Gene expression profiling of two different E. coli ABU strains during biofilm growth in human urine.
Global gene expression profiling of asymptomatic bacteriuria Escherichia coli during biofilm growth in human urine.
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View SamplesComparison of gene expression profile of E. coli 83972 grown in minimal lab media, in urine and in 3 individual patients.
Global gene expression profiling of the asymptomatic bacteriuria Escherichia coli strain 83972 in the human urinary tract.
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View SamplesGlobal transcription profiling of E. coli strains CFT073, Nissle 1917 and 83972 grown exponentially in MOPS, exponentially in human urine and in biofilms in human urine.
Comparison of probiotic Escherichia coli Nissle 1917 and 83972, and UPEC strain CFT073: biofilm formation, growth, competition and transcriptomics
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View SamplesInvestigation of lipid metabolism as a function of three experimental factors: 1) aerobicity (aerobic vs anaerobic, or 'A' vs 'O'), 2) nutrient limitation (carbon vs nitrogen limitation, or 'C' vs 'N'), 3) temperature (30C vs 15C, or 'T' vs 't') using a full factorial design.
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View SamplesMicroglia are phagocytic cells that survey the brain and perform neuroprotective functions in response to tissue damage, but their activating receptors are largely unknown. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial immunoreceptor whose loss-of-function mutations in humans cause presenile dementia, while genetic variants are associated with increased risk of neurodegenerative diseases. In myeloid cells, TREM2 has been involved in the regulation of phagocytosis, cell proliferation and inflammatory responses in vitro. However, it is unknown how TREM2 contributes to microglia function in vivo. Here, we identify a critical role for TREM2 in the activation and function of microglia during cuprizone (CPZ)-induced demyelination. TREM2-deficient (TREM2(-/-)) mice had defective clearance of myelin debris and more axonal pathology, resulting in impaired clinical performances compared to wild-type (WT) mice. TREM2(-/-) microglia proliferated less in areas of demyelination and were less activated, displaying a more resting morphology and decreased expression of the activation markers MHC II and inducible nitric oxide synthase as compared to WT. Mechanistically, gene expression and ultrastructural analysis of microglia suggested a defect in myelin degradation and phagosome processing during CPZ intoxication in TREM2(-/-) microglia. These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage.
TREM2 regulates microglial cell activation in response to demyelination in vivo.
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View SamplesE-cadherin, a protein encoded by the CDH1 gene is the dominant epithelial cell adhesion molecule playing a crucial role in epithelial tissue polarity and structural integrity. The progression of 90% or more carcinomas is believed to be mediated by disruption of normal E-cadherin expression, subcellular localization or function. Despite the strong correlation between E-cadherin loss and malignancy the mechanism through how this occurs is not known in most sporadic and hereditary epithelial carcinomas. Previous works have shown the importance of CDH1 intron 2 sequences for proper gene and protein expression supporting the possibility of these being cis-modulators of E-cadherin expression/function. but when co-expressed it led to reduced cell-cell adhesiveness, increased invasion and angiogenesis. By expression array analysis, IFITM1 and IFI27 levels were found to be increased upon CDH1a overexpression. Importantly, CDH1a was found to be de novo expressed in gastric cancer cell lines when compared to normal stomach.
Transcription initiation arising from E-cadherin/CDH1 intron2: a novel protein isoform that increases gastric cancer cell invasion and angiogenesis.
Specimen part, Cell line
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