Keratinocytes are the major constituent of epithelial cells at mucosal surfaces and skin, which cover organs, internal cavities and the body. Traditionally, keratinocytes have been considered as an inert component of the multilayered epithelium to protect the subepithelial compartments from the pathogenic microorganisms, toxic stimuli and physical trauma. However, accumulated researches of the airway, gastrointestinal tract and skin have demonstrated that keratinocytes function in the development of the immune system, promotion of pathologic inflammation and even impose diverse decisions on immune cells.
Genome-wide analysis reveals the active roles of keratinocytes in oral mucosal adaptive immune response.
Specimen part, Time
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Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.
Age, Specimen part
View SamplesWe used microarrays to detail the global programme gene expression of Phf8 knock out and wild type mice
Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.
Age, Specimen part
View SamplesEctromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. ECTV causes mousepox in most strains of mice, including BALB/c and DBA/2, and these are therefore classified as susceptible mice. Conversely, C57BL/6 and certain 129 strains display limited pathology and a very low mortality, and are thus classified as resistant. To understand the host genetic factors of different mouse strains in response to ECTV infection, we carried out a microarray analysis using Affymetrix Gene-Chip Mouse Genome Arrays of spleen tissues from BALB/c and C57BL/6 mice at 3 and 10 days post-ECTV infection.
Comparison of Host Gene Expression Profiles in Spleen Tissues of Genetically Susceptible and Resistant Mice during ECTV Infection.
Sex, Specimen part, Time
View SamplesPolycomb group (PcG) proteins are epigenetic silencers whose dysregulation is frequently linked to cancer via mechanisms that remain unclear. Using conditional knock-out mice in a colitis-associated colorectal cancer (CAC) model, we found that Bmi1 and Mel18 are important initiation and maintenance factors during CAC tumorigenesis. Epithelial depletion of both Bmi1 and Mel18, but not either gene alone, significantly reduces tumor growth and multiplicity.
BMI1 and MEL18 Promote Colitis-Associated Cancer in Mice via REG3B and STAT3.
Specimen part
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ATF4 plays a pivotal role in the development of functional hematopoietic stem cells in mouse fetal liver.
Specimen part
View SamplesIn this study, we demonstrated that deletion of the activating transcription factor 4 (ATF4) resulted in severely impaired HSC expansion in the fetal liver at E12.5 and E15.5. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region at E11.5 was not significantly affected. Furthermore, the HSC-supporting ability of both endothelial and stromal cells in fetal liver was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed down-regulated expression of a panel of cytokines in ATF4-/- stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor-A (VEGFA).
ATF4 plays a pivotal role in the development of functional hematopoietic stem cells in mouse fetal liver.
Specimen part
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Atrial identity is determined by a COUP-TFII regulatory network.
Age, Specimen part
View SamplesAtria and ventricles exhibit distinct molecular profiles that produce structural and functional differences between the two cardiac compartments. However, factors that determine these differences remain largely undefined. Cardiomyocyte-specific COUP- TFII ablation produces ventricularized atria that exhibit ventricle-like action potentials, increased cardiomyocyte size, and development of extensive T-tubules.
Atrial identity is determined by a COUP-TFII regulatory network.
Age, Specimen part
View SamplesThe gastrointestinal (GI) tract can have significant impact on the regulation of the whole body metabolism and may contribute to the development of obesity and diabetes. To systemically elucidate the role of the GI tract in obesity, we performed a transcriptomic analyses in different parts of the GI tract of two obese mouse models: ob/ob and high-fat diet (HFD) fed mice. Compared to their lean controls, both obese mouse groups had significant amount of gene expression changes in the stomach (ob/ob: 959; HFD: 542), much more than the number of changes in the intestine. Despite the difference in genetic background, the two mouse models shared 296 similar gene expression changes in the stomach. Among those genes, some had known associations to obesity, diabetes and insulin resistance. In addition, the gene expression profile strongly suggested an increased gastric acid secretion in both obese mouse models, probably through an activation of the gastrin pathway. In conclusion, our data reveal a previously unknown dominant connection between the stomach and obesity.
Significant obesity-associated gene expression changes occur in the stomach but not intestines in obese mice.
Specimen part
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