two factors on inflammatory responses, we generated mice lacking both Hes1 and Hey1 (DKO). WT and DKO BMDMs were then untreated or exposed to LPS for 3 hours, and microarray was performed to examine global gene expression profiles to identify Hes1 and Hey1-regulated inflammatory genes
Publication Title
No associated publication
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Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
Description
To determine hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic hypoxic environment, equivalent to an altitude of 6500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic, normobaric conditions by exposing them to ambient air in Philadelphia (c. 50 mts above sea level).
Publication Title
No associated publication
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No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
Description
To understand hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic chemical hypoxic environment, for 2 weeks. Control, age-machted mice were maintained under normoxic conditions.
Publication Title
No associated publication
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
Description
To determine hypoxia mediated changes in whole blood, normal swiss webster mice were gradually exposed to a chronic hypobaric hypoxic environment up to 8500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic conditions in Kathmandu (c. 1300 mts above sea level).
Publication Title
No associated publication
Alternate Accession IDs
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
Description
Interferon is effective at inducing complete remissions in patients with Chronic Myelogenous Leukemia (CML), and evidence supports an immune mechanism. Here we show that the Type I Interferons (alpha and beta) regulate expression of the Interferon consensus sequence binding protein (ICSBP) in bcr-abl transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of bcr-abl induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the Type I Interferons and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the anti-leukemic response of interferons suggest new strategies for immunotherapy of CML.
Publication Title
ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.
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No sample metadata fields
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