To clarify the functional role of migratory liver-resident leukocytes (LRLs) in the pre-metastatic lung, we identify differentially expressed genes and address biological significance in the liver.
Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.
Specimen part, Disease, Disease stage
View SamplesTo understand the molecular mechanisms mediating Liver Resident Leukocytes (LRL) relocalization from the liver to the lungs in response to tumor progression, isolated LRLs from the liver and lungs of tumor-stimulating mice using a cell sorter. LRLs remaining in the liver displayed increased liver signature when compared to those that migrated into the lungs.
Hepato-entrained B220<sup>+</sup>CD11c<sup>+</sup>NK1.1<sup>+</sup> cells regulate pre-metastatic niche formation in the lung.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations (i.e., I363V, A384T, R397W) through knock-in mutagenesis in mice.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations in mice.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations in mice. The I363V and R397W mutations were loss-of-function mutations, causing multi-organ inflammation by globally compromising Treg cell physiology. By contrast, the A384T mutation induced a distinctive tissue-restricted inflammation by specifically impairing the ability of Treg cells to compete with pathogenic T cells in certain non-lymphoid tissues.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesSo far, we have found PMA induced USP2b isoform in myeloid leukemia cell lines such as HL60, THP-1, and U937.
Ubiquitin-specific protease 2-69 in macrophages potentially modulates metainflammation.
Treatment
View SamplesMyeloid leukemia cell lines HL60, THP-1, and U937 undergo macrophage-like differentiation after treatment with phorbol ester.
Ubiquitin-specific protease 2-69 in macrophages potentially modulates metainflammation.
Cell line, Time
View SamplesThe accumulation of intramyocellular lipid (IMCL) is recognized as an important determinant of insulin resistance, and is increased by a high-fat diet (HFD). However, the effects of HFD on IMCL and insulin sensitivity are highly variable.
Increased intramyocellular lipid/impaired insulin sensitivity is associated with altered lipid metabolic genes in muscle of high responders to a high-fat diet.
Sex, Specimen part, Time
View SamplesBreast cancer is a curable disease if it is diagnosed at an early stage. However, only little options are left once the tumor is metastasized to distant organs, and more than 90% of breast cancer death is attributed to metastatic disease. The process of metastasis is highly complex and involves many steps for successful colonization of tumor cells at a target organ. According to the cancer stem cell (CSC) theory, which still remains a hypothesis, these metastatic cells must have stem cell-like capability for their self-renewal in addition to their invasive ability. Therefore, it has been predicted that a metastatic stem cell, which is distinct from a cancer stem cell, must exist in the primary tumor mass. To identify genes that are involved in metastasis of CSCs, we isolated CSC populations from a well-established model cell line of breast cancer, MDA-MB231, and that of highly metastatic variants, 231BoM-1833 and 231BrM-2a, using CD24, CD44 and EpCAM (ESA), which have been identified as surface markers for CSCs in breast cancers. Overall yield of CSCs from these cells ranged from 2% to 4%. We then performed global expression profile analysis for these CSCs using the Affymetrix Human Gene 1.0ST array.
Hyaluronan synthase HAS2 promotes tumor progression in bone by stimulating the interaction of breast cancer stem-like cells with macrophages and stromal cells.
Cell line
View Samples